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Acyclovir provides protection against 6-OHDA-induced neurotoxicity in SH-SY5Y cells through the kynurenine pathway
(Elsevier, 2025) Sezen, Selma; Karadayi, Mehmet; Yesilyurt, Fatma; Burul, Feyza; Gulsahin, Yusuf; Ozkaraca, Mustafa; Okkay, Ufuk
Parkinson's disease is one of the most prevalent neurodegenerative disorders worldwide. The kynurenine pathway associated with oxidative stress and neuroinflammation is recognized to contribute to its pathophysiology, although the exact mechanism is not fully elucidated. In neuroinflammation, IDO-1 catalyzes the conversion of tryptophan to neurotoxic QUIN through the kynurenine pathway. Consequently, QUIN increases oxidative stress via nNOS and NMDA, which causes neurodegeneration. Few studies have reported on the effect of different antiviral drugs in Parkinson's disease; the exact mechanism is still unknown. The antiviral acyclovir has been shown to have neuroprotective properties and can cross the blood-brain barrier. We examined acyclovir's effects and potential mechanisms in the 6-OHDA-induced in vitro model of Parkinson's disease in SHSY5Y cells using biochemical, immunocytochemical, and in silico methods. MTT assay demonstrated that acyclovir significantly decreased cell mortality induced by the neurotoxic 6-OHDA at dosages of 3.2 mu M, 6.4 mu M, 12.8 mu M, 25.6 mu M, and 51.2 mu M. In immunocytochemical analysis, acyclovir treatment decreased alpha-synuclein and TNF-alpha expressions in cells. In biochemical analyses, while IL-17A and TOS levels decreased depending on varying doses (1.6 mu M, 3.2 mu M, 6.4 mu M, 12.8 mu M), TAC levels increased. Using in silico analyses to investigate the mechanism showed that acyclovir docked with TNF-alpha, IL-17A, IDO-1, nNOS, alpha-synuclein, and NMDA. The findings demonstrated that acyclovir had neuroprotective effects by modulating the kynurenine pathway and decreasing neurodegeneration via QUIN inhibition in an in vitro Parkinson's disease model. Although the
Amelioration of oxidative damage parameters by carvacrol on methanol-induced liver injury in rats
(Int Press Editing Centre Inc, 2022) Gursul, Cebrail; Ozcicek, Adalet; Ozkaraca, Mustafa; Mendil, Ali Sefa; Coban, Taha Abdulkadir; Arslan, Aynur; Ozcicek, Fatih
The methanol metabolite that causes hepatotoxicity is formic acid, generating reactive oxygen radical formation and cell damage. Carvacrol is an antioxidant monoterpenic phenol produced from Thymus vulgaris. This study aimed to investigate the effects of carvacrol on methanol-induced oxidative liver damage in rats. Eighteen rats were divided into three groups. Methotrexate was administered orally for 7 days to methotrexate+methanol (MTM) and methotrexate+methanol+carvacrol (MMC) groups. Methotrexate was given before methanol to cause methanol poisoning. Distilled water was given to the healthy group (HG) as a solvent. At the end of the 7th day, 20% methanol was administered orally at a dose of 3 g/kg to the MTM and MMC groups. Four hours after methanol administration, 50 mg/kg carvacrol was injected intraperitoneally into the MMC group. Animals were sacrificed 8 h after carvacrol injection. Biochemical markers were studied in the excised liver tissue and blood serum samples, and histopathological evaluations were made. Severe hemorrhage, hydropic degeneration, pycnosis, and mononuclear cell infiltration were observed in the liver of the MTM group. Additionally, the levels of malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly higher, and total glutathione (tGSH) and total antioxidant status (TAS) were significantly lower in the MTM group compared to HG (P<0.001). Carvacrol prevented the increase in MDA, TOS, ALT and AST levels with methanol and the decrease in tGSH and TAS levels (P<0.001), and alleviated the histopathological damage. Carvacrol may be useful in the treatment of methanol-induced liver damage.
