Early renal tubulointerstitial changes and their interventions with Shenkang Injection in diabetic rats
Liu, Y.; Ma, Q.; Yang, G.; Zhao, J.; Liu, S.; Ao, Q.; Du, J.; Wang, X.; Cheng, Q.
Zhonghua Yi Xue Za Zhi 95(4): 289-293
2015
ISSN/ISBN: 0376-2491 PMID: 25877247 Document Number: 679381
To explore whether renal tubulointerstitial lesions are early renal pathological changes and its interventions in diabetic rats. The type 2 diabetic rat model was induced by a high-sugar and high-fat diet with a low-dose intraperitoneal injection of streptozotocin. And Shenkang Injection (SKI) was used as an intervention drug. A total of 30 Sprague-Dawley rats were divided randomly into diabetic (DM), DM+SKI (DMSK) and normal control (NC) groups. The general status, blood biochemical parameters, microalbuminuria and urinary N-acetyl-D-glueosaminidas (NAG) were recorded. The insulin resistance of diabetic rats was detected with hyperinsulinemic-euglycemic clamp test.Renal pathological changes were evaluated with periodic acid-Schiff (PAS) staining. The expression of Toll-like receptor 4 (TLR4) in kidney tissue and renal interstitial CD68(+) cells was detected with immunohistochemistry. The levels of microalbuminuria, urinary NAG, glomerular volume, renal tubular score, TLR4 expression and renal interstitial CD68(+) cells significantly increased in DM rats with body weight loss and insulin resistance (IOD value of TLR4: 6 289.86 ± 272.45 vs 207.14 ± 22.37; CD68(+) cells: 8.79 ± 0.79 vs.1.23 ± 0.52). All changes in DM rats improved after SKI intervention (P < 0.05). Renal tubulointerstitial lesions are early renal damages in type 2 diabetic rats.SKI can attenuate diabetic tubulointerstitial damage and delay the progression of diabetic nephropathy associated with the inhibition of TLR4 expression and inflammation-mediated macrophage infiltration.