肾缺血再灌注损伤 z-bo 2020-12-18 401

　　Objective 　To explore the effect of G protein-coupled estrogen receptor (GPER) on oxidative stress, and its protective effect and possible mechanism on renal ischemia-reperfusion injury. Methods After ovariectomy, female SD rats were randomly divided into ovariectomized group (OVX), renal ischemia reperfusion group (OVX+I/R), estrogen intervention group (OVX+I/R+E2), GPER specific Agonist G1 intervention group (OVX+I/ R+ G1), estrogen+GPER specific blocker G15 intervention group (OVX+I/ R+G15+E2) (8 in each group). The blood creatinine (Cr) and urea nitrogen (BUN) levels of rats in each group were measured, the pathological morphology of kidney tissue was observed by HE staining, and the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in kidney tissue of each group were detected. Western blot was used to detect the expression levels of p-PI3K and p-Akt proteins in kidney tissue. Results Compared with the OVX group, the blood Cr and BUN levels in the OVX+I/R group increased (P<0.01), the renal tissue pathological damage (HE staining) was obvious (P<0.01), and the oxidative stress reaction increased (P<0.01), p-PI3K, p-Akt protein expression levels were significantly reduced (P<0.01); Compared with the OVX+I/R group, the blood Cr and BUN levels in the E2 and G1 intervention groups were reduced ( P<0.01), renal tissue pathological damage is alleviated (P<0.01), oxidative stress is alleviated (P<0.01), and p-PI3K, p-Akt protein expression levels increase (P<0.01). 01), and GPER specific blocker G15 can partially eliminate the protective effect of E2 on renal ischemia-reperfusion injury. Conclusion E2 and GPER agonist G1 can reduce oxidative stress and reduce renal ischemia-reperfusion injury in rats, and the protective effect of E2 on I/R may be mediated by GPER, and its mechanism may involve the activation of PI3K/Akt signaling pathway .