首页> 外文期刊>Drug delivery. >Hepatoprotective and neuroprotective activity of liposomal quercetin in combating chronic arsenic induced oxidative damage in liver and brain of rats.
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Hepatoprotective and neuroprotective activity of liposomal quercetin in combating chronic arsenic induced oxidative damage in liver and brain of rats.

机译:脂质体槲皮素抗击慢性砷诱导的大鼠肝脏和脑部氧化损伤的肝保护和神经保护活性。

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CONTEXT: Arsenic is a naturally occurring toxicant that causes acute and chronic adverse health effects, including cancer. OBJECTIVE: The study was performed to evaluate the therapeutic efficacy of liposome entrapped flavonoidal quercetin in combating arsenic toxicity mediated oxidative damage in hepatocytes and brain cells in rat model. MATERIALS AND METHODS: Hepatic and neuronal cell damage in rats was made by daily arsenic (6 mg/kg b wt, 9 mg/kg b wt and 12 mg/kg b wt) treatment via oral route for four consecutive months. Liposomal quercetin (2.71 mg QC/kg b. wt) were injected s.c. on rats treated with 12 mg/kg b. wt. NaAsO(2) twice a week for four months. RESULTS AND DISCUSSION: Inorganic arsenic deposition was found to be most significant in hepatic (9.32 +/- 0.100 microg/g tissue) and neuronal (6.21 +/- 0.090 microg/g tissue) cells of rats treated with 12 mg/kg b wt of arsenite. Antioxidant levels in hepatic and neuronal cells were reduced significantly by the induction of arsenic. Liposomal quercetin was found most potent for a complete prevention of arsenite-induced reduction in antioxidant levels in the liver and brain of rats. Arsenic induced a substantial increase in hepatic hydroxyproline (HP) and Liposomal quercetin treatment resulted in complete replenishment of the HP level to normal. Liposomal quercetin completely prevented the arsenite-induced upregulation of cytochrome c expression in liver and brain significantly suggesting that the protective effect of Liposomal quercetin could be related to the reduction of arsenic deposition in both the organs. CONCLUSION: Thus, Liposomal quercetin might prove to be of therapeutic potential against arsenite-induced hepatic and neuronal cell damage in rats.
机译:上下文:砷是一种天然毒物,会引起包括癌症在内的急性和慢性不利健康影响。目的:研究脂质体包裹的类黄酮槲皮素在大鼠模型中对抗砷毒性介导的肝细胞和脑细胞氧化损伤的治疗效果。材料与方法:连续四个月每天口服砷(6 mg / kg b wt,9 mg / kg b wt和12 mg / kg b wt)对大鼠的肝和神经细胞造成损害。皮下注射槲皮素(2.71 mg QC / kg b.wt)。在接受12 mg / kg的大鼠身上b。重量NaAsO(2)每周两次,持续四个月。结果与讨论:在用12 mg / kg b wt处理的大鼠的肝(9.32 +/- 0.100 microg / g组织)和神经元(6.21 +/- 0.090 microg / g组织)细胞中,无机砷沉积最为明显亚砷酸盐。诱导砷可显着降低肝细胞和神经元细胞的抗氧化水平。发现脂质体槲皮素最有效地完全预防砷引起的大鼠肝脏和大脑中抗氧化剂水平的降低。砷诱导肝羟脯氨酸(HP)大量增加,脂质体槲皮素治疗可将HP水平完全补充至正常水平。脂质体槲皮素完全阻止了砷诱导的肝脏和大脑中细胞色素c表达的上调,这表明脂质体槲皮素的保护作用可能与减少两个器官中的砷沉积有关。结论:脂质体槲皮素可能被证明具有抗砷剂对大鼠肝和神经细胞损伤的治疗潜力。

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