Anticancer activity of lycopene in HT-29 colon cancer cell line
(Humana Press Inc, 2023) Ataseven, Dilara; Ozturk, Aysegul; Ozkaraca, Mustafa; Joha, Ziad
An inverse association between serum lycopene levels and the risk of cancers has been pointed out by many prospective and retrospective epidemiological studies which prompted more studies to be performed on animal models and cell cultures in order to test this hypothesis. The aim of the present study was to evaluate the antiproliferative and pro-apoptotic effect of lycopene on colon cancer HT-29 cell line. The effect of lycopene on the viability of HT-29 cell line was investigated using XTT assay. The levels of Bcl-2, cleaved caspase 3, BAX, cleaved PARP, and 8-oxo-dG in lycopene-treated HT-29 cells were measured using ELISA. Gamma-H2AX and cytochrome c expression was assessed semi-quantitatively using immunofluorescence staining. Lycopene at doses of 10 and 20 mu M produced a significant antiproliferative effect on HT-29 cells compared to the control (p < 0.05). The IC50 value of lycopene in HT-29 cells was found to be 7.89 mu M for 24 h. Lycopene (7.89 mu M) significantly elevated cleaved caspase 3 (p < 0.01), BAX, and cleaved PARP, 8-oxo-dG levels (p < 0.05). The levels of gamma-H2AX foci are significantly higher while the levels of cytochrome-c are lower (p < 0.05) in lycopene-treated HT-29 cells. These results indicate that lycopene has an antiproliferative apoptotic and genotoxic effect on HT-29 colon cancer cell line.
Apoptosis is induced by sub-acute exposure to 3-MCPD and glycidol on Wistar Albino rat brain cells
(Elsevier, 2021) Sevim, Cigdem; Ozkaraca, Mustafa; Kara, Mehtap; Ulas, Nergis; Mendil, Ali Sefa; Margina, Denisa; Tsatsakis, Aristidis
3-chloropropane-1,2-diol (3-MCPD) and its toxic metabolite glycidol were classified by the International Agency for Research on Cancer (IARC) as belonging to group 2B and 2A for humans. This study aimed to determine the sub-acute toxicity of these agents. Rats were exposed to 3-MCPD at 0.87 and 10 mg/kg/bw and glycidol (2,4 and 37,5 mg/kg/bw) for 90 days. miR-21 gene expression levels significantly decreased in all group's cerebellar tissues compared with control. Exposure to 10 mg/kg/bw 3-MCPD showed significant increases in PTEN in brain as compared to control group. The Akt gen expressions were significantly decreased in 3-MCPD and glycidol groups when compared to control group brains. Additionally, Caspase 3 and AIF immunopositivity significantly increased in 3-MCPD high dose and glycidol high dose groups in cerebellum granular layers compared to control. The results of the present study conclude that 3-MCPD and glycidol can induce apoptosis in rat brain tissue.
Ascorbic acid mitigates doxorubicin-induced spleen injury in rats: Histopathological and immunohistochemical insights
(Univ Karachi, 2024) Gezer, Arzu; Ozkaraca, Mustafa; Sari, Ebru Karadag; Bedir, Gursel; Aydin, Pelin; Asker, Hasan; Abd El-Aty, Am
This study assessed the protective potential of ascorbic acid against doxorubicin-induced spleen tissue damage in rats. Twenty-eight male Sprague-Dawley rats were divided into four groups. The control group received saline every other day at a dose of 1mL throughout the experiment. The ascorbic acid group was administered 50mg/kg of ascorbic acid daily for 10 days. The doxorubicin group received a single dose of 15mg/kg of doxorubicin on day 7. The ascorbic acid + doxorubicin group received both 50mg/kg of ascorbic acid daily for 10 days and a single dose of 15mg/kg of doxorubicin on day 7. After the experiment, splenic tissue samples were examined histopathologically and immunohistochemically. Histopathological analysis revealed edema, destruction, and degeneration in the doxorubicin group, but these changes were alleviated in the ascorbic acid-treated group, approaching control group levels. Immunohistochemical analysis showed increased CD4(+) and CD8(+) cell immunopositivity in the ascorbic acid + doxorubicin group compared to the doxorubicin group. Biochemical tests indicated that doxorubicin reduced superoxide dismutase activity and increased malondialdehyde levels, whereas ascorbic acid mitigated these effects. The findings suggest that ascorbic acid may have a protective role against doxorubicin-induced spleen injury in rats.
Ascorbic acid mitigates doxorubicin-induced spleen injury in rats: Histopathological and immunohistochemical insights
(Univ Karachi, 2024) Gezer, Arzu; Ozkaraca, Mustafa; Sari, Ebru Karadag; Bedir, Guersel; Aydin, Pelin; Asker, Hasan; Abd El-Aty, Am
This study assessed the protective potential of ascorbic acid against doxorubicin-induced spleen tissue damage in rats. Twenty-eight male Sprague-Dawley rats were divided into four groups. The control group received saline every other day at a dose of 1mL throughout the experiment. The ascorbic acid group was administered 50mg/kg of ascorbic acid daily for 10 days. The doxorubicin group received a single dose of 15mg/kg of doxorubicin on day 7. The ascorbic acid + doxorubicin group received both 50mg/kg of ascorbic acid daily for 10 days and a single dose of 15mg/kg of doxorubicin on day 7. After the experiment, splenic tissue samples were examined histopathologically and immunohistochemically. Histopathological analysis revealed edema, destruction, and degeneration in the doxorubicin group, but these changes were alleviated in the ascorbic acid -treated group, approaching control group levels. Immunohistochemical analysis showed increased CD4(+) and CD8(+) cell immunopositivity in the ascorbic acid + doxorubicin group compared to the doxorubicin group. Biochemical tests indicated that doxorubicin reduced superoxide dismutase activity and increased malondialdehyde levels, whereas ascorbic acid mitigated these effects. The findings suggest that ascorbic acid may have a protective role against doxorubicin-induced spleen injury in rats.
