Regulating role of ethyl acetate fraction of Tephrosia tinctoria pers. in carbohydrate metabolism and oxidative stress in diabetic rats

[Display omitted] •The efficacy of TTEA for antidiabetic activity proved in metabolic level.•TTEA inhibits the gluconeogenesis by decreasing the level of Malate dehydrogenase.•TTEA enhanced the level of glycolysis and TCA cycle enzymes except Malate dehydrogenase.•TTEA regulated most of the antidiab...

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Veröffentlicht in:Biomedicine & pharmacotherapy 2019-06, Vol.114, p.108842-108842, Article 108842
Hauptverfasser: Krishnasamy, Rajaram, Periyasamy, Sureshkumar
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Sprache:eng
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Zusammenfassung:[Display omitted] •The efficacy of TTEA for antidiabetic activity proved in metabolic level.•TTEA inhibits the gluconeogenesis by decreasing the level of Malate dehydrogenase.•TTEA enhanced the level of glycolysis and TCA cycle enzymes except Malate dehydrogenase.•TTEA regulated most of the antidiabetic targets significantly. Traditionally, Tephrosia tinctoria (TT) is used as antimicrobial, larvicidal, antidiabetic and antioxidant agents. In the present study, the diabetes was induced in male albino - rats using alloxan (140 mg/kg b.w.) and treated with ethyl acetate extract (100 and 200 mg/kg b.w.) of T. tinctoria (TTEA) orally for 28 days. The effects of TTEA on biochemical paramets were studied. The results of this comprehensive study revealed that the TTEA significantly restored the altered parameters in alloxan-induced diabetic rats. The diabetes-induced elevated levels of glycogenolysis and gluconeogenesis metabolism were significantly controlled by TTEA. In the same, the decreased glycogenesis, glycolysis and TCA cycle metabolisms were significantly increased by TTEA. The enzymatic and non- enzymatic antioxidant levels were significantly elevated in TTEA treated diabetic rats and also the total non-enzymatic antioxidants capacity of serum and liver homogenate were calculated though DPPH inhibition. To conclude, this study demonstrates the anti-diabetic effect of TTEA possibly mediated through regulating carbohydrate metabolism and antioxidant status.
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2019.108842