Protective Effect Of Valsartan On Endoplasmic Reticulum Stress Induced By Diabetic Nephropathy In
Recently, Xuzhou Medical College researchers published a paper to investigate the effects of valsartan on renal podocyte apoptosis and the expression of endoplasmic reticulum stress markers GRP78 and caspase12 in rats with diabetic nephropathy. It is pointed out that valsartan exerts its protective effect on diabetic nephropathy by slowing the endoplasmic reticulum stress and possibly by inhibiting the endoplasmic reticulum-specific caspase12 pathway and decreasing the apoptosis of podocytes. This article was published in the 12th issue of "Armed Police Medicine" in 2015.
Male SD rats were randomly divided into normal control group and experimental group. Rats in experimental group were given intraperitoneal injection of streptozotocin to establish diabetic model, and then were randomly divided into model group and valsartan group. Normal control group and model group were given once / d reverse osmosis water, valsartan group Valsartan (8 mg / kg) was given orally once daily for 6 weeks. The expression levels of nephrin, GRP78 and caspase12 were analyzed, and the indexes of blood glucose, blood urea nitrogen, creatinine and 24 h urine protein were observed.
At the 6th week of modeling, the number of apoptotic cells in model group was significantly higher than that in normal control group. The expression of GRP78 (6.75 ± 0.65) and caspase12 (11.51 ± 0.32) in model group were significantly higher than that of GRP78 (1.57 ± 0.39), caspase12 (2.66 ± 0.57) (P <0.05). The nephrin expression in the model group (2.29 ± 0.15) was lower than that in the normal control group (5.71 ± 0.53) (P <0.05). Compared with the model group, the number of apoptotic cells in valsartan group was decreased. The expression of GRP78 (3.14 ± 1.00), caspase12 (8.08 ± 2.48) was decreased (P <0.05), while the nephrin (3.35 ± 0.40) decreased slightly (P <0.05).