Nephroprotective Effect of Estradiol and Moreinga Oleifera Extract in Ovarictomized Rat

Document Type : Original Article

Authors

1 Clinical Physiology department, Faculty of Medicine, Menoufia University

2 Pharmacology Department, Faculty of Medicine, Menoufia University

3 Histology and cell Biology Department, Faculty of Medicine, Menoufia University

4 Anatomy and Embryology Department, Faculty of Medicine, Menoufia University

5 Physiology department, faculty of medicine , menufia university

Abstract

Estrogen deficiency occurring during menopause seems to increase renal oxidative stress which may predispose to renal malfunctioning. We evaluate the reno-protective effects of estradiol and Moreinga Oleifera supplementation in a rat model of menopause trying to clarify the mechanism(s) by which these therapies may execute its reno- protective effects on oxidative stress and inflammatory changes in the kidney of rat model of menopause.
Forty female albino rats were divided into 5 groups, 8 rats in each group, as follows: (Control group) divided into A receive no treatment and B receive vehicle only, (sham group) received sesame oil, ovariectomized non treated group (OV) received sesame oil, Ovariectomized-estradiol treated group (OVEst) and Ovariectomized Moreinga Oleifera treated group (OVMO). Serum urea, creatinine, creatinine clearance and serum tumour necrosis factor α (TNFα) were estimated. Superoxide dismutase (SOD), malondialdehyde (MDA) and Interleukin 10 (IL10) mRNA gene expressions in kidney tissue were measured. Also histopathological, immunohistochemical and morphometrical studies for kidney tissue were performed.
OVEST and OVMO showed significant decrease in serum urea, creatinine, TNF-α and MDA level in kidney tissue but significant increase in kidney tissue SOD and IL10 mRNA gene expression in kidney tissue when compared to the OV group. Also, histopathological alterations were ameliorated. The improving effects on the kidney tissues, may be due to the inflammatory gene modifications including reduction of pro-inflammatory cytokines TNF-α and increase in anti-inflammatory IL-10 mRNA expression, reduced oxidative stress and mechanistic downregulation of NF-ĸB, and iNOS expression.

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