Literature DB >> 26279435

Effect of the Total Extract of Averrhoacarambola (Oxalidaceae) Root on the Expression Levels of TLR4 and NF-κB in Streptozotocin-Induced Diabetic Mice.

Xiaohui Xu1, Tao Liang, Xing Lin, Qingwei Wen, Xingmei Liang, Weisi Li, Feizhang Qin, Ni Zheng, Jianjun Ming, Renbin Huang.   

Abstract

BACKGROUND: Averrhoacarambola L., which is a folk medicine used in diabetes mellitus (DM) in ancient China, has been reported to have anti-diabetic efficacy. AIMS: The aim of this study was to evaluate the hypoglycemic effect of the extract of Averrhoacarambola L. root (EACR) on the regulation of the Toll-like receptor 4 (TLR4)-Nuclear-factor kappa B (NF-κB) pathway in B) pathway in streptozotocin (STZ)-induced diabetic mice.
METHODS: the mice were injected with STZ (120 mg/kg body weight) via a tail vein. After 72 h, the mice with FBG ≥ 11.1 mmol/L were confirmed as having diabetes. Subsequently, the mice were treated intragastrically with EACR (300, 600, 1200 mg/kg body weight/d) and metformin (320 mg/kg body weight/d) for 14 days.
RESULTS: As a result the serum fasting blood glucose (FBG), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels were decreased following EACR administration. Immunohistochemical analysis revealed that the pancreatic tissue expression levels of TLR4 and NF-κB were downregulated after EACR administration. EACR suppressed pancreatic mRNA expression level of TLR4 and blocked the downstream NF-κB pathway in the pancreas. According to Western blot analysis EACR suppressed pancreatic TLR4 and NF-κB protein expression levels. Histopathological examination of the pancreas showed that STZ-induced pancreas lesions were alleviated by the EACR treatment.
CONCLUSION: These findings suggest that the modulation of the IL-6 and TNF-α inflammatory cytokines and the suppression of the TLR4-NF-κB pathway are most likely involved in the anti-hyperglycemic effect of EACR in STZ-induced diabetic mice.
© 2015 S. Karger AG, Basel.

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Year:  2015        PMID: 26279435     DOI: 10.1159/000430194

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


  5 in total

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