动物造模,大鼠肾缺血再灌注 z-bio 2021-07-12 339

　　OBJECTIVE: To study the effects of repeated hypoxic preconditioning (RHP) on liver injury caused by renal ischemia-reperfusion injury (IRI) in rats, and to preliminarily explore its mechanism of action.

　　Methods: 120 male SD rats were randomly divided into 4 groups (n=30): hypoxia preconditioning surgery group (RHP group), hypoxia preconditioning sham surgery group (RHPS group), and normal pressure surgery group (IRI group) And normal pressure sham operation group (group S). The rats were pretreated in a hypobaric oxygen chamber for 5 days to establish a kidney IRI model. In the HP and IRI groups, the right kidney was removed, the left renal hilum was clamped and released for 45 minutes to establish renal ischemia. -Reperfusion model, RHPS group and S group only remove the right kidney, and the left kidney is ischemia-no reperfusion therapy. Serum alanine aminotransferase (ALT), IL-17A, and TNF-α levels were measured at 2, 8 and 24 hours after reperfusion to produce liver homogenate superoxide dismutase (SOD) and nitric oxide (NO). I did it. Content, Western blot test, determination of liver p-PI3K and p-AKT levels, and histopathological examination to observe the changes in liver structure.

　　Results: Compared with the IRI group, the histopathological examination of the rats in the RHP group at 2, 8, and 24 hours after reperfusion showed that the damage was reduced, the serum ALT level was reduced, and the TNF-α level was reduced. 24 hours after reperfusion (P0.05)); the expression of P-PI3K and P-AKT in the RHP group was higher than that in the IRI group (Pu003c0.05), and the difference was particularly significant after 8 hours of reperfusion.

　　Conclusion: RHP has a protective effect on IRI-induced kidney and liver injury in rats, but it is not achieved by inhibiting IL-17A.