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Asian Journal of Biological Sciences
Year: 2020  |  Volume: 13  |  Issue: 2  |  Page No.: 228 - 236

Role of PPARγ/Anti-inflammatory Axis in the Protective Effect of Ellagic Acid Against FSD/STZ-induced Gestational Diabetes in Rats

Adel Abdel-Moneim, Ahmed Hosni, Eman Salah Abdel-Reheim and Ahmed Ismail    

Abstract: Background and Objective: Ellagic acid (EA) is a natural polyphenol compound with promising anti-diabetic effects. This study examined the safe effects of EA from Padina boryana against fatty-sucrosed diet (FSD)/streptozotocin (STZ)-induced gestational diabetes mellitus (GDM), referring to the role of peroxisome proliferator-activated receptor gamma (PPARγ)/anti-inflammatory axis. Materials and Methods: Female albino Wistar rats were allocated into three groups. Group I fed with normal diet (ND). Group II and III were fed FSD for 8 weeks (five pre-gestational and three gestational). Rats of group III were administered with a daily oral dose of 50 mg kg–1 EA 1 week before mating onward. At the 7th day of the gestation, to induce GDM, FSD-fed dams were injected intraperitoneally with STZ (25 mg kg–1 b.wt.). Results: Pre-mating administration of EA controlled the body weight loss, hyperphagia, glucose intolerance and insulin resistance during the gestational period than in diabetic dams. EA also reduced levels of total cholesterols, triglycerides, hepatic lipid peroxidation, fructosamine and nitric oxide levels, while it significantly increased levels of high-density lipoprotein-cholesterol, liver glycogen, glutathione and catalase activity. In addition, EA supplementation markedly attenuated serum levels of tumor necrosis factor-alpha and leptin while adiponectin level was elevated. These effects coincided with up-regulation of the visceral adipose tissue PPARγ expression at term pregnancy. Besides, EA nearly normalized number of viable fetuses, implantation loss sites as well as fetal insulin and glucose levels. Conclusion: EA safely ameliorates gestational hyperglycemia in rats via potential association of PPARγ and anti-inflammatory biomarkers that suppress the oxidative stress status.

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