Metformin induces apoptosis via uterus mitochondrial permeability transition pore opening and protects against estradiol benzoate-induced uterine defect and associated pathophysiological disorder in female Wistar rats
نویسندگان
چکیده
Abstract Background Some antitumor or anticancer agents have been shown to execute cell death by induction of mitochondrial permeability transition (mPT) pore opening in order elicit their chemotherapeutic effect. Therefore, this study investigated the effect metformin on via rat uterus mPT and estradiol benzoate-induced uterine defect associated pathophysiological disorder female rat. Mitochondria were isolated using differential centrifugation. The opening, cytochrome c release ATPase activity determined spectrophotometrically. Caspases 9 3 activities, MDA levels SOD, GSH ELISA technique. Histological histochemical assessments section carried out standard methods. Results Metformin at concentrations 10–90 μg/mL, showed no significant mATPase c. However, oral administration caused enhancement activation caspases significantly 300 400 mg/kg. protected against benzoate (EB)-induced other disorder. It also improved antioxidant defense system. histological evaluation revealed protective cellular architecture while examination severe hyperplasia EB-treated rats, remarkably reversed co-treatment. Conclusion This suggests that high doses induces apoptosis protects EB-induced (hyperplasia)
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ژورنال
عنوان ژورنال: Bulletin of the National Research Centre
سال: 2021
ISSN: ['2522-8307', '1110-0591']
DOI: https://doi.org/10.1186/s42269-021-00562-6