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    Intranasal miRNAs-17/20 Administration Alleviates Early Brain Injury After Subarachnoid Hemorrhage in Rats
    (Springer, 2023) Malcok, U. A.; Doganlar, O.; Tufekcioglu, N. K.; Ovali, M. A.; Aykora, D.; Doganlar, Z. B.; Buyuk, B.
    Early brain injury (EBI) in the first 24-72 h is the leading cause of mortality and disability related to subarachnoid hemorrhage (SAH). Both melatonin and microRNAs (miRs) are involved in the regulation of a number of neuronal molecular signaling procedures in the central nervous system, ranging from hypoxia, inflammation to neuronal apoptosis. The present study was performed to explore the effect of miRs-17/20 and combined treatment with melatonin on early brain injury after SAH and underlying molecular mechanisms in rats. In this study 54 Wistar albino rats were divided into six experimental groups: Sham, SAH, SAH + Melatonin, SAH+miRs-17/20 control, SAH+MEL+miRs-17/20, and SAH+MEL+miRs-17/20. The Garcia's Neurological Scoring Scale and motor coordination tests were used for clinical observation. H&E staining was performed to evaluate pathological score. The gene expression levels were determined by qRT-PCR and key proteins were quantitated by Western blot assay. miRs-17/20 with or without melatonin treatment suppressed the expression and activity of both the HIF1/VEGF/MMPs and the IL6R/JAK2/STAT3 axis. miRs-17/20 with or without melatonin treatment also mitigated the clinical impairment, pyknosis, and edema in the hippocampus and cortex and neurodegeneration induced by SAH. Our results show that miRs-17/20 alleviated EBI by reducing hypoxic conditions, hypoxia-induced molecular signaling, and neuronal apoptosis.
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    Protective effect of an L-type calcium channel blocker, amlodipine, on paracetamol-induced hepatotoxicity in rats
    (Sage Publications Ltd, 2018) Kaya, H.; Polat, B.; Albayrak, A.; Mercantepe, T.; Buyuk, B.
    Paracetamol (P), one of the most popular and commonly used analgesic and antipyretic agents, causes hepatotoxicity in overdoses. Amlodipine (AML), an L-type calcium channel blocker, has been shown to have anti-inflammatory activity by reversing the effect of calcium in the inflammation pathogenesis. In this study, the hepatoprotective activity of AML on P-induced hepatotoxicity was evaluated. Thirty male albino Wistar rats were divided into five groups: (1) control, (2) 2 g/kg of P, (3) 2 g/kg of P + 5 mg/kg of AML, (4) 2 g/kg of P + 10 mg/kg of AML, and (5) 10 mg/kg of AML. Some liver enzymes, oxidative parameters, cytokine mRNA expressions, histopathology, and immunohistochemical studies were performed in liver and blood samples. The serum levels of alanine aminotransferase and aspartate aminotransferase and the mRNA expression of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta in the liver tissues were significantly increased in the group treated with P. The superoxide dismutase and glutathione parameters decreased and malondialdehyde levels increased in the livers of the rats treated with P. All these parameters were increased with both doses of the AML similar to the control group. A histopathological examination of the liver showed that AML administration ameliorated the P-induced inflammatory liver damage. In immunohistochemical staining, the expression of TNF-alpha in the cytoplasm of the hepatocytes was increased in the P group but not in other treatment groups when compared to the control. In conclusion, AML treatment showed significant protective effects against P-induced hepatotoxicity by increasing the activity of antioxidants and reducing inflammatory cytokines.