Objective To investigate the protective mechanism of phyllostachysin A on hepatic ischemia-reperfusion injury in rats.
Methods Thirty SD rats were randomly divided into sham operation group, model group and RA group, with 10 rats in each group. Rats in the RA group were injected with RA (10 mg/kg) by tail vein at 24 h and 1 h before modeling, respectively, while the sham-operated group and the model group were injected with an equal volume of 0.9% NaCl solution (physiological saline). After anesthesia, the rats were clipped into the hepatic blood vessel for 60 minutes, resulting in 70 % ischemia in the liver. After 6 hours of blood flow recovery, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) were detected. ) content, ELISA method was used to detect superoxide dismutase (SOD), malondialdehyde (MDA), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor- The content of α (TNF-α), HE and TUNEL staining were used to observe the liver pathological damage and hepatocyte apoptosis, and Western blotting was used to detect the B-lymphoma-2-associated X protein (Bax) and B-lymphoma-2 protein in the liver. (Bcl-2) and cysteine protease-3 (Caspase-3) expression levels.
Results Compared with the model group, the contents of ALT, AST and LDH in serum of RA group decreased (P<0.05), the contents of MDA, IL-1b, IL-6 and TNF-a in liver tissue decreased (P<0.05), and the content of SOD increased (P<0.05); In the RA group, the liver tissue structure was intact, the number of apoptotic cells decreased, and the apoptotic rate decreased (P<0.01), the levels of Bax and Caspase-3 decreased, and the level of Bcl-2 increased (P<0.05).
Conclusion RA injection before ischemia-reperfusion can improve the liver function of rats after ischemia-reperfusion, reduce the release of oxidative and inflammatory factors, and reduce the apoptosis of hepatocytes by down-regulating the protein expressions of Bax and Caspase-3, thereby protecting the liver.