Protective Effect of Valsartan on Podocyte Injury in Rats with Diabetic Nephropathy
American Journal of Life Sciences
Volume 6, Issue 3, June 2018, Pages: 47-51
Received: Dec. 5, 2018;
Published: Dec. 6, 2018
Views 125 Downloads 40
Qingfen Wang, Department of Nephrology, Binzhou People's Hospital, Binzhou, China
Rui Li, Department of Nephrology, Binzhou People's Hospital, Binzhou, China
Weiwei Li, Department of Nephrology, Binzhou People's Hospital, Binzhou, China
Lei Wang, Department of Urology, Binzhou People's Hospital, Binzhou, China
To investigate the mechanism of valsartan protecting podocytes and inhibiting renal injury in diabetic rats. The rat model of diabetic nephropathy was induced by combination of valsartan and high-sugar and high-fat diet. The urinary protein content, renal index, inflammatory and antioxidant indexes in the kidney, renal pathological changes and podocyte holes were investigated. Membrane WT1 and P-Cadherin protein expression levels. Compared with the model group, the 24h urine protein content of valsartan was significantly decreased (P<0.05). Valsartan significantly inhibited the body weight of the model group (P<0.01), and significantly inhibited The increase of renal index (P<0.05); the high and middle doses of valsartan could significantly reduce the levels of IL-β, TNF-α and IL-6 in rat kidney (P<0.05-0.01). The valsartan high and middle dose groups significantly reduced MDA content in rat kidney (P<0.05), and significantly increased SOD activity (P<0.05). HE and PAS staining showed that valsartan was used in model group rats. The pathological changes were alleviated, and the glomerular morphology returned to normal. The protein expression of WT1 and P-Cadherin in the kidney of DN rats by Western blot showed that P- in the kidney tissue of valsartan rats. The expression levels of Cadherin and WT1 protein were significantly increased (P<0.05). Valsartan can regulate the expression of podocyte membrane proteins WT1 and P-Cadherin to protect podocytes, and then repair renal function and anti-diabetic nephropathy.
Protective Effect of Valsartan on Podocyte Injury in Rats with Diabetic Nephropathy, American Journal of Life Sciences.
Vol. 6, No. 3,
2018, pp. 47-51.
Wadie W, El-Tanbouly DM. Vinpocetine mitigates proteinuria and podocytes injury in a rat model of diabetic nephropathy. European journal of pharmacology. 2017; 814: 187-95.
Peng T, Chang X, Wang J, Zhen J, Yang X, Hu Z. Protective effects of tacrolimus on podocytes in early diabetic nephropathy in rats. Molecular medicine reports. 2017; 15 (5): 3172-8.
Mukhi D, Nishad R, Menon RK, Pasupulati AK. Novel Actions of Growth Hormone in Podocytes: Implications for Diabetic Nephropathy. Frontiers in medicine. 2017; 4: 102.
Liu Y, Zhang J, Wang Y, Zeng X. Apelin involved in progression of diabetic nephropathy by inhibiting autophagy in podocytes. Cell death & disease. 2017; 8 (8): e3006.
Huang SS, Ding DF, Chen S, Dong CL, Ye XL, Yuan YG, et al. Resveratrol protects podocytes against apoptosis via stimulation of autophagy in a mouse model of diabetic nephropathy. Scientific reports. 2017; 7: 45692.
Hsu YH, Li HH, Sung JM, Chen WY, Hou YC, Weng YH, et al. Interleukin-20 targets podocytes and is upregulated in experimental murine diabetic nephropathy. Experimental & molecular medicine. 2017; 49 (3): e310.
Guo Y, Song Z, Zhou M, Yang Y, Zhao Y, Liu B, et al. Infiltrating macrophages in diabetic nephropathy promote podocytes apoptosis via TNF-alpha-ROS-p38MAPK pathway. Oncotarget. 2017; 8 (32): 53276-87.
Zhang H, Luo W, Sun Y, Qiao Y, Zhang L, Zhao Z, et al. Wnt/beta-Catenin Signaling Mediated-UCH-L1 Expression in Podocytes of Diabetic Nephropathy. International journal of molecular sciences. 2016; 17 (9).
Tharaux PL, Huber TB. How Is Proteinuric Diabetic Nephropathy Caused by Disturbed Proteostasis and Autophagy in Podocytes? Diabetes. 2016; 65 (3): 539-41.
Sawada K, Toyoda M, Kaneyama N, Shiraiwa S, Moriya H, Miyatake H, et al. Upregulation of alpha3beta1-Integrin in Podocytes in Early-Stage Diabetic Nephropathy. Journal of diabetes research. 2016; 2016: 9265074.
Liu F, Zong M, Wen X, Li X, Wang J, Wang Y, et al. Silencing of Histone Deacetylase 9 Expression in Podocytes Attenuates Kidney Injury in Diabetic Nephropathy. Scientific reports. 2016; 6: 33676.
Ji ZZ, Xu YC. Melatonin protects podocytes from angiotensin II-induced injury in an in vitro diabetic nephropathy model. Molecular medicine reports. 2016; 14 (1): 920-6.
He Y, Zhang M, Wu Y, Jiang H, Fu H, Cai Y, et al. Aberrant activation of Notch-1 signaling inhibits podocyte restoration after islet transplantation in a rat model of diabetic nephropathy. Cell death & disease. 2018; 9 (10): 950.
Zhang Y, Chen X, Yuan L, Wu J, Guo N, Liu J. Down-regulation of IRAK1 attenuates podocyte apoptosis in diabetic nephropathy through PI3K/Akt signaling pathway. Biochemical and biophysical research communications. 2018; 506 (3): 529-35.
Lei X, Zhang L, Li Z, Ren J. Astragaloside IV/lncRNA-TUG1/TRAF5 signaling pathway participates in podocyte apoptosis of diabetic nephropathy rats. Drug design, development and therapy. 2018; 12: 2785-93.
Wang Y, Li H, Song SP. beta-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/beta-Catenin Pathway. Medical science monitor: international medical journal of experimental and clinical research. 2018; 24: 1724-32.
Pan Y, Jiang S, Hou Q, Qiu D, Shi J, Wang L, et al. Dissection of Glomerular Transcriptional Profile in Patients With Diabetic Nephropathy: SRGAP2a Protects Podocyte Structure and Function. Diabetes. 2018; 67 (4): 717-30.
Wang XB, Zhu H, Song W, Su JH. Gremlin Regulates Podocyte Apoptosis via Transforming Growth Factor-beta (TGF-beta) Pathway in Diabetic Nephropathy. Medical science monitor: international medical journal of experimental and clinical research. 2018; 24: 183-9.
Lv Z, Hu M, Fan M, Li X, Lin J, Zhen J, et al. Podocyte-specific Rac1 deficiency ameliorates podocyte damage and proteinuria in STZ-induced diabetic nephropathy in mice. Cell death & disease. 2018; 9 (3): 342.