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
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.
Available from: Kwangwon Lee
- "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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ABSTRACT: Lindera obtusiloba Blume, a native plant of East Asia, has traditionally been used as a folk medicine for liver disease. We studied the in vitro antioxidant and in vivo hepatoprotective activities of a 70% ethanolic extract of L. obtusiloba (LOE) containing 62.9% quercitrin and 22.0% afzelin. LOE prevented tert-butyl hydroperoxide (t-BHP)-induced oxidative damage in HepG2 cells. Along with its high antioxidant potency in vitro, our animal study confirmed that pretreatment with LOE (500 or 2,000 mg/kg) for 7 days prior to a single dose of t-BHP (i.p.; 0.5 mmol/kg) significantly lowered the serum levels of alanine and aspartate aminotransferases. In addition, glutathione levels were increased in the liver, and lipid peroxidation levels were decreased in a dose-dependent manner. The histopathological examinations of rat livers showed that LOE significantly reduced the incidence of liver lesions induced by t-BHP. Therefore, we concluded that LOE has merit as a potent candidate to protect the liver against oxidative damage.
Available from: Ruhi Turkmen
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ABSTRACT: The aim of this study was to clarify the effects of dietary supplementation with Yucca schidigera (Ys) on lipid peroxidation (LPO), antioxidant activity, some biochemical parameters and histopathological changes in arsenic-exposed mice. Forty Swiss albino male mice were divided into five equal groups. Group I (control group) was given normal diet and tap water for 28 days. Group II (arsenic group) was given normal diet and 100 mg/L arsenic along with drinking water for 28 days. Groups III-V were given three different doses of Ys (50, 100 and 200 mg/kg) in supplemented diet and arsenic (100 mg/L) along with drinking water throughout the entire period of 28 days. The arsenic significantly increased serum biochemical parameters and malondialdehyde levels in blood and tissue. However, arsenic significantly decreased tissue glutathione concentration, erythrocyte superoxide dismutase and catalase activities. In contrast, dietary supplementation of Ys, in a dose-dependent manner, resulted in reversal of arsenic-induced oxidative stress, LPO and activities of antioxidant enzymes. Moreover, Ys also exhibited protective action against the arsenic-induced focal gliosis and hyperemi in brain, necrosis and degeneration in liver, degeneration and dilatation in Bowman's capsule of kidney and hyaline degeneration in heart tissue of mice. Consequently, our results demonstrate that Ys especially high-dose supplementation in diet decreases arsenic-induced oxidative stress and enhances the antioxidant defence mechanism and regenerate of tissues in Swiss albino mice.
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