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Redox Report
Communications in Free Radical Research
Volume 23, 2018 - Issue 1
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Research Articles

Galangin, a natural flavonoid reduces mitochondrial oxidative damage in streptozotocin-induced diabetic rats

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ABSTRACT

Objective: We designed this study to observe the effect of galangin on damaged mitochondria in the liver of diabetic rats.

Methods: Male albino Wistar rats were made diabetic by injecting streptozotocin (STZ) intraperitoneally (40 mg kg−1 body weight (BW)). Galangin (8 mg kg−1 BW) or glibenclamide (600 µg kg−1 BW) was given orally daily once for 45 days to both healthy and diabetic rats.

Results: Diabetic rats showed significant (P < 0.05) increase in liver mitochondrial oxidant [Thiobarbituric acid reactive substance (TBARS)] level and a significant decrease in enzymatic [superoxide dismutase (SOD), glutathione peroxidase (GPx)] and non-enzymatic (reduced glutathione (GSH)) antioxidant levels when compared with healthy rats. The mitochondrial enzymes isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (α-KGDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) and mitochondrial respiratory chain enzymes NADH-dehydrogenase and Cytochrome c-oxidase were decreased significantly (P < 0.05) in diabetic rats when compared with healthy rats. A natural flavonoid galangin administered to hyperglycemia-induced rats resulted in the following findings as compared to hyperglycemia-induced control rats: the oxidant levels decreased significantly (P < 0.05); the enzymatic and non-enzymatic antioxidant levels increased significantly (P < 0.05) and the function of mitochondrial enzymes and the mitochondrial respiratory chain enzymes increased significantly (P < 0.05).

Conclusion: From the results, we conclude that galangin could maintain liver mitochondrial function in diabetic rats.

Acknowledgements

The authors extend their sincere appreciation to the Deanship of Scientific Research at the King Saud University for its funding of this research through the Research Group Project No. RGP-249.

Disclosure statement

No potential conflict of interest was reported by the authors.