Abstract

In order to study the effect of changes in TRPC6 protein pathway on podocyte injury in hypertensive mice, 20 WT mice were randomly divided into the control group and the experimental group. Acute hypertension model was established by ligating abdominal aorta for 15 min in the experimental group mice. After successful establishment of the mouse model, in vivo freezing technology is used in all mice to prepare tissue samples for the experiment. H and E staining, SABC-DAB immunohistochemical staining, Western blot and calcium ion detections were made on kidney tissue samples of mice. Urine samples of mice were collected to test urinary albumin. The results showed that compared to the control group, the glomerular tubules and Bowman capsules in the experimental group were swollen, the expression of TRPC6 channels in podocytes increased, the concentration of calcium increased sharply and the concentration of albumin in urine also increased sharply. These results showed that hypertension could cause opening of TRPC6 channel to increase the calcium ion concentration leading to podocyte damage. The ability of damaged podocytes to deal with albumin is weakened and a large increase of albumin would cause further increase of Ca2+ concentration, that aggravated damage to podocytes this initiated a vicious circle. This study thus laid a foundation for exploring the mechanism of podocyte injury caused by hypertensions