Objective To investigate the protective effect of hepatocyte growth-promoting factor ( PHGF) against liver ischemia-reperfusion injury in rats and its mechanism of its action. Methods A total of 80 healthy male Sprague-Dawley rats were randomly divided into experimental group ( PHGF group) and control group ( NS group) , with 40 rats in each group. A rat model of liver ischemia-reperfusion injury was established by 70% liver ischemia caused by the occlusion of blood flow in the middle and left lobes of the liver, with an ischemia time of 21 minutes. The rats in the PHGF group were given intraperitoneal injection of PHGF for intervention before surgery, and those in the NS group were given an equal volume of normal saline. Serum and liver tissue samples were collected before surgery and on days 1, 3, 5, and 7 after surgery, and the levels of alanine aminotransferase ( ALT) , aspartate aminotransferase ( AST) , and total bilirubin ( TBil) were measured; HE staining was used to observe pathological changes; real-time PCR was used to measure the mRNA expression of mitochondrial transcription factor A ( TFAM) in the liver. The independent samples t-test was used for comparison of continuous data between two groups. Results HE staining showed that compared with the NS group, the PHGF group had significantly lower degrees of hepatocyte swelling, inflammatory cell infiltration, and hepatocyte necrosis under a light microscope. Liver biochemistry showed that on days 1, 3, 5, and 7 after surgery, the PHGF group had significantly lower serum levels of ALT, AST, and TBil than the NS group ( t = 11. 879, 16. 019, 22. 168, 10. 235, 9. 041, 12. 936, 18. 759, 8. 142, 10. 108, 11. 014, 13. 245, and 9. 968, all P < 0. 001) . Real-time PCR showed that on days 1, 3, and 5 after surgery, the PHGF group had a significantly higher mRNA level of TFAM in the liver than the NS group ( t =7. 998, 14. 764, and 13. 861, all P < 0. 001) . Conclusion PHGF preconditioning exerts a protective effect against liver ischemia-reperfusion injury in rats, possibly by upregulating the expression of TFAM to alleviate liver ischemia-reperfusion injury.
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