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    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.
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    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.
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    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.
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    Nobiletin reduces 5-FU-induced lung injury with antioxidative, anti-inflammatory and anti-apoptotic activities
    (Springer, 2025) Uslu, Gozde Atila; Uslu, Hamit; Coban, Taha Abdulkadir; Ozkaraca, Mustafa; Mendil, Ali Sefa; Aygormez, Serpil
    Like other chemotherapeutic agents, 5-fluorouracil (5-FU) targets cancerous cells, but it also causes many unwanted side effects on healthy tissues and cells. Based on the undesirable effects of 5-FU, the aim of this study was to determine how 5-FU affects lung tissue and whether nobiletin has any protective effect. The study consisted of negative control, Nobiletin, 5-FU and Nobiletin + 5-FU groups. Nobiletin and Nobiletin + 5-FU groups received 10 mg/kg Nobiletin i.g. for 7 days. On day 8, 100 mg/kg 5-FU was administered i.p. to 5-FU and Nobiletin + 5-FU groups. Biochemical and immunohistochemical analyses were performed on the lung tissues dissected at the end of the study. 5-FU caused growth retardation, disturbed the oxidant-antioxidant balance by increasing MDA levels and decreasing GSH levels, triggered cellular apoptosis by increasing Bax and caspase-3 levels and decreasing Bcl-2, also increased lung tissue inflammation and damage by increasing NF kappa B and IL-1 beta levels. However, it was determined that Nobiletin prevented the disruption of the oxidant-antioxidant balance, showed significant anti-apoptotic effects, especially by reducing Bax levels and partially modulating caspase-3 and Bcl-2 levels, and also exhibited anti-inflammatory effects by reducing NF kappa B and IL-1 beta levels and supported the normal development of animals. Our results showed that nobiletin pretreatment showed anti-inflammatory activity by inhibiting the NF kappa B pathway in 5-FU-induced lung injury, suppressed oxidative stress with its antioxidant activity and was effective in modulating cellular apoptosis with its anti-apoptotic activity. In conclusion, Nobiletin has been shown to have an important potential in reducing fluorouracil-induced tissue damage by acting through multiple pathways.
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    The Effect of Adenosine Triphosphate, Benidipine, Sugammadex, and their Combinations upon Cardiac Damage after Temporary Clamping of the Abdominal Aorta in Rats
    (Colegio Farmaceuticos Provincia De Buenos Aires, 2022) Emir, Izzet; Altuner, Durdu; Gulaboglu, Mine; Coban, Taha Abdulkadir; Suleyman, Bahadir; Mammadov, Renad; Ozkaraca, Mustafa
    The aim of our study was to biochemically and histopathologically investigate the protective effect of adenosine triphosphate (ATP), benidipine, sugammadex and (ATP + benidipine + sugammadex) ABS against cardiac damage induced by abdominal clamping and unclamping (ACU) procedure in rats. Rats utilized were divided into six groups as Healthy (HG), Abdominal ACU (AACC), ATP + AACU (ATPG), Benidipine + AACU (BNDG), Sugammadex + AACU (SDXG), ABS + AACU (ABSG). One hour before anesthesia, ATP (25 mg/kg; ip) was administered to the ATPG group, Benidipine (4 mg/kg orally) was administered to the BNDG group, Sugammadex (4 mg/kg ip) was administered to the SDXG and ABS was administered with this specified dose and method to the ABSG group. Distilled water as a solvent was injected to AACC and HG groups. One hour after, laparotomy was performed to the rats, and the abdominal cavity was reached. Ischemia was provided for one hour and then reperfusion for 2 h placing an atraumatic clamp on the suprarenal abdominal aorta of the animals in all groups (except from the HG). The heart tissues extracted from the killed animals were examined biochemically and histopathologically. ATP and benidipine suppressed the increase of oxidant and proinflammatory cytokines better than sugammadex. The ABSG group was found to be almost the same as the healthy group biochemically and histopathologically (p > 0.05). ABS drug form alone was possible to be much more beneficial rather than ATP, benidipine and sugammedex in the treatment of cardiac damage induced by AACU procedure.