动物造模 z-bio 2022-02-18 290

　　Objective: To investigate the role of TRPV4 receptor in angiotensin II (Ang II)-induced renal damage by using transient receptor potential vanilloid isoform 4 knockout (TRPV4 - / - ) mice.

　　Methods: The experimental mice were divided into sham-operated group and Ang II-treated group. The Ang II-dependent hypertension model was established by subcutaneous perfusion of Ang II in wild-type and TRPV4 - / - mice, while the sham-operated mice were only perfused subcutaneously. saline. After 4 weeks of treatment, the systolic blood pressure of the tail artery of the mice was measured. 24-h urinary albumin excretion and 8-isomer prostaglandins. Changes in serum creatinine, and at the same time the changes in renal histopathology were classified...

　　Results: Compared with the corresponding sham-operated group, the blood pressure of the Ang II-treated mice increased, the excretion of urinary albumin and 8-isoprostaglandin increased, and the serum creatinine increased at the same time (P < 0.05); The degree of glomerular fibroid sclerosis and tubulointerstitial injury were significantly aggravated, and the level of renal collagen was increased (P < 0.05). Except for blood pressure, knockout of TRPV4 significantly inhibited all the above pathological changes, thereby alleviating the renal damage induced by Ang II (P < 0.05).

　　Conclusion: In the process of AngII-induced hypertension, TRPV4 gene knockout can significantly attenuate the renal damage induced by the above process. Therefore, the above findings suggest that the TRPV4 receptor plays an important pathophysiological role in promoting Ang II-induced renal damage.