动物造模,肾炎小鼠模型 z-bio 2022-09-28 310

　　Objective To investigate the similarities and differences between unilateral nephrectomy (UNX) mouse Habu nephritis model and normal mouse Habu nephritis model in renal function, renal pathology and expression of glomerular villin 1 (VIL 1) and their molecular mechanisms.

　　Methods Twenty four six week old SPF male C57BL6 mice (18~20g) were randomly divided into two groups: experimental group (n=12) and control group (n=12). Habu nephritis model (HSV UNX group) was established by tail vein injection of green bamboo leaf snake venom (HSV) after receiving UNX, and control group (n=12) was established by tail vein injection of snake venom after sham operation; The renal function of the mice in the two groups was detected by blood biochemistry, and the pathological changes in the renal tissues of the mice in the two groups were observed by periodate Schiff staining; Further, we analyzed the expression of glomerular proteins of the two groups by proteomics, screened out the differential proteins between the two groups, and studied the effect and mechanism of differential proteins on cell proliferation and apoptosis in mouse mesangial cells in vitro.

　　Results The levels of serum creatinine and urea nitrogen in HSV-UNX group were significantly higher than those in HSV group (all P<0.01), the level of mesangial dissolution in renal tissue was higher than that in HSV group (P<0.001), and the level of mesangial proliferation was lower than that in HSV group (P<0.001); Proteomic analysis and Western blotting confirmed that the expression of VL1 in HSV-UNX mice was lower than that in HSV mice; In mouse mesangial cells, knockdown of VIL1 expression can promote cell apoptosis (P<0.01) and inhibit cell proliferation (P<0.05) by up regulating the expression of caspase3, Bax, p21 and p27 proteins.

　　Conclusion The expression of VIL1 is down regulated in the single nephrectomy model of Habu nephritis in mice. The down-regulation of VIL1 can lead to the decline of glomerular self repair ability and aggravate the damage of renal function by inhibiting cell proliferation and promoting cell apoptosis.