期刊
DRUG DELIVERY
卷 18, 期 6, 页码 451-459出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/10717544.2011.577110
关键词
Hepatocellular; neuronal; reactive oxygen species; antioxidants; blood-brain barrier
资金
- Indian Council of Medical Research (ICMR), Government of India [58/17/2003-BMS]
- Council of Scientific and Industrial Research (CSIR), Government of India, New Delhi
ze 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 (6mg/kg b wt, 9 mg/kg b wt and 12 mg/kg b wt) treatment via oral route for four consecutive months. Liposomal quercetin (2.71mg QC/kg b. wt) were injected s.c. on rats treated with 12 mg/kg b. wt. NaAsO2 twice a week for four months. Results and Discussion: Inorganic arsenic deposition was found to be most significant in hepatic (9.32 +/- 0.100 mu g/g tissue) and neuronal (6.21 +/- 0.090 mu g/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.
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