A study on the protective effects and mechanisms of ercao qinggan tang to immunological liver injury in rats
SU Linhon
Abstract
SU Linhon
Abstract
ObjectiveTo study the protection and mechanisms of ercao qinggan tang to immunological liver injury in rats.MethodsThe immunological liver injury rat model was produced by intraperitoneal injection with BCG plus LPS.Normal control group,immunological liver injury model group,Cyclophosphamide(CTX) group,ercao qinggan tang low dose group and ercao qinggan tang high dose group were set up.The levels of aminotransferase(ALT),aspartate aminotransferase(AST),tumor necrosis factor-α(TNF-α),interleukin-12(IL-12) in blood plasma of the five groups were examined.The rates of apoptosis of hepatocytes were analyzed by flow cytometry.The expression of Bax and Bcl-2 was detected qualitatively and quantitatively by immunohistochemistry assay using an image analysis system.ResultsThe levels of ALT and AST in the ercao qinggan tang(large dose group and small dose group) and CTX group were lower than those of the immunological liver injury model group.ALT was(547±76)、(576±69)、(538±72)、(547±76)U/L respectively and AST was(536±72)、(585±74)、(526±71)、(627±92)U/L respectively.The differences between the ercao qinggan tang groups or CTX and the model group were significant(P0.01 or P0.05).The levels of TNF-α and IL-12 in the ercao qinggan tang groups and the CTX group were lower than those of the model group,and the differences were significant(P0.05).The rates of hepatocytes apoptosis of the ercao qinggan tang treatment group or the CTX group were lower than that of the model group,and the differences were significant(P0.01 or P0.05).The comparing ratios of Bax and Bcl-2 proteins(Bax/Bcl-2) expression in hepatocytes in ercao qinggan tang high dose group and CTX group were significantly lower than that of that the model(P0.01 or P0.05).ConclusisonErcao qinggan tang can decrease the levels of TNF-α and IL-12 in plasma and inhibit hepatocytes apoptosis to protect immunological injury to liver in rats.
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ObjectiveTo study the protection and mechanisms of ercao qinggan tang to immunological liver injury in rats.MethodsThe immunological liver injury rat model was produced by intraperitoneal injection with BCG plus LPS.Normal control group,immunological liver injury model group,Cyclophosphamide(CTX) group,ercao qinggan tang low dose group and ercao qinggan tang high dose group were set up.The levels of aminotransferase(ALT),aspartate aminotransferase(AST),tumor necrosis factor-α(TNF-α),interleukin-12(IL-12) in blood plasma of the five groups were examined.The rates of apoptosis of hepatocytes were analyzed by flow cytometry.The expression of Bax and Bcl-2 was detected qualitatively and quantitatively by immunohistochemistry assay using an image analysis system.ResultsThe levels of ALT and AST in the ercao qinggan tang(large dose group and small dose group) and CTX group were lower than those of the immunological liver injury model group.ALT was(547±76)、(576±69)、(538±72)、(547±76)U/L respectively and AST was(536±72)、(585±74)、(526±71)、(627±92)U/L respectively.The differences between the ercao qinggan tang groups or CTX and the model group were significant(P0.01 or P0.05).The levels of TNF-α and IL-12 in the ercao qinggan tang groups and the CTX group were lower than those of the model group,and the differences were significant(P0.05).The rates of hepatocytes apoptosis of the ercao qinggan tang treatment group or the CTX group were lower than that of the model group,and the differences were significant(P0.01 or P0.05).The comparing ratios of Bax and Bcl-2 proteins(Bax/Bcl-2) expression in hepatocytes in ercao qinggan tang high dose group and CTX group were significantly lower than that of that the model(P0.01 or P0.05).ConclusisonErcao qinggan tang can decrease the levels of TNF-α and IL-12 in plasma and inhibit hepatocytes apoptosis to protect immunological injury to liver in rats.
Key concepts: Medicine, Intraperitoneal injection, Cyclophosphamide, Liver injury, Apoptosis, Immunohistochemistry, Tumor necrosis factor alpha, Internal medicine