Literature DB >> 24802264

Protective effects of total extracts of Averrhoa carambola L. (Oxalidaceae) roots on streptozotocin-induced diabetic mice.

Xiaohui Xu1, Tao Liang, Qingwei Wen, Xing Lin, Jingzhi Tang, Qiaoyun Zuo, Liqun Tao, Feifei Xuan, Renbin Huang.   

Abstract

BACKGROUND: In Chinese culture, the roots of Averrhoa carambola L. have long been used for medical purposes due to their potent pharmaceutical activities, such as improving digestive function and treating diabetes.
METHODS: Recently, we prepared extracts of Averrhoa carambola L. root (EACR), which were isolated from Averrhoa carambola L. roots using ethanol or water. This study was designed to investigate the potential effects of EACR on streptozotocin (STZ) diabetic mice and to explore the underlying mechanism of these effects. Male mice were injected with STZ through the tail vein (120 mg/kg body weight) and were identified as a diabetic mouse model when the level of blood glucose was ≥11.1 mmol/L. Subsequently, the mice were administered EACR (150, 300, 600, 1200 mg/kg body weight/d) and metformin (320 mg/kg body weight/d) via intragastric gavage for three weeks.
RESULTS: The results indicated that EACR significantly decreased the serum levels of blood glucose, total cholesterol (TC), triglycerides (TGs) and free fatty acids (FFAs), whereas the content of serum insulin was elevated. In addition, the expressions of apoptosis-related regulators (including caspase-3, caspase-8 and caspase-9) and the apoptosis-induced protein Bax were markedly down-regulated by EACR, whereas the expression of the anti-apoptotic Bcl-2 protein was notably increased. Furthermore, EACR could protect the diabetic mice against the STZ-induced apoptosis of pancreatic β cells.
CONCLUSION: Taken together, these findings indicate that EACR plays an effective hyperglycemic role that is associated with ameliorating metabolic functions and with inhibiting apoptosis in pancreas tissue.
© 2014 S. Karger AG, Basel.

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Year:  2014        PMID: 24802264     DOI: 10.1159/000358695

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


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