montelukast and Endometrial-Hyperplasia

To study the possible protective role of montelukast in endometrial hyperplesia (EH) rat model, induced by estradiol valerate (EV).. Thirty six female albino Wistar rats were classified into 7 groups: normal control, EV (2 mg/kg/day, p.o.), montelukast (10 mg/kg/day, p.o.), montelukast (1 mg/kg/day, p.o.) + EV (2 mg/kg/day, p.o.), montelukast (10 mg/kg/day, p.o.) + EV (2 mg/kg/day, p.o.), montelukast (20 mg/kg/day, p.o.) + EV (2 mg/kg/day, p.o.) groups. Uterine malondialdehyde (MDA), superoxide dismutase (SOD), total nitrites (NO) and serum total antioxidant capacity (TAC) were determined. Uterine, serum total cholesterol, high density lipoprotein (HDL) and tumor necrosis factor (TNF)-α were measured. Histopathological examination of the uterine tissue was also done. In addition, immunohistochemistry was done using Phosphatase and tensin homolog (PTEN) and inducible nitric oxide synthase (iNOS) antibodies.. Our results showed that montelukast in dose dependant manner improves oxidative stress, lipids profile and TNF α which were affected by EV. Moreover, immunohistochemical examination revealed that montelukast markedly reduced iNOS expression, while expression of PTEN was markedly enhanced, as compared to EV group. The protective effects of montelukast were also verified histopathologically.. Montelukast in dose dependant manner provided biochemical and histo-pathological improvement in EV induced EH, through its anti-inflammatory, antioxidant activity and inhibition of iNOS expression with induction of PTEN expression.

Topics: Acetates; Animals; Anti-Inflammatory Agents; Antioxidants; Cholesterol; Cyclopropanes; Disease Models, Animal; Dose-Response Relationship, Drug; Endometrial Hyperplasia; Estradiol; Female; Nitric Oxide Synthase Type II; Oxidative Stress; Quinolines; Rats; Rats, Wistar; Sulfides; Tumor Necrosis Factor-alpha