动物造模,TRPV4 z-bo 2022-02-04 386

　　Objective: To use transient receptor potential vanilloid type 4 (TRPV4) gene knockout (TRPV4-/-) mice to study the kidney damage caused by TRPV4 receptor in angiotensin II (angiotensin II, Ang II) In the role.

　　Method: Did you divide the experimental mice into sham operation group and AngII treatment group? An AngII-dependent hypertension model was established by subcutaneously injecting AngII in wild-type and TRPV4-/- mice, while mice in the sham-operated group were physiologically perfused with saline. 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. Serum creatinine changes and renal histopathological changes occur simultaneously...

　　Result: Compared with the corresponding sham operation group, did the blood pressure of the AngII treatment group increase? The excretion of urinary albumin and 8-isomer prostaglandin increased with the increase of serum creatinine (P\u003c0.05); glomerular capillary sclerosis and tubular interstitial damage accompanied by increased renal collagen levels were significantly worse (P\u003c0.05). Except for 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 hypertension caused by AngII, 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.