Assessment of antimicrobial activity and In Vitro wound healing potential of ZnO nanoparticles synthesized with Capparis spinosa extract
(Springer Heidelberg, 2023) Sezen, Selma; Ertugrul, Muhammed Sait; Balpinar, Ozge; Bayram, Cemil; Ozkaraca, Mustafa; Okkay, Irmak Ferah; Hacimuftuoglu, Ahmet
Agents that will accelerate wound healing maintain their clinical importance in all aspects. The aim of this study is to determine the antimicrobial activity of zinc oxide nanoparticles (ZnO NPs) ZnO nanoparticles obtained by green synthesis from Capparis spinosa L. extract and their effect on in vitro wound healing. ZnO NPs were synthesized and characterized using Capparis spinosa L. extract. ZnO NPs were tested against nine ATCC-coded pathogen strains to determine antimicrobial activity. The effects of different doses (0.0390625-20 mu g/mL) of NPs on cell viability were determined by MTT assay. The effect of ZnO NPs doses (0.0390625 mu g/mL, 0.078125 mu g/mL, 0.15625 mu g/mL, 0.3125 mu g/mL, 0.625 mu g/mL, 1.25 mu g/mL) that increase proliferation and migration on wound healing was investigated in an in vitro wound experiment. Cell culture medium obtained from the in vitro wound assay was used for biochemical analysis, and plate alcohol-fixed cells were used for immunohistochemical staining. It was determined that NPs formed an inhibition zone against the tested Gram-positive bacteria. The ZnO NPs doses determined in the MTT test provided faster wound closure in in-vitro conditions compared to the DMSO group. Biochemical analyses showed that inflammation and oxidative status decreased, while antioxidant levels increased in ZnO NPs groups. Immunohistochemical analyses showed increased expression levels of Bek/FGFR2, IGF, and TGF-beta associated with wound healing. The findings reveal the antimicrobial effect of ZnO nanoparticles obtained using Capparis spinosa L. extract in vitro and their potential applications in wound healing.
Assessment of oxidative DNA damage, oxidative stress responses and histopathological alterations in gill and liver tissues of Oncorhynchus mykiss treated with linuron
(Sage Publications Ltd, 2021) Topal, Ahmet; Gergit, Arzu; Ozkaraca, Mustafa
We investigated changes in 8-hydroxy-2-deoxyguanosine (8-OHdG) activity which is a product of oxidative DNA damage, histopathological changes and antioxidant responses in liver and gill tissues of rainbow trout, following a 21-day exposure to three different concentrations of linuron (30 mu g/L, 120 mu g/L and 240 mu g/L). Our results indicated that linuron concentrations caused an increase in LPO levels of liver and gill tissues (p < 0.05). While linuron induced both increases and decreases in GSH levels and SOD activity, CAT activity was decreased by all concentrations of linuron (p < 0.05). The immunopositivity of 8-OHdG was detected in the hepatocytes of liver and in the epithelial and chloride cells of the secondary lamellae of the gill tissues. Our results suggested that linuron could cause oxidative DNA damage by causing an increase in 8-OHdG activity in tissues, and it induces histopathological damage and alterations in the antioxidant parameters of the tissues.
Black Garlic Extract Modulates Endothelin Expression and Ovulatory Function in Monosodium Glutamate Treated Rats
(Wiley, 2025) Gezer, Arzu; Aras, Sukran Yediel; Ozkaraca, Mustafa; Baygutalp, Nurcan Kilic; Gundogdu, Gulhande; Sari, Ebru Karadag; Bedir, Gursel
Monosodium glutamate (MSG), a widely used food additive, has been associated with various health concerns, including potential reproductive toxicity. This study investigated the protective effects of black garlic (BG) ethanol extract against MSG-induced ovarian damage in rats. Thirty-two female rats in estrus were randomly divided into four groups (n = 8 per group): control (saline), BG (250 mg/kg BW), MSG (4 mg/g BW), and BG+MSG (combined treatment). Treatments were administered daily for 14 days. Ovarian tissues were collected for histopathological, immunohistochemical (IHC), and biochemical analyses. Histopathological examination revealed a significant reduction in cystic follicles in the BG+MSG group compared to the MSG group (p < 0.0001). IHC analysis showed decreased immunoreactivity of endothelin-1 and endothelin-2 in the BG+MSG group compared to the MSG group (both p < 0.01). Biochemical assays demonstrated significantly increased follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estradiol levels in the BG+MSG group compared to the MSG group (all p < 0.05), while progesterone levels were significantly lower in the MSG group compared to the BG+MSG group (p < 0.05). These findings suggest that BG ethanol extract may mitigate MSG-induced ovarian dysfunction in rats by alleviating degenerative changes in follicles and modulating hormonal levels. This study provides insights into potential natural interventions for MSG-related reproductive toxicity.
