Mori cortex prevents kidney damage through inhibiting expression of inflammatory factors in the glomerulus in streptozocin-induced diabetic rats
نویسندگان
1 Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
2 Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
3 Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
4 Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
5 Department of Nephrology, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo, Zhejiang, PR China
6 Center for Pharmacogenetics, University of Pittsburgh School of Pharmacy, Pittsburgh, PA 15261, USA
7 Department of Prevention and Health, Changhai Hospital, Second Military Medical University, Shanghai, PR China
8 Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
9 Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
10 Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
11 Department of Nephrology, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo, Zhejiang, PR China
12 Department of Nephrology, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo, Zhejiang, PR China
13 Runliang Diabetes Laboratory, Diabetes Research Center, Ningbo University. Ningbo, Zhejiang, PR China
doi
10.22038/ijbms.2017.8842چکیده
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.
