动物造模,肾缺血再灌注 z-bio 2022-07-08 466

　　Objective To investigate the effect of rapamycin on the heart injury of distant organs after renal ischemia-reperfusion in rats.

　　Methods Forty rats were randomly divided into four groups: blank group, sham-operated group, RIR group and rapamycin-treated group, with 10 rats in each group. Rats in the rapamycin-treated group received rapamycin by gavage. Rats in each group were sacrificed 24 h after surgery, and blood, spleen and heart were collected. Plasma levels of creatine kinase (CK), creatine kinase isoenzyme (CK-MB), serum creatinine (SCr) and blood urea nitrogen (BUN) were determined. The degree of cardiac pathological damage was expressed by semi-quantitative analysis of PAS staining. Cell apoptosis was detected by TUNEL kit. Flow cytometry to measure the percentage of NKT cell numbers. RT-qPCR method was used to detect CXC chemokine ligand 10 (CXCL10), hypoxia-inducible factor-1α (hypoxia-inducible factoR-1α, HIF-1α) mRNA and vascular endothelial growth factor (VEGF) mRNA expression.

　　Results The serum BUN and SCr values in the RIR group were higher than those in the sham operation group. The levels of serum CK and CK-MB in the rapamycin-treated group were lower than those in the model group. The semiquantitative score of cardiac pathological damage showed that the pathological damage score of the rapamycin-treated group was significantly lower than that of the RIR group. The percentage of NKT cells in the heart and peripheral blood in the rapamycin-treated group was significantly higher than that in the RIR group. The percentage of spleen NKT cells in the rapamycin-treated group was lower than that in the RIR group. The expression levels of HIF-1α mRNA and VEGF mRNA in the rapamycin-treated group were lower than those in the RIR group. The expression level of CXCL10 mRNA in the rapamycin-treated group was higher than that in the RIR group.

　　Conclusion RAPA can significantly up-regulate the expression level of CXCL10 and promote the accumulation of NKT cells in the heart from spleen to peripheral blood. RAPA can also inhibit the expression level of HIF-1α and thus exert a protective effect on the heart after RIR.