Chlorogenic Acid Attenuates Doxorubicin-Induced Oxidative Stress and Markers of Apoptosis in Cardiomyocytes via Nrf2/HO-1 and Dityrosine Signaling
(Mdpi, 2023) Cicek, Betul; Hacimuftuoglu, Ahmet; Yeni, Yesim; Danisman, Betul; Ozkaraca, Mustafa; Mokhtare, Behzad; Kantarci, Mecit
(1) Background: Doxorubicin (DOX) is extensively used for cancer treatments; however, its clinical application is limited because of its cardiotoxic adverse effects. A combination of DOX and agents with cardioprotective properties is an effective strategy to ameliorate DOX-related cardiotoxicity. Polyphenolic compounds are ideal for the investigation of novel cardioprotective agents. Chlorogenic acid (CGA), an essential dietary polyphenol found in plants, has been previously reported to exert antioxidant, cardioprotective, and antiapoptotic properties. The current research evaluated CGA's in vivo cardioprotective properties in DOX-induced cardiotoxicity and the probable mechanisms underlying this protection. (2) Methods: CGA's cardioprotective properties were investigated in rats that were treated with CGA (100 mg/kg, p.o.) for fourteen days. The experimental model of cardiotoxicity was induced with a single intraperitoneal (15 mg/kg i.p.) injection of DOX on the 10th day. (3) Results: Treatment with CGA significantly improved the DOX-caused altered cardiac damage markers (LDH, CK-MB, and cTn-T), and a marked improvement in cardiac histopathological features accompanied this. DOX downregulated the expression of Nrf2/HO-1 signaling pathways, and the CGA reversed this effect. Consistently, caspase-3, an apoptotic-related marker, and dityrosine expression were suppressed, while Nrf2 and HO-1 expressions were elevated in the cardiac tissues of DOX-treated rats after treatment with the CGA. Furthermore, the recovery was confirmed by the downregulation of 8-OHdG and dityrosine (DT) expressions in immunohistochemical findings. (4) Conclusions: CGA demonstrated a considerable cardioprotective effect against DOX-induced cardiotoxicity. One of the possible mechanisms for these protective properties was the upregulation of the Nrf2/HO-1-dependent pathway and the downregulation of DT, which may ameliorate oxidative stress and cardiomyocyte apoptosis. These findings suggest that CGA may be cardioprotective, particularly in patients receiving DOX-based chemotherapy.
Cilomilast, a PDE4 Inhibitor, Suppresses CD4++ and CD8++ T Cell Proliferation in the Thymus and Spleen of Rats: Mechanism of Glutathione Reduction
(Univ Agriculture, Fac Veterinary Science, 2024) Gezer, Arzu; Baygutalp, Nurcan Kilic; Cengiz, Mustafa; Gur, Bahri; Ozkaraca, Mustafa
Cilomilast is an oral phosphodiesterase-4 (PDE4) inhibitor recommended for treating COPD. However, its side effects and low therapeutic index remain an unresolved problem in clinical practice. This study aimed to evaluate the effects of cilomilast on the spleen and thymus tissues of rats. For experimental studies, 24 male Sprague-Dawley rats weighing 200-220g were randomly divided into three experimental groups: The procedures were repeated for 7 days for the control, sham, and cilomilast groups. Blood and tissue samples were collected from the rats under anesthesia on day 8 of the experiment for analysis. p<0.05 at a 95% confidence level was considered to indicate statistical significance. Severe tissue damage in the thymus and spleen was observed in the cilomilast group. In the thymus and spleen tissues of the control and sham groups, CD4+ + and CD8+ + cell immunopositivity were more intense, while the density of these cells was significantly reduced in the cilomilast group. In addition, glutathione (GSH) levels decreased, and nitric oxide levels increased in both tissues of the cilomilast group. However, in-silico results showed that the decrease in GSH levels is due to the enzymes gamma-glutamylcysteine synthase and glutathione synthase, which act as catalysts in the two-step GSH biosynthesis mechanism. Suppression of the immune system targets both harmful and compensatory pathways so that both beneficial mechanisms and pathological changes can be blocked. To eliminate these cilomilast-induced side effects and enable more effective clinical application, it may be recommended to develop formulations such as lipid-based inhaled forms or nano-drug delivery systems including dendrimers, reverse micelle systems, polymeric or lipid-based carriers as an alternative to conventional application.
