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    Effect of Pantoprazole, a Proton Pump Inhibitor, on Morphine Tolerance in Rats
    (Maik Nauka/Interperiodica/Springer, 2024) Sahin, Bilal; Gunes, Handan
    Pantoprazole's neuroprotective effects and its role in altering processes linked to apoptosis, inflammation, and oxidative stress were demonstrated. Consequently, this study aimed to explore how pantoprazole influences the development of morphine tolerance and the associated mechanisms, including apoptosis, oxidative stress, and inflammation. Six groups of rats were created: saline, 10 mg/kg pantoprazole, 5 mg/kg morphine, morphine tolerance, morphine + pantoprazole, and morphine tolerance + pantoprazole. Hot plate and tail-flick tests were utilized to detect the analgesic effect. Following the analgesic tests, samples of the dorsal root ganglion (DRG) tissues were collected. Oxidative stress parameters (total oxidant status, total antioxidant status), inflammation parameters (Pro-IL-1 beta, IL-1 beta, NLRP-3), and apoptosis proteins (Caspase-1, Caspase-3, Capsape-9) were detected in dorsal root ganglions (DRG) tissues. Pantoprazole showed a weak but statistically significant analgesic activity when given alone. Furthermore, pantoprazole potentiated the antinociceptive effect of morphine and prevented the development of tolerance to morphine. Moreover, it increased total antioxidant status and decreased total oxidant status as well as caspase-1 when given with single-dose morphine and after tolerance induction. Furthermore, pantoprazole decreased Pro-IL-1 beta, IL-1 beta, Caspase-3 and Capsape-9 levels after tolerance development. Collectively, pantoprazole produces a weak analgesic activity and boosts the morphine's analgesic effect. On the other hand, pantoprazole can prevent tolerance development. These effects likely arise through the modulation of pathways associated with oxidative stress, inflammation and apoptosis pathways.
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    Protective Effect of Melatonin and Mycophenolate Mofetil Against Nephrotoxicity Induced by Tacrolimus in Wistar Rats
    (Kafkas Univ, Veteriner Fakultesi Dergisi, 2022) Koc, Suleyman; Aktas, Ahmet; Sahin, Bilal; Ozkaraca, Mustafa
    Although Tacrolimus (TAC) is a potent and well-tolerated drug, it has some side effects. Melatonin and mycophenolate mofetil (MMF) have some protective properties against drug-induced damage. We aimed to evaluate TAC-induced nephrotoxicity and the protective effect of melatonin and MMF against this injury in rats. The animals were divided into five equal groups (n): Control group (untreated), group II TAC, group III as the TAC + melatonin, group IV as the TAC + MMF, and group V as the TAC + melatonin + MMF. TAC was applied orally, 2 mg/kg once daily. Melatonin and MMF were applied orally 10 mg/kg once and 40 mg/kg once daily, respectively. In the TAC group, kidney tissue malondialdehyde (MDA), total oxidative status (TOS), interleukin-1, and tumor necrosis factor-alpha levels were higher, and catalase and total antioxidant status (TAS) levels were lower. Severe histopathologic changes such as glomerular congestion, intertubular hemorrhage, hyaline formation, degenerative-necrotic tubules epithelium, and mononuclear cell infiltration were seen in the TAC group. There was a clear improvement in the groups in which melatonin and MMF were used together with TAC. It was shown that TAC causes nephrotoxicity through oxidative stress. Melatonin and MMF together or separately protect the kidney against oxidative stress damage caused by TAC.
