Estradiol valerate-induced endometrial hyperplasia in rats: A possible role for NFκB and caspase-3

Document Type : Original Article

Author

Pharmacology department, Faculty of medicine, Minia university

Abstract

Endometrial hyperplasia is induced by estradiol valerate (EV), however the underline mechanism is not fully understood. The aim of this study is to examine the impact of EV dosing on oxidative stress, inflammation, and apoptosis. The rats were allocated into two groups: Group 1 (Control) was given 1 ml of 0.5% aqueous solution of carboxy methyl celluse (CMC) as the drug's vehicle. Group 2 (EV-treated) received 2 mg/kg/day Estradiol valerate (EV) suspended in CMC orally. The rats were sacrificed 10 days later and utrine tissues were harvested for histopathological and biochemical analysis. Biochemical tests used for assessing oxidative marker malonaldehyde (MDA) and serum total antioxidant capacity (TAC). Interestingly, EV- treated group showed a remarkable histopathological and biochemical changes. It showed a significant increases in uterine MDA levels and decreases in uterine TAC and caspase-3 levels with increases in NFκB expression.

In conclusion, EV induced endometrial hyperplasia via oxidative stress damage, induction of NFκB and reduction in apoptotic marker (caspase-3).

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