Morin a Flavonoid Exerts Antioxidant Potential in Streptozotocin-induced Hepatotoxicity

Osama A Alkhamees

doi:10.19026/bjpt.4.5382

Abstract

Although diabetic hepatopathy is potentially less common, it may be appropriate for addition to the list of target organ conditions related to diabetes. This study was designed to evaluate the hepatoprotective activity of morin in Streptozotocin (STZ)-induced diabetes rats. Morin (15 and 30 mg/kg/day) was treated to diabetic rats for five consecutive weeks. In serum, fasting glucose and Alkaline Phosphatase (ALP) levels were estimated and found significant increase in diabetic group as compared to controls. Nucleic acids, total protein, Malondialdehyde (MDA), Total Glutathione (T-GSH), Non-Protein Sulphydral (NP-SH) levels and Superoxide Dismutase (SOD) activity was measured in hepatic cells. Oxidative stress was confirmed by increasing MDA and decreasing T-SHG, NP-SH and nucleic acid levels and SOD activity in hepatic cells of diabetic rats. Morin treatment to diabetic rats significantly reduced the STZ-induced oxidative stress by following decrease MDA and increase T-GSH, DNA levels and increase SOD activity in hepatic cells respectively. These biochemical findings were matched with histopathological verifications. The findings obtained from this study indicate that morin exerts protection to STZ-induced diabetic rats against oxidative stress. This could be due to prevention or inhibition of lipid peroxidative system by its antioxidant and hepatoprotective effect. In conclusion, morin has been shown to possess antidiabetic effect in STZ-induced detoxication and antioxidant properties. But the exact underlying mechanism needs to be elucidated.

Highlights

Diabetes Mellitus (DM) is one of the most prevalent chronic metabolic disorder and a major health problem around the world
Numerous studies have reported that DM is associated with oxidative stress, leading to an increased production of Reactive Oxygen Species (ROS) where they formed as natural toxic byproducts of the normal metabolism of oxygen, including superoxide radical (O2-), hydrogen peroxide (H2O2) and hydroxyl radical (OH) or diminution of antioxidant defense system (Vincent et al, 2004)
All experimental procedure including euthanasia was conducted in accordance with the National Institute of Health Guide for the Care and Use of Laboratory Animals, Institute for Laboratory Animal Research (NIH Publications No 80-23; 1996) as well as Ethical Guidelines of the Experimental Animal Care Centre, College of Pharmacy, King Saud University (KSU), Riyadh, Kingdom Saudi Arabia (KSA)

Summary

Introduction

Diabetes Mellitus (DM) is one of the most prevalent chronic metabolic disorder and a major health problem around the world. Numerous studies have reported that DM is associated with oxidative stress, leading to an increased production of Reactive Oxygen Species (ROS) where they formed as natural toxic byproducts of the normal metabolism of oxygen, including superoxide radical (O2-), hydrogen peroxide (H2O2) and hydroxyl radical (OH) or diminution of antioxidant defense system (Vincent et al, 2004). Inference of oxidative stress in the pathogenesis of diabetes mellitus is suggested by ROS generation and due to non-enzymatic protein glycosylation, auto-oxidation of glucose; weaken antioxidant enzyme and formation of peroxides (Vincent et al, 2004; Pari and Latha, 2005). Lipid Peroxidation (LPO) is a key marker of oxidative stress. It is a free radical-induced progression causing oxidative worsening of polyunsaturated fatty acids that eventually consequences in extensive membrane damage and dysfunction. The noteworthy extent of LPO products that was measured as Thiobarbituric

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Conclusion