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    Protective effect of ursodeoxycholic acid and resveratrol against tacrolimus induced hepatotoxicity
    (Taylor & Francis Ltd, 2023) Koc, Suleyman; Aktas, Ahmet; Sahin, Bilal; Ozer, Hatice; Zararsiz, Gozde Erturk
    Tacrolimus (TAC) is a potent and well-tolerated immunosuppressive drug, but serious side effects including nephrotoxicity and hepatotoxicity have been reported. Ursodeoxycholic acid (UDCA) and resveratrol (RSV) exhibit hepatoprotective effects in liver diseases. We investigated the hepatoprotective effect of UDCA and RSV against TAC induced hepatotoxicity. We divided 40 male rats into five equal groups: A) control group, B) TAC group, C) TAC + UDCA group, D) TAC + RSV group, E) TAC + UDCA + RSV group. We administered 0.5 mg/kg TAC once daily, 25 mg/kg UDCA twice daily and 10 mg/kg RSV once daily. The drugs in the experimental groups were given by gavage from the first day of the study and continued for 21 days. Histopathologic and biochemical analyses were performed on day 22. In group B, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-alpha (TNF), interleukin-1 (IL-1), interleukin-6 (IL-6), total oxidative status (TOS) and malondialdehyde (MDA) levels were higher compared to group A, and catalase (CAT), superoxide dismutase (SOD) levels and total antioxidant status (TAS) were lower compared to group A. Severe cellular swelling, degeneration and focal necrosis were more evident in group B than in groups C-E. Histopathological improvement was observed in groups C-E, where UDCA and RSV were combined, compared to group B. We found that UDCA and RSV, together or separately, protected the liver against oxidative stress damage caused by TAC.
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    The Effects of Proton Pump Inhibitors (Pantoprazole) on Pentylenetetrazole-Induced Epileptic Seizures in Rats and Neurotoxicity in the SH-SY5Y Human Neuroblastoma Cell Line
    (Springer/Plenum Publishers, 2021) Taskiran, Ahmet Sevki; Ergul, Mustafa; Gunes, Handan; Ozturk, Aysegul; Sahin, Bilal; Ozdemir, Ercan
    Recent studies have shown that proton pump inhibitors have positive effects on the nervous system. However, its effect on epileptic seizure and neuronal damage are still unclear. In this study, it was aimed to investigate the effect of pantoprazole on pentylenetetrazole-induced epileptic seizures in rats and neurotoxicity in the SH-SY5Y cell line. Animals were divided into three groups: control, saline (1 mL/kg serum physiologic), and pantoprazole (10 mg/kg). Pentylenetetrazole (45 mg/kg) was given to induce a seizure and a passive avoidance test trial was carried out to evaluate memory function. 8-hydroxy-2 '-deoxyguanosine (8-OHdG), caspase-3, and brain-derived neurotrophic factor (BDNF) levels were measured in the brain by commercial kits. SH-SY5Y cells were treated with saline or pantoprazole for one hour, and then pentylenetetrazole (30 mu m) was added to the medium to induce neurotoxicity. After 24 h, cell viability, total antioxidant, total oxidant status, and apoptosis were measured in SH-SY5Y cells. It was found that pantoprazole treatment postponed epileptic seizure onset, protected memory, reduced 8-OHdG, caspase-3, and also increased BDNF in the brain. In addition, it blocked pentylenetetrazole toxicity, apoptosis, increased antioxidant, and decreased oxidant status in SH-SY5Y cells. Pantoprazole significantly improved seizure, oxidative stress, and apoptosis. Thus, pantoprazole could be used as a supportive therapeutic agent in epilepsy.
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    The Role of Nitric Oxide Pathway in the Anti-Epileptogenic Effect of Valproic Acid in the Pentylenetetrazole-Kindling Model in Rats
    (Maik Nauka/Interperiodica/Springer, 2023) Sahin, Bilal; Filiz, Ahmet Kemal; Joha, Ziad
    Though valproic acid (VPA) is used to treat seizures, more investigations have been needed to understand the effect of VPA on the nitric oxide pathway in epilepsy. Our investigation aimed to study the effect of VPA on cortical and hippocampal NOS isomers in epileptogenesis processes in the PTZ kindling model of epilepsy in the rat to reveal its mechanisms of action. Twenty-four male Wistar albino rats were used in this study. The animals were divided into four groups control, PTZ without VPA, and PTZ with VPA at two doses (100 and 200 mg/kg) Rats were kindled by injections of PTZ (35 mg/kg) with drugs or vehicle 30 minutes before, once every other day for 12 times and their behavior was observed. After completing the epileptic model process, nitric oxide pathway markers (eNOS, nNOS, iNOS, and NO) in the cortex and hippocampus were assessed by using ELISA methods. VPA suppressed seizure stages and decreased nNOS, iNOS, and NO levels while increasing eNOS levels in the hippocampus and cerebral cortex. The effect of VPA on nitric oxide pathway was found to contribute to its anti-epileptic activity.
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