Protective Effect Of Yulangsan Polysaccharide On Acute Chemical Liver Injury In Mice

Objective: To observe the protective effect of Yulangsan polysaccharide (YLSPS) on acute chemical liver injury in mice. Methods: The models of CCl₄, AP and D-GalN induced acute liver injury in mice with the method of subcutaneous injection were used to study the protective effects of YLSPS. Kunming mice were randomly divided into NC group, liver-injured group, high-, medium- and low- dose of YLSPS groups (0.4, 0.2 and 0.1 g/ kg respectively), and biphenyldicarboxylate (BPDC) group. The indexes of liver, spleen and thymus were observed. The activities of AST, ALT and ALP, the content of Alb, the ability of T-AOC in serum, the content of MDA, and the activity of SOD in liver tissue were investigated. Hematoxylineosin (HE) stain was used to examine the degree of hepatic injury. Results: Compared with model group, YLSPS could obviously reduce the weights of liver and thymus, but had no effect on the weight of spleen. The activities of AST, ALT and ALP, and the content of MDA could be lessened; the content of Alb, the ability of T-AOC, and the activity of SOD could be increased (P<0.01 or P<0.05). The degree of hepatic injury could be lessened. Conclusion: YLSPS has protective effect on acute chemical liver injury. The mechanism may be related to attenuating free radical and inhibiting the effect on lipid peroxidation. Objective: To observe the protective effect of YLSPS on immunity liver injury in mice. Methods: Kunming mice were randomly divided into NC group, liver-injured group, high-, medium- and low- dose of YLSPS groups (0.4, 0.2 and 0.1 g/ kg respectively), and biphenyldicarboxylate (BPDC) group. The animals were intragastrically administered with drugs for 12 days. The models of BCG and LPS induced immunity liver injury in mice with the method of vena caudalis injection at 60 min after the end administration of drug were established. The activities of AST, ALT and LDH in serum, the content of NO in hepatic microsome, the activities of SOD and GSH-PX, the contents of MDA and GSH, and the expressions of Bcl-2 and Bax in liver tissue were investigated. HE stain was used to examine the degree of hepatic injury. Results: Compared with model group, YLSPS could obviously reduce the activities of AST, ALT and LDH, the contents of NO and MDA, and the expression of Bax. The activities of SOD and GSH-PX, the content of GSH and the expression of Bcl-2 could be increased (P<0.01 or P<0.05). The degree of hepatic injury could be lessened. Conclusion: YLSPS has protective effect on immunity liver injury. The mechanism may be related to attenuating free radical and inhibiting the effect on lipid peroxidation. Objective: To observe the protective effect of YLSPS on hepatic injury induced by alcohol in mice. Methods: Kunming mice were randomly divided into NC group, liver-injured group, high-, medium- and low- dose of YLSPS groups (0.4, 0.2 and 0.1 g/ kg respectively). The animals were intragastrically administered with drugs for 30 days. Then, 50% alcohol was administered (i.g.) to YLSPS-treated groups and model group at a dose of 10 ml/ kg to induce the acute alcoholic hepatic injury at 60 min after the end administration of drug. The activities of AST, ALT and the content of TG in serum, the activities of SOD, GSH-PX and AH, the contents of GSH, Cyt P450 and Cyt b₅ in hepatic microsome, and the expressions of Bcl-2 and Bax in liver tissue were investigated. HE stain was used to examine the degree of hepatic injury. Results: Compared with model group, YLSPS could obviously reduce the activities of AST, ALT, the content of TG, and the expression of Bax. The activities of SOD, GSH-PX and AH, the contents of GSH, Cyt P450 and Cyt b₅, and the expression of Bcl-2 could be increased (P<0.01 or P<0.05). The number of fat droplet stained by HE dye in test groups was less than model group (P<0.01). Conclusion: YLSPS has protective effect on hepatic injury induced by alcohol. The mechanism may be related to attenuating free radical; inhibiting effect on lipid peroxidation, and inducing the activities of hepatic microsomal enzymes. Objective: To observe the protective effect of YLSPS on liver injury induced by cyclophosphamide (CY) in mice. Methods: Kunming mice were randomly divided into NC group, liver-injured group, high-, medium- and low- dose of YLSPS groups (0.4, 0.2 and 0.1 g/ kg respectively), and biphenyldicarboxylate (BPDC) group. The animals were intragastrically administered with drugs for 10 days. The models of CY induced liver injury in mice with the method of intraperitoneal injection at 2,4, 6, 8, and 10 days after the first administration of drug were established. The indexes of thymus and spleen were observed. The activities of AST, ALT and LDH, the contents of TNF-a and lysozyme (LSZ) in serum were investigated. Results: Compared with model group, YLSPS could obviously reduce the activities of AST, ALT and LDH. The index of thymus, the contents of TNF-a and lysozyme could be obviously increased (P<0.01 or P<0.05). Conclusion: YLSPS has protective effect on liver injury induced by CY. The mechanism may be related to strengthenning the nonspecific immunologic function.