Zhonghua yi xue za zhi · 2015
[Regulation of hydrogen sulfide on transporter protein Bsep and Mdr2 in acute liver failure].
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Wang Xinguo, Wang Bingyuan, Huang Qian, Zhang Bo, Hua Zhong
Аннотация
OBJECTIVE: To observe the effect of hydrogen sulfide on Bsep and Mdr2 in acute liver failure induced by thioacetamide.
METHODS: Twenty-four male SD rats were randomly divided into thioacetamide (TAA) induced model group (n=6), control group (n=6), TAA+sodium hydrosulfide group (n=6), and TAA+ propargylglycine group (n=6). TAA was given to enterocoelia at the dose of 600 mg/kg for the model group, sodium hydrosulfide group and propargylglycine group rats.Sodium hydrosulfide with the dose of 0.15 mmol/kg and propargylglycine of 30 mg/kg was injected into enterocoelia one hour before the TAA used. All rats were sacrificed and serum specimen was collected to test hydrogen sulfide and hepatic function. The method of Western blot and Immunohistochemistry were used to measure the expression of Bsep and Mdr2 in the liver.
RESULTS: The Liver function of TAA group rats was severely injured [ALT(524.0±32.0) vs (28.3±8.4) U/L]. It was worsen by application of sodium hydrosulfide [ALT(861.9±55.1) U/L] while recovered [ALT(59.5±10.2) U/L)] by propargylglycine. The level of bilirubin and bile acid was significantly higher in the TAA group rats than in the normal control group, and the application of sodium hydrosulfide caused bile acids increased further besides of bilirubin. On the contrary, the levels of bile acids and bilirubin were significantly decreased with PPG application. The level of hydrogen sulfide in the serum of the TAA group rats was higher than normal group rats'. That was elevated by sodium hydrosulfide and decreased by propargylglycine.Severely edema, necrosis and inflammatory cell infiltration were observed in TAA group rats, which worse by sodium hydrosulfide and released by propargylglycine. The expression of Bsep and Mdr2 down regulated in TAA and deteriorated by sodium hydrosulfide application and relieved by propargylglycine application.
CONCLUSION: Hydrogen sulfide exacerbated the Bsep and Mdr2 loss in the liver failure and contributed to high serum concentration of bile acids.
METHODS: Twenty-four male SD rats were randomly divided into thioacetamide (TAA) induced model group (n=6), control group (n=6), TAA+sodium hydrosulfide group (n=6), and TAA+ propargylglycine group (n=6). TAA was given to enterocoelia at the dose of 600 mg/kg for the model group, sodium hydrosulfide group and propargylglycine group rats.Sodium hydrosulfide with the dose of 0.15 mmol/kg and propargylglycine of 30 mg/kg was injected into enterocoelia one hour before the TAA used. All rats were sacrificed and serum specimen was collected to test hydrogen sulfide and hepatic function. The method of Western blot and Immunohistochemistry were used to measure the expression of Bsep and Mdr2 in the liver.
RESULTS: The Liver function of TAA group rats was severely injured [ALT(524.0±32.0) vs (28.3±8.4) U/L]. It was worsen by application of sodium hydrosulfide [ALT(861.9±55.1) U/L] while recovered [ALT(59.5±10.2) U/L)] by propargylglycine. The level of bilirubin and bile acid was significantly higher in the TAA group rats than in the normal control group, and the application of sodium hydrosulfide caused bile acids increased further besides of bilirubin. On the contrary, the levels of bile acids and bilirubin were significantly decreased with PPG application. The level of hydrogen sulfide in the serum of the TAA group rats was higher than normal group rats'. That was elevated by sodium hydrosulfide and decreased by propargylglycine.Severely edema, necrosis and inflammatory cell infiltration were observed in TAA group rats, which worse by sodium hydrosulfide and released by propargylglycine. The expression of Bsep and Mdr2 down regulated in TAA and deteriorated by sodium hydrosulfide application and relieved by propargylglycine application.
CONCLUSION: Hydrogen sulfide exacerbated the Bsep and Mdr2 loss in the liver failure and contributed to high serum concentration of bile acids.