Abstract
To investigate the effect of specific knockout of SHP2 in mononuclear macrophages on renal ischemia-reperfusion injury and its molecular mechanism. The structural, functional, and pathological changes in the mouse kidney were detected by ultrasound testing. The relative fluorescence intensity of α-SMA, Col1, Col3, and Vim was measured by immunofluorescence staining, and ELISA was performed to detect the concentrations of blood urea nitrogen (BUN), creatinine (Crea), and uric acid (UA). The relative protein expressions of relevant proteins in the mouse kidney tissue were detected by western blotting. Specific knockout of SHP2 could improve both renal function and structure, reduce the relative fluorescence intensity of α-SMA, Col1, Col3 and Vim, lower the concentrations of BUN, Crea, and UA and the expressions of TNF-α, IFNγ, p-NFκB, and p-MyD88, and increase the expressions of p-MerTK, p-FAK, p-PI3K, and p-IκB. The above results illustrate that specific knockdown of macrophage SHP2 promotes macrophage M2 polarization and alleviates renal ischemia-reperfusion injury. The above results illustrate that specific knockdown of macrophage SHP2 promotes macrophage M2 polarization and attenuatesll renal ischemia-reperfusion injury. Specific knockout of macrophage SHP2 promotes macrophage M2 polarization and alleviates renal ischemia-reperfusion injury.