ABSTRACT
Objective To investigate the effect of G protein?coupled estrogen receptor (GPER) on the diastolic function of renal interlobular artery and reduce renal ischemia?reperfusion injury in rats. Methods Female ovariectomized rats were divided into control group; ischemia?reperfusion injury (IRI) group;GPER?specific agonist (G1) intervention group;GPER?specific blocker+GPER?specific agonist (G15+G1) intervention group. Histopathological examination (HE staining), renal function test and Paller score were used to identify the success of the model and the degree of kidney damage. In vitro microvascular pressure diameter measuring instrument was used to detect the relaxation and contraction activity of renal interlobular artery in each group. Immunofluorescence technique was used to observe the expression of GPER on the renal interlobular artery. Westernblotting was used to detect the expression of GPER protein in renal interlobular artery of rats in each group. The NO content was determined by a nitrate reductase method. Results Compared with IRI group, serum BUN, Scr level and Paller score in G1 intervention group were significantly decreased (all P<0.05). The systolic rate of renal interlobar artery was significantly increased [(40.76 ± 1.57)％ vs (29.78 ± 1.87)％, P<0.05]. The results of immunofluorescence showed that GPER was expressed in renal interlobular artery smooth muscle cells and endothelial cells, and the expression of IRI group was higher than that of the control group. The expression of G15+G1 intervention group was lower than that of G1 intervention group (all P<0.05). Compared with the IRI group, the NO content in the G1 intervention group increased significantly (all P<0.05). Conclusions During renal ischemia ?reperfusion injury, GPER may regulate the systolic and diastolic activity of the renal interlobar artery by increasing the content of NO, so as to alleviate the renal ischemia?reperfusion injury.
ABSTRACT
Objective To investigate the effect of estrogen (E2) on the connexin43 (Cx43) expression of renal interlobar arteries after renal ischemia-reperfusion injury (I/R).Methods The experiment was carried out in vivo using an SD rat I/R model.SD rats were randomly divided into normal group,sham-operation group,I/R group,and estrogen-intervention group.The functional changes of the kidney were analyzed after 24 hours of I/R;nephridial tissue section was stained by hematoxylin-eosin (HE),and Paller scores were used to evaluate the degree of kidney damage.Pressure myography was utilized to detect the vasomotor function of renal interlobar arteries.Immunofluorescence technique,qRT-PCR and Western blot were applied to determine the expression of Cx43 in renal interlobar arteries in different groups.Results Estrogen markedly decreased the levels of Cr and BUN in the serum of I/R rats (P＜0.05),and the damage of the kidney tissue could be improved noticeably.The vasomotor rate of renal interlobar arteries was (24.80 ± 3.70)％ after I/R and (41.60 ± 3.50)％ after treatment with estrogen,which was higher than that of I/R group (P＜0.05).The expression of Cx43 was lower in renal interlobar arteries of estrogen-intervention group than that in I/R group (P＜0.01).Conclusion Estrogen may reduce vascular tension and boost dilation of the artery by inhibiting Cx43 expression and GJ function.Therefore,estrogen may attenuate the damage of I/R and improve renal function.
ABSTRACT
Objective To observe the effects of propofol intervention on renal ischemia-reperfusion injury on the expression of Cx43 in rat renal interlobar artery.Methods Male SD rats were randomly divided into control 4h and 24h groups (control), sham operation 4h and 24h groups (sham), ischemia reperfusion 4h and 24h groups (I/R), propofol 4h and 24h groups (propofol), and fat emulsion 4h and 24h groups (intralipid).Ischemia/reperfusion model was prepared by resection of right kidney and noninvasive arterial occlusion of left kidney, with renal ischemia for 45min and reperfusion for 4h or 24h depending on different group.Serum urea nitrogen (BUN) and creatinine (Cr) were detected by automatic biochemical analyzer.HE staining was used to observe the pathological changes of renal tissue.The changes of renal artery systolic and diastolic lobes were examined by pressure myographic technique.The expression of Cx43 protein in renal interlobar artery was analyzed by Western blot.Results The concentrations of serum BUN and Cr in sham group did not differ significantly from those in the blank control group.Renal HE staining showed no significant lesions;the pressure myogram of motor renal interlobar artery contraction rate showed no significant difference.The expression of Cx43 protein did not change significantly.Compared with sham operation group, the concentrations of serum BUN and Cr in ischemia-reperfusiongroup were significantly increased.HE slices kidney showed that the pathological changes of renal tissue became obvious;pressure motor indicated renal interlobar artery contraction rate was decreased;the expression of Cx43 protein was increased significantly (P<0.05).Compared with ischemia-reperfusion group, the concentrations of serum BUN and Cr in propofol group were decreased;renal HE slices showed reduced renal tissue lesions, increased renal interlobar artery contraction rate, and decreased expression of Cx43 protein (P<0.05).Conclusion Propofol can change renal ischemia-reperfusion injury by reducing the expression of Cx43 protein in vasomotor in renal interlobar artery.