Protective Effects Of Longyanshen Polysaccharide On Hepatorenal Damage Induced By Chronic Fluorosis In Rats

Objective:To investigate the protective effects of Longyanshen Polysaccharide (LYS) on hepatorenal damage induced by chronic fluorosis in rats and its related mechanisms.Methods:Sixty wistar rats were randomly divided into 5 groups:the normal control group, the chronic fluorosis model control group, the LYSP low dose group, the LYSP medium dose group and the LYSP high dose group. Except the normal control group, the other groups were given sodium fluorid in drinking water ([F-]=150 mg·L-1) for 12 weeks to establish chronic fluorosis model. Eight weeks after the administration of sodium fluorid, The LYSP low dose group, LYSP medium dose group and LYSP high dose group were treated with different doses of Longyanshen Polysaccharide(ig), the normal control group and the model control groups were treated with normal saline. All rats were sacrificed to obtain the liver and kidney tissues after the treatment for 4 weeks:1. The serum F ion concentration ([F-]) and biochemical indicators were determined. The Ca2+ concentrations in serum, liver tissues and kidney were surveryed. 2. Total anti-oxidation capacity (T-AOC) and the contents of malondiadehyde (MDA), metabolic product of lipid peroxidation in liver and kidney tissues were surveryed. Meanwhile the contents of NO were studied.3. Activities antioxidases (GSH-Px & SOD) and the activities of NOS in fluoride-exposed rat liver and kidney tissues were determined.4. Chronic fluorosis rat liver tissues and kidney tissues were taken to make histological section for observing the changes. The Bcl-2 and Bax protein expressions of the liver and kidney tissues were determined by immunohistochemical method.Results:1. The serum [F"] in model group was increased significantly, compared with normal control group (P＜＜0.01). Differences between model group and LYSP group were insignificant(P>0.05). Meanwhile CO2-CP were found no significant difference (P＞0.05). Compared with model group, the levels of TP, A/G, and UA in LYSP-treated groups were increased significantly (P＜0.01 or P＜0.05), while the levels of ALT, AST, T-BIL, y-GT, BUN, CR, ALP and LDH in LYSP-treated groups were decreased significantly (P<0.01).2. The Ca2+ concentration in serum of model group was reduced significantly, compared with control group (P＜0.01). Meanwhile, Ca2+ concentration in hepatorenal tissues were increased significantly (P＜0.01). Differences between in model group and LYSP group were insignificant (P＞0.05). 3. Compared with model group, the content of MDA, NO in hepatic tissues of LYSP group were reduced significantly (P＜0.01), while the liver T-AOC, GSH-Px and SOD were increased significantly (P＜0.01). The activities of tNOS and iNOS in hepatic tissues of LYSP group were reduced significantly. 4. Compared with model group, the content of MDA, NO in nephridial tissues of LYSP group were reduced significantly (P＜0.01), while the nephridial tissues SOD, GSH-Px were increased significantly (P＜0.01). The activities of tNOS, iNOS in the nephridial tissues of LYSP group were reduced significantly.5. The histopathological examination showed that LYSP could lessen the degree of hepatorenal damages induced by chronic fluorosis obviously compared with model group.The Bcl-2 and Bax protein expressions of the liver were insignificant compared with control group.Compared with control group, the Bcl-2 and Bax protein expressions of nephridial tissues were increased significantly (P＜0.01). Compared with model group, the expression of Bcl-2 protein in nephridial tissues were increased significantly in LYSP-treated groups (P＜0.01 or P＜0.05), the expresion of Bax protein and the ratio of Bax protein to Bcl-2 protein were decreased significantly in nephridial tissues (P＜0.01 or P＜0.05).Conclusion:Longyanshen Polysaccharide can protect hepatorenal damage induced by chronic fluorosis in rats. The mechanism may be related to anti-oxidative activity, increasing the activity of activities antioxidases.Meanwhile the up-regulation of protein expressions of Bcl-2 and down-regulation of the expressions of Bax protein may account for the protection of nephridial damage.