Development and in vitro characterization nanoemulsion containing the methanol extract of Hypericum linarioides for wound healing: In vitro scratch assay
(Elsevier, 2024) Kaplan, Afife Busra Ugur; Yesilyurt, Fatma; Guven, Leyla; Cetin, Meltem; Lacin, Burak Batuhan; Ozkaraca, Mustafa; Yilmaz, Mustafa Abdullah
It was aimed to develop and in vitro characterize the methanol extract of Hypericum linarioides (MHL)-containing nanoemulsion formulation (MHL-NEF) to heal the wound effectively. MHL-NEF was prepared and its droplet size, polydispersity index (PDI), viscosity, pH and zeta potential (ZP) values were determined. The effect of MHL and MHL-NEF on human dermal fibroblast cell viability was examined by MTT assay. Also, their wound healing potential was evaluated using the scratch assay. The droplet size, PDI, ZP, pH and viscosity values for the MHL-NEF were found to be 157.67 +/- 7.61 nm, 0.268 +/- 0.036, (-)40.20 +/- 6.79 mV, 4.27 +/- 0.01, and 1.82 +/- 0.01 cP, respectively. In the cell viability assay, the highest percentage of living cells was obtained at concentration of 0.4 mu g/mL for the MHL and MHL-NEF. In the scratch assay, MHL-NEF showed significantly ameliorated wound closure (%) rates at 24 and 30 h than the groups of control, MHL and blank-NEF (NEF without MHL) (p < 0.001). Immunofluorescence staining was carried out. TGF-beta 1 and FGFR-2 expressions in MHL-NEF-treated fibroblast cells increased significantly at 24 h compared to the groups of control, MHL, and B-NEF (p < 0.001). Our findings show that MHL-NEF may be promising for better wound healing. (c) 2024 SAAB. Published by Elsevier B.V. All rights reserved.
Docosahexaenoic acid eliminates endoplasmic reticulum stress and inflammatory pathways in diabetic rat keratopathy
(Elsevier, 2024) Gezer, Arzu; Ozkaraca, Mustafa; Ustundag, Hilal; Soydan, Menekse; Alkanoglu, Omer; Bedir, Gursel
Diabetic keratopathy, characterized by corneal structural changes, is a common complication of diabetes mellitus (DM). Docosahexaenoic acid (DHA), an omega-3 fatty acid, has shown potential therapeutic benefits in various diabetic complications. This study aimed to investigate the protective effect of DHA on corneal tissue in streptozotocin (STZ)-induced type 2 DM in rats. Forty male Sprague-Dawley rats were randomly assigned to four groups (n = 10 per group): Control, DHA, DM, and DM + DHA. The DHA group received DHA by oral gavage at a dose of 100 mg/kg daily for 10 days. In the DM group, diabetes was induced by a single intraperitoneal injection of STZ at 50 mg/kg. Confirmation of diabetes induction was based on monitoring fasting blood glucose levels on the third day post-injection. The DM + DHA group underwent the same diabetes induction protocol with STZ and received DHA at 100 mg/kg daily via oral gavage for 10 consecutive days. Corneal tissue samples were collected at the end of the study period for histopathological, immunohistochemical, qRT-PCR, and ELISA analyses. Histopathological analysis showed significant edema, angiogenesis, and degeneration in the DM group compared to the control (p < 0.001). DHA treatment significantly mitigated these changes, approaching control levels (p < 0.01). Immunohistochemistry showed increased VEGFR2 and iNOS expression in the DM group, which was significantly reduced in the DM + DHA group (p < 0.01). qRT-PCR results indicated a significant decrease in Bcl-2 expression (p < 0.001) and an increase in ATF-6, IRE1, NF-kappa B, TNF-alpha, IL-1 beta, NLRP3, Bax, and Caspase-3 expressions in the DM group (p < 0.001). ELISA analyses revealed significantly elevated levels of inflammatory markers NF-kappa B, TNF-alpha, IL-1 beta, and IL-6 in the DM group compared to the control (p < 0.001). DHA treatment significantly upregulated Bcl-2 and downregulated apoptotic and inflammatory markers (p < 0.01). DHA demonstrated significant protective effects against STZ-induced corneal damage in diabetic rats by modulating apoptotic and inflammatory pathways. These findings suggest that DHA may be a promising therapeutic agent for preventing diabetic keratopathy.
