动物造模,血管紧张素II,小鼠肾损害 z-bio 2021-10-21 304

　　Objective: To study the role of TRPV4 receptor in angiotensin II (angiotensin II, Ang II)-induced nephropathy, this gene uses transient receptor potential vanilloid type 4 (TRPV4) gene knockout (TRPV4-/- ) Mice.

　　Method: Did you divide the experimental mice into sham operation group and AngII treatment group? By subcutaneously injecting AngII into wild-type and TRPV4-/- mice, an AngII-dependent hypertension model was established, and mice in the sham operation group were subcutaneously perfused. Salt water only. Four weeks after treatment, the systolic blood pressure of the tail artery of the mouse was measured. 24-hour urine albumin excretion and 8 isoform prostaglandins. The changes in kidney histopathology and changes in serum creatinine were separated at the same time.

　　Result: Compared with the corresponding sham operation group, did the blood pressure of the mice in the AngII treatment group increase? Urinary albumin and 8-isomer prostaglandin excretion serum creatinine levels significantly increased (P\u003c0.05), glomerular fibrotic sclerosis with increased renal collagen levels and renal tubular interstitial damage (P\u003c0 .05). In addition to blood pressure, TRPV4 gene knockout can significantly inhibit all the above pathological changes, thereby reducing the kidney damage caused by AngII (P\u003c0.05).

　　 Conclusion: In the process of AngII-induced hypertension, TRPV4 gene knockout can significantly reduce the kidney damage caused by the above process. Therefore, the above findings indicate that TRPV4 receptor plays an important pathophysiological role in promoting AngII-induced nephropathy.