Tangshen Formula Attenuates Colonic Structure Remodeling in Type 2 Diabetic Rats.

Pengmin Chen,Meihua Yan,Haojun Zhang,Xin Yang,Lin Pan,Huicun Zhang,Ping Li,Yun Zhang,Xin Li,Jingbo Zhao,Tingting Zhao

doi:10.1155/2017/4064156

Abstract

Aim. This study investigated the effect and mechanism of the Chinese herbal medicine Tangshen Formula (TSF) on GI structure remodeling in the rat model of diabetes. Methods. Type 2 diabetic rats were used. Wet weight per unit length, layer thicknesses, levels of collagens I and III, nuclear factor kappa B (NF-κB), interferon-γ (IFN-γ), interleukin-6 (IL-6), transforming growth factor-β1 (TGF-β1), and Smad2/3 expression in the rat colon were measured. Results. Compared with the control group animals, wet weight and layer thicknesses of the colon increased, and expressions of collagens I and III, NF-κB, IFN-γ, IL-6, TGF-β1, and Smad2/3 increased significantly in the diabetic animals. TSF inhibited increase in colonic wet weight and layer thicknesses, downregulated expressions of collagens I and III in the mucosal layer, and downregulated expressions of NF-κB, IFN-γ, IL-6, TGF-β1, and Smad2/3 in the colon wall. Furthermore, level of expression of NF-κB was associated with those of TGF-β1 and Smad2/3. Expression of TGF-β1 was associated with the most histomorphometric parameters including colonic weight, mucosal and muscle thicknesses, and levels of collagens I and III in mucosal layer. Conclusion. TSF appears to attenuate colonic structure remodeling in type 2 diabetic rats through inhibiting the overactivated pathway of NF-κB, thus reducing expressions of TGF-β1.

Highlights

People with diabetes mellitus (DM) often have gastrointestinal (GI) motility disorders
Marked differences in body weight between the NC and DM groups and between the NC and Tangshen Formula (TSF) groups were evident at week 9, which was 3 weeks after administering citrate buffer or STZ (P < 0.01) and continued through the end of the experiment
The present study found that the muscle thickness of the colon increased in the DM group but this increase was inhibited in the TSF group

Summary

Introduction

People with diabetes mellitus (DM) often have gastrointestinal (GI) motility disorders. Disorders of transit and motility in the colon [4,5,6] likely contribute to constipation in diabetes [7]. It is well known that in diabetes the muscle and mucosal layers, functions of neurons and interstitial cells of Cajal, and GI hormone levels are impaired [1, 8]. Dysfunctions of neurons and interstitial cells of Cajal in diabetes seem to be mainly responsible for GI motility disorder, the role of muscle and mucosal layer remodeling in GI motility remains unclear and needs to be investigated further. How diabetic enteropathy affects the colon is not entirely understood [1]. Histomorphologic remodeling of the colon wall may be involved in the pathogenesis of colon motility dysfunction [9]

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Results

Conclusion