Dose-Dependent Pulmonotoxic Effects of Favipiravir in Rats Biochemical and Histopathological Evaluation
(Asian Network Scientific Information-Ansinet, 2025) Suleyman, Zeynep; Altuner, Durdu; Suleyman, Halis; Coban, Taha Abdulkadir; Ozkaraca, Mustafa
Background and Objective: Favipiravir is associated with more serious side effects at higher doses. This experimental study proposed to investigate the effect of favipiravir on dose-dependent lung toxicity in rats biochemically and histopathologically. Materials and Methods: The rats were divided into four groups as healthy (HG), 100 mg/kg favipiravir (FAV-100), 200 mg/kg favipiravir (FAV-200) and 400 mg/kg favipiravir (FAV-400). Favipiravir 100, 200 and 400 mg/kg doses were administered by oral gavage to the other groups except HG. To the HG group, only distilled water (0.5 mL) was applied in the same way. This procedure was repeated twice a day for a week. Then, the rats were euthanised with high-dose anaesthesia and lung tissues were removed. Oxidative stress parameters such as malondialdehyde (MDA), Total Glutathione (tGSH), superoxide dismutase (SOD), total oxidant status (TOS) and total antioxidant status (TAS) were examined. After the one-way ANOVA, the Tukey's post hoc test was performed. Results: Favipiravir dose-dependently increased MDA and TOS also decreased tGSH, SOD and TAS in rat lung tissue. As favipiravir was given in increasing doses, it was easier to observe the changes between the different groups. This was also supported by the histopathological data. Histopathologically, interstitial pneumonia and lymphoid hyperplasia were mild in the 100 mg/kg favipiravir group, severe at high doses. Conclusion: As the dose of favipiravir increased, oxidant levels increased and antioxidant levels decreased in the lung tissue. In line with these results, it was observed that favipiravir caused a dose-dependent pulmonotoxic effect in rats.
Early administration of milrinone ameliorates lung and kidney injury during sepsis in juvenile rats
(Wiley, 2022) Keskin, Halil; Tavaci, Taha; Halici, Hamza; Yuksel, Tugba Nurcan; Ozkaraca, Mustafa; Bilen, Arzu; Kose, Duygu
Background A sepsis model was created, induced by cecal ligation and puncture (CLP), in juvenile rat groups. Milrinone (MIL), which is known to have a modulatory effect on pro-inflammatory cytokines, was administered to the designated rat groups in the early period before severe sepsis developed. The study was aimed at investigating the possible protective effects of milrinone on the lung and kidney tissues of rats in the late phase of sepsis. Methods The rat pups were divided into seven groups with six animals in each group: (1) healthy rats who received no drug; (2) CLP-S12 (sacrificed at hour 12); (3) CLP-S24 (sacrificed at hour 24); (4) CLP-MIL1-S12 (administered with 0.5 mg/kg milrinone at hour 1 and sacrificed at hour 12); (5) CLP-MIL1-S24 (administered with 0.5 mg/kg milrinone at hour 1 and sacrificed at hour 24): (6) CLP-MIL12-S24 (administered with 0.5 mg/kg milrinone at hour 12 and sacrificed at hour 24), (7) and CLP-MIL1,12-S24 (administered with 0.5 mg/kg milrinone at hours 1 and 12 and sacrificed at hour 24). Results Significant differences were found between the early and late administration of milrinone in terms of both molecular and histopathological results. The results showed that the tissues were significantly preserved in the groups in which milrinone had been started in the early period compared to the sepsis control groups and the groups in which milrinone had been started in the late period. Conclusions In addition to the positive inotropic effects of milrinone, its immunomodulatory properties that result in decreased cytokine storm can be beneficial during early period of sepsis.
Effect of Astragalus microcephalus wild extract and Vitamin E–Selenium combination on Cadmium–induced damage in rat ovaries
(Universidad del Zulia, Facultad de Ciencias Veterinarias, 2024) Kurt, Begum; Kara, Haki; Sahın, Mahmut; Kumru, Alper Serhat; Ozkaraca, Mustafa
This study was conducted to investigate the protective effect of Astragalus (AST) extract alone and in combination with vitamin E (vit E) + selenium (Se) against the toxicity induced by cadmium (CdCl2) in rat ovaries. Thirty–six female Wistar rats were divided into six groups. AST was administered at a dose of 5 mg·kg-1, Cd at a dose of 2 mg·kg-1, and Vit E (60 mg·kg-1) + Se (1 mg·kg-1) orally for a duration of 15 days. The levels of MDA, GSH–Px, SOD, and CAT were analyzed in the blood and tissue samples to assess oxidative stress. Additionally, the levels of estrogen, FSH, LH, Inhibin B, and Antimullerian hormones were measured in the serum samples. The ovarian tissues were examined histopathologically and immunohistochemically for 8–OhDG, Caspase 3, and LC3B immunoreactivity. In the group exposed to CdCl2, MDA levels significantly increased, while antioxidant parameters showed significant decreases (P<0.05). Although significant improvements were observed in the groups treated with AST alone, more significant improvements were seen in the groups treated with both AST and Vit E + Se (P<0.05). It was concluded that AST extracts alone and in combination with Vit E + Se exhibited protective effects against ovarian toxicity caused by Cd exposure and may be effective against metal toxicity. © (2024), (Universidad del Zulia, Facultad de Ciencias Veterinarias). All rights reserved.
