动物造模 z-bio 2023-04-12 672

　　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 pathological manifestations and glomerular villin 1 (VIL 1) expression and its molecular mechanism.

　　Methods Twenty-four 6-week-old SPF-grade male C57BL6 mice (18-20 g) were randomly divided into 2 experimental groups (n=12). After receiving UNX, the Habu nephritis model (HSV-UNX group) was established by tail vein injection of Bamboo leaf snake venom (HSV). ), and the control group (n=12) received sham surgery and then received venom tail vein injection to construct Habu nephritis model HSV group); the renal function levels of mice in the two groups were detected by blood biochemistry, and periodic acid-Schiff staining was used to observe the small size of the mice in the two groups. Pathological changes of rat kidney tissue; further analysis of glomerular protein expression between the two groups by proteomics, screening of differentially expressed proteins between the two groups, in vitro mouse mesangial cells to study the effect of differential proteins on cell proliferation and apoptosis function and mechanism.

　　Results The levels of serum creatinine and blood urea nitrogen in the HSV-UNX group were significantly higher than those in the HSV group (all P<0.01), the level of renal mesangial lysis was higher than that in the HSV group (P<0.0001), and the level of mesangial proliferation was lower than that in the HSV group (P<0.01). HSV group (P<0.001); proteomic analysis and Western blotting confirmed that the expression of VL1 in HSV-UNX group was lower than that in HSV group; in mouse mesangial cells, knockdown of VIL1 expression could up-regulate caspase3, Bax, The expression of p21 and p27 proteins promoted cell apoptosis (P<0.01) and inhibited cell proliferation (P<0.05).

　　Conclusion The expression of VIL1 is down-regulated in uninephrectomy Habu nephritis mouse model. Down-regulation of VIL1 can reduce the self-repair ability of glomeruli and aggravate renal function damage by inhibiting cell proliferation and promoting cell apoptosis.