Mori cortex prevents kidney damage through inhibiting expression of inflammatory factors in the glomerulus in streptozocin-induced diabetic rats

Authors

  • Bingyang Liu Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
  • Chun Luo Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
  • Fuyan Wang Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
  • Hailai Ni Department of Prevention and Health, Changhai Hospital, Second Military Medical University, Shanghai, PR China
  • Lili Ma Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
  • Pangjie Xu Department of Nephrology, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo, Zhejiang, PR China
  • Shizhong Bu Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
  • Song Li Center for Pharmacogenetics, University of Pittsburgh School of Pharmacy, Pittsburgh, PA 15261, USA
  • Xiaohui Qiu Department of Nephrology, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo, Zhejiang, PR China
  • Xinrong Zou Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
  • Yang Xi Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
  • Yanyan Yuan Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
  • Yudong Chu Department of Nephrology, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo, Zhejiang, PR China
Abstract:

Objective(s): It has been widely reported that Mori cortex extract (MCE) is used for the treatment of diabetes mellitus in traditional medicine. The present study was designed to investigate its mechanism of action in the treatment of diabetic nephropathy (DN). We assessed whether MCE preventive treatment ameliorates kidney damage in high-fat diet and streptozotocin (STZ)-induced type 2 diabetic rats. Materials and Methods: Rats were fed a high-fat diet and injected with STZ. MCE was given to rats daily at 10 g/kg. Fasting blood glucose (FBG) and postprandial plasma glucose were measured. Blood and urine biochemical parameters, renal tissue morphology, and inflammation were investigated. Results: Prevention with MCE significantly decreased FBG and homoeostasis model assessment (HOMA) of IR (HOMA-IR) levels and increased insulin levels in diabetic rats. MCE prevention significantly decreased levels of KW/BW, BUN, Cr, and 24 hr urinary protein. MCE inhibited glomerular basement membrane thickening, tubular epithelial cell hypertrophy, and glomerular capillary dilation. MCE also prevented the disappearance of bowman’s space and renal tubular lumen and decreased collagen deposition in rat kidney. Moreover, MCE reduced the levels of inflammatory factors (MCP-1 and TNF-α) and fibrosis factors (collagen IV and fibronectin). Conclusion: MCE prevents DN through inhibition of inflammation and fibrosis in a rat model. It might provide a safe and effective way to prevent DN.

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Journal title

volume 20  issue 6

pages  715- 721

publication date 2017-06-01

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