Effect of taxifolin on acrylamide-induced oxidative and proinflammatory lung injury in rats: Biochemical and histopathological studies
(Pharmacotherapy Group, 2022) Demir, Omer Faruk; Elma, Bekir; Suleyman, Bahadir; Ozkaraca, Mustafa; Mammadov, Renad; Suleyman, Halis; Coban, Taha Abdulkadir
Purpose: To examine the probable beneficial effects of taxifolin against acrylamide damage in lung tissue. Methods: 18 male albino Wistar rats were divided into healthy (HG), acrylamide (AG) and taxifolin + acrylamide (TAG) groups. Once a day for 30 days, acrylamide was orally administered to the AG group (50 mg/kg), while ACL (50 mg/kg) and TAX (20 mg/kg) were orally administered to TAG group. Protein concentration, malondialdehyde (MDA), and total glutathione (tGSH) levels as well as oxidant and antioxidant molecules concentrations of the rat lung tissues were measured. In addition, degree of mononuclear (MN) cell infiltration and bronchial-associated lymphoid tissue (BALT) hyperplasia was evaluated by the degree of hyperplasia (absent, mild, moderate, severe). The histopathological and biochemical data the groups were compared. Results: When compared in terms of MDA levels, it was found that the AG group had high MDA levels, and the TAG group had low MDA levels. (p < 0.001). TAG group was found to have a higher tGSH level than the AG group (p < 0.001). Compared to the AG group, lower TOS and higher TAS levels were obtained in the TAG group (p < 0.001). In addition, when TOS levels of TAG and HG groups were compared, the TOS levels between the two groups were statistically insignificant (p = 0.213). It has been observed that TAX administration prevents the increase in NF-KB level. When the NF-KB levels of the AG and TAG groups were compared with each other, there was a statistically significant difference (p = 0.001). In the AG group, severe MN cell hyperplasia and BALT hyperplasia were observed histopathologically. It was determined that these findings were alleviated in the TAG group. A histopathologically significant difference was found between AG and TAG groups (p < 0.05). Conclusion: Taxifolin has beneficial effects against lung injury caused by acrylamide, a health damaging environmental factor. Regular use of taxifolin can be recommended, especially in people who are known to have intense contact with acrylamide. There is a need for research studies on this subject.
Effects of dexpanthenol on 5-fluorouraci-induced nephrotoxicity, hepatotoxicity, and intestinal mucositis in rats: a clinical, biochemical, and pathological study
(Walter De Gruyter Gmbh, 2025) Tastemur, Seyma; Ekici, Mehmet; Mendil, Ali Sefa; Ozkaraca, Mustafa; Ataseven, Hilmi
Background5-fluorouracil (5-FU) is a broad-spectrum drug that has a wide range of side effects. Patients may experience severe comorbidities as a result of these toxic side effects, making it impossible for them to continue chemotherapy. Despite the fact that various molecules have been experimented, there is no literature data on the efficacy of dexpanthenol (DXP) for mitigating the toxic effects of 5-FU.ObjectiveTo investigate the protective effects of DXP on nephrotoxicity, hepatotoxicity, and intestinal toxicity induced by 5-FU in rats.MethodsTwenty-eight male Wistar-Albino rats aged 16 weeks were randomly assigned to four groups. We created a rat model of intestinal mucositis, nephrotoxicity, and hepatotoxicity through intraperitoneal 5-FU (35 mg/kg for 4 d) injection. 500 mg/kg and 1000 mg/kg of DXP were administered to the treatment groups. The effects of dexpanthenol were evaluated clinically, biochemically, histopathologically, and immunohistochemically (inducible nitric oxide synthase [iNOS], cyclooxygenase-2 [COX-2], 8-hydroxyguanosine [8-OHdG], and nuclear factor kappa B [NF-kappa B]).Results5-FU caused a decrease in body weight and food intake, and an increase in diarrhea scores in rats. 5-FU led to significant disruptions in the hepatic biochemical markers (aspartate transaminase [AST], alanine transaminase [ALT], alkaline phosphatase [ALP], total bilirubin, direct bilirubin, and lactate dehydrogenase [LDH]), renal biochemical markers (blood urea nitrogen [BUN], creatinine, and uric acid), and protein and albumin, which are markers of both hepatic and renal functions. Severe pyknosis and mononuclear cell infiltrations were observed in the liver, and mononuclear cell infiltration and tubular degeneration in the kidneys. Jejunum and colon showed villous hyperemia and hemorrhage, respectively, along with mononuclear cell infiltration. Furthermore, 5-FU increased the immunohistochemical expressions of iNOS, COX-2, 8-OHdG, and NF-kappa B in the examined tissues. The administration of DXP at doses of 500 mg/kg and 1000 mg/kg demonstrated significant mitigation of the toxic effects induced by 5-FU on the liver, kidney, jejunum, and colon.ConclusionDXP showed protective effects against nephrotoxicity, hepatotoxicity, and intestinal toxicity caused by 5-FU. These findings suggest that DXP may serve as a potential therapeutic agent to alleviate the severe side effects of 5-FU chemotherapy, thereby improving patient tolerance and quality of life. Further clinical studies are warranted to validate these results and explore the translational potential of DXP in human cancer therapy.
