Hepatoprotective and neuroprotective activity of liposomal quercetin in combating chronic arsenic induced oxidative damage in liver and brain of rats

Biomembrane Division, Indian Institute of Chemical Biology, 4, Raja S.C. Mullick Road, Kolkata-700032, India.
Drug Delivery (Impact Factor: 2.56). 05/2011; 18(6):451-9. DOI: 10.3109/10717544.2011.577110
Source: PubMed


Arsenic is a naturally occurring toxicant that causes acute and chronic adverse health effects, including cancer.
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.
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.
Inorganic arsenic deposition was found to be most significant in hepatic (9.32 ± 0.100 µg/g tissue) and neuronal (6.21 ± 0.090 µg/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.
Thus, Liposomal quercetin might prove to be of therapeutic potential against arsenite-induced hepatic and neuronal cell damage in rats.

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    • "The hepatoprotective effects of antioxidant compounds of plants on liver damage caused by t-BHP-induced oxidative stress in rats has previously been studied by our group (Lee et al., 2005; Kim et al., 2007; Yang et al., 2012). Many other researchers provide similar evidence of plant based antioxidant effects towards hepatoprotective effects (Ghosh et al., 2011; Ha et al., 2010; Pradeep et al., 2010). This study demonstrated the high antioxidant activity of LOE and quercitrin and afzelin with increased cell viability observed under oxidative stress, as well as TP and TF contents, DPPH scavenging activity and FRAP assays. "
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