Found programs:
Authors:Li Jingling; Yin Chenghong
Keywords:endotoxemia;liver;renin-angiotensin system;inflammatory response;stress response
DOI:10.19405/j.cnki.issn1000-1492.2022.01.022
〔Abstract〕 Objective To investigate the changes of liver renin-angiotensin(RAS) system as well as its relationship with liver function in endotoxemia rats. Methods Totally 90 rats were randomly divided into control group and 2, 4, 8, 12, 24, 48, 72 h and 7 d after injection group, which were prepared for sepsis model by tail vein injection of LPS except for the control group. Animals in the control group were collected samples at 8 h after injection, while animals in the model group were collected samples at each time points(2, 4, 8, 12, 24, 48, 72 h and 7 d). Heart blood was collected to measure liver markers alanine amine aminotransferase(ALT), aspartate aminotransferase(AST), lactate dehydrogenase(LDH), RAS markers renin-angiotensin(PRA), angiotensin converting enzyme(ACE) and angiotensin Ⅱ(Ang Ⅱ). Liver tissues were extracted to observe the pathology characteristics and detect PRA, ACE, Ang Ⅱ and angiotensin type 1 receptor(AT1 R) mRNA. Results The levels of AST, ALT and LDH in the model group gradually increased after LPS injection, and AST and LDH in the model group were higher than those in the control group at 4~48 h, ALT in the model group was higher than that in the control group at 2 to 48 h, and the differences were statistically significant(P<0.05). The circle and liver PRA level in the model group increased rapidly after injection, which was higher than that in the control group at 2 to 48 h. The circle and liver levels of ACE and Ang Ⅱ increased after injection too, which were both higher than those in the control group at 2 to 28 h, and the difference was statistically significant(P<0.05). The expression of AT1 R mRNA in the model group gradually increased after injection, which was higher than that in the control group at 4 to 48 h, and the difference was statistically significant(P<0.05). Conclusion Liver function damage caused by endotoxemia may be related to the activation of local RAS in the liver.