Evaluated periodontal tissues and oxidative stress in rats with neuropathic pain-like behavior
(Springer, 2023) Toraman, Ayse; Toraman, Emine; Ozkaraca, Mustafa; Budak, Harun
Background Oxidative stress has a critical effect on both persistent pain states and periodontal disease. Voltage-gated sodium NaV1.7 (SCN9A), and transient receptor potential ankyrin 1 (TRPA1) are pain genes. The goal of this study was to investigate oxidative stress markers, periodontal status, SCN9A, and TRPA1 channel expression in periodontal tissues of rats with paclitaxel-induced neuropathic pain-like behavior (NPLB). Methods and results Totally 16 male Sprague Dawley rats were used: control (n=8) and paclitaxel-induced pain (PTX) (n=8). The alveolar bone loss and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels were analyzed histometrically and immunohistochemically. Gingival superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities (spectrophotometric assay) were measured. The relative TRPA1 and SCN9A genes expression levels were evaluated using quantitative real-time PCR (qPCR) in the tissues of gingiva and brain. The PTX group had significantly higher alveolar bone loss and 8-OHdG compared to the control. The PTX group had significantly lower gingival SOD, GPx and CAT activity than the control groups. The PTX group had significantly higher relative gene expression of SCN9A (p=0.0002) and TRPA1 (p=0.0002) than the control in gingival tissues. Increased nociceptive susceptibility may affect the increase in oxidative stress and periodontal destruction. Conclusions Chronic pain conditions may increase TRPA1 and SCN9A gene expression in the periodontium. The data of the current study may help develop novel approaches both to maintain periodontal health and alleviate pain in patients suffering from orofacial pain.
Exploring the anti-inflammatory activity of boron compounds through the miR-21/PTEN/AKT pathway in cecal ligation and puncture-induced sepsis
(Spandidos Publ Ltd, 2025) Sevim, Cigdem; Ozkaraca, Mustafa; Kara, Mehtap; Taghizadehghalehjoughi, Ali; Genc, Sidika; Yeni, Yesim; Mendil, Ali Sefa
The present study investigated the impact of boric acid (BA) and borax (BX) on markers of inflammation and modifications in miR-21/PTEN/AKT pathway genes in the liver and kidney tissues of Sprague Dawley male rats with sepsis induced by cecal ligation and puncture (CLP). A total of 60 male Sprague Dawley rats were randomly divided into 6 groups, each containing 10 animals as follows: Control, CLP (where the model was created), 20 mg/kg BX (CLP + BX1), 40 mg/kg BX (CLP + BX2), 20 mg/kg BA (CLP + BA1) and 40 mg/kg BA (CLP + BA2). Liver and kidney tissues were analyzed for histopathological changes, immunopositivity for tumor necrosis factor-alpha, interleukin (IL)-6 and IL-10, and gene expression of microRNA-21 (miR-21), phosphatase and tensin homolog (PTEN) and AKT. Gene expression analysis in the liver tissues revealed a significant decrease in miR-21, and a marked but not significant decrease in PTEN levels in the CLP group, while AKT expression was significantly increased in the CLP group, and was significantly decreased in CLP + BA1 group compared with in the CLP group. In the kidney tissues, miR-21 levels were significantly decreased in the CLP group, but the CLP + BA2 group showed a significant increase compared with in the CLP group. These results suggest the potential therapeutic benefits of low-dose BA and BX in ameliorating sepsis-induced tissue damage, emphasizing the need for further exploration of their mechanisms of action.

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