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首页> 外文期刊>Human and Experimental Toxicology >Novel effect of Daflon and low-dose gamma-radiation in modulation of thioacetamide-induced hepatic encephalopathy in male albino rats
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Novel effect of Daflon and low-dose gamma-radiation in modulation of thioacetamide-induced hepatic encephalopathy in male albino rats

机译:Daflon和低剂量γ-辐射在雄性白化大鼠硫代乙酰胺诱导的肝癌调节中的新疗效

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摘要

This study was designed to evaluate the hepato and neuroprotective activity of Daflon and low-dose gamma radiation on thioacetamide (TAA)-induced liver damage and hepatic encephalopathy (HE) in rats. Effect of daily Daflon treatment (100 mg/kg body weight, Per OS (p.o.) for consecutive 3 days) and/or fractionated low-dose gamma-radiation (LDR; 0.25 Gy, twice the total dose of 0.5 Gy at the 1st and 3rd day, respectively) was evaluated against TAA (300 mg/kg, intraperitoneal x 3) induced liver damage and HE in rats. Serum aspartate transaminase, alanine transaminase, gamma-glutamyltransferase, total bilirubin, ammonia, and manganese were estimated to evaluate liver function. In addition, malondialdehyde (MDA) as well as reduced glutathione (GSH), glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT) were determined to assess antioxidant capacity in liver tissue. Moreover, hepatic apoptotic markers (cysteine-dependent aspartate-directed proteases 3, 8 (caspase-3, 8) and cytochrome C) were estimated to indicate hepatic apoptosis. HE was evaluated through the determination of whole brain ammonia, manganese, MDA, GSH, GPX, SOD, CAT, and caspase-3. The cognitive and locomotor deficits were assessed via step through passive avoidance test, activity cage (actophotometer), gamma-aminobutyric acid, and N-methyl-D-aspartate/adenosine triphosphate-neuronal nitric oxide synthase/nitric oxide-cyclic guanosine monophosphate axis in rats' cerebella and hippocampi. The involvement of hypoxia inducible factor-1 alpha, aquaporine-4, and matrix metalloproteinase 9 in association with the brain water content (%) in the whole brain as an index for brain edema was also evaluated. The obtained results showed a marked amelioration of the aforementioned biochemical parameters and behavioral tasks which is supported by histopathological and immunohistochemical examination. It could be concluded that Daflon and LDR afforded hepatoprotection and neduroprotection against TAA-induced acute liver damage and HE.
机译:本研究旨在评估Daflon和低剂量γ辐射对硫代酰胺(TAA)诱导的肝损伤和肝脑病变(HE)在大鼠中的肝细胞和低剂量γ辐射的神经保护活性。每日Daflon治疗的影响(连续3天/ kg体重,每次(PO))和/或分级低剂量γ-辐射(LDR; 0.25 GY,次数为0.5 GY的两倍)分别评估了TaA(300mg / kg,腹膜内x 3)诱导肝损伤和大鼠的第3天。估计血清天冬氨酸转氨酶,丙氨酸转氨酶,γ-戊二酰转移酶,总胆红素,氨和锰,以评估肝功能。此外,确定丙二醛(MDA)以及还原的谷胱甘肽(GSH),谷胱甘肽过氧化物酶(GPX),超氧化物歧化酶(SOD)和过氧化酯酶(猫),以评估肝组织中的抗氧化能力。此外,估计肝细胞凋亡标记物(依赖于半胱氨酸依赖性天冬氨酸导向的蛋白酶3,8(Caspase-3,8)和细胞色素C)以表明肝细胞凋亡。他通过确定全脑氨,锰,MDA,GSH,GPX,SOD,猫和Caspase-3进行评估。通过步骤通过被动避免试验,活性笼(测距力计),γ-氨基丁酸和N-甲基-D-天冬氨酸/腺苷三磷酸 - 神经元一氧化氮合酶/一氧化氮 - 环状鸟苷一单磷酸盐轴来评估认知和运动运动缺陷大鼠的脑和海马。还评估了缺氧诱导因子-1α,Aquaporine-4和基质金属蛋白酶9与脑水质含量(%)相关联的脑水含量(%)作为脑水肿指数相关联。所得结果表明,上述生化参数和行为任务的显着改善,其由组织病理学和免疫组化检查支持。可以得出结论,Daflon和Ldr提供肝脏应戊二术和NeDuroproctention,免受Taa诱导的急性肝损伤和他。

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