线粒体通透性转变（mPT）孔已成为与细胞凋亡失调情况相关的药物进化的动力。一些化合物通过 mPT 孔打开来阻止肿瘤/癌症。环丙沙星已被证明可以阻碍某些癌细胞的生长并影响细胞凋亡。然而，本研究使用大鼠模型，研究了其通过 mPT 孔开放和苯甲酸雌二醇 (EB) 诱导的子宫内膜增生对线粒体介导的细胞死亡的影响。使用差速离心分离线粒体。测定孔的开放、细胞色素 c 释放 (CCR)、线粒体 ATP 酶 (mATPase) 活性、线粒体脂质过氧化 (mLPO)、半胱天冬酶 3 和 9 水平以及肝 DNA 碎片。对肝脏和子宫切片的组织学评估以及 Bax、caspase 3 和抗凋亡 Bcl-2 水平的免疫表达水平进行定量。结果表明，环丙沙星引起 mPT 孔开放、CCR、mATPase 活性，影响 mLPO、caspases 3 和 9 激活以及肝 DNA 片段化。肝脏切片的组织学显示，在 100 mg/kg 剂量下，出现中度至显着的播散性充血，而较高剂量则显示出严重的肝损伤。在 EB 治疗的大鼠中检测到严重的 EH，而治疗组中的环丙沙星可减轻这种情况。环丙沙星上调 Bax 和 caspase 表达，同时下调抗凋亡 Bcl-2 表达。环丙沙星通过 mPT 孔开放诱导线粒体介导的细胞死亡，并通过 Bax/caspase/Bcl-2 信号通路减轻大鼠模型中 EB 诱导的 EH。© 2023。作者获得 Springer-Verlag GmbH 德国的独家许可，施普林格自然的一部分。

Mitochondrial permeability transition (mPT) pore has become a motive for drug evolvement pertinent to dysregulated apoptosis situations. Some chemical compounds impede tumor/cancer via the inception of mPT pore opening. Ciprofloxacin has been demonstrated to hinder growth and effect apoptosis in some cancer cells. However, using a rat model, this study investigated its effect on mitochondrial-mediated cell death via mPT pore opening and estradiol benzoate (EB)-induced endometrial hyperplasia. Mitochondria were isolated using differential centrifugation. The opening of the pore, cytochrome c release (CCR), mitochondrial ATPase (mATPase) activity, mitochondrial lipid peroxidation (mLPO), caspases 3 and 9 levels, and hepatic DNA fragmentation were determined. Histological evaluation of hepatic and uterine sections and immunoexpression levels of Bax, caspase 3, and anti-apoptotic Bcl-2 levels were quantified. The results show that ciprofloxacin caused mPT pore opening, CCR, mATPase activity, effected mLPO, caspases 3 and 9 activations, and hepatic DNA fragmentation. The histology of the liver section showed moderate to marked disseminated congestion at 100 mg/kg, while higher doses showed severe hepatic damage. Severe EH was detected in the EB-treated rats which was attenuated by ciprofloxacin in the treatment group. The Bax and caspase expressions were upregulated by ciprofloxacin while anti-apoptotic Bcl-2 was downregulated. Ciprofloxacin induces mitochondrial-mediated cell death via mPT pore opening and mitigates EB-induced EH in rat models via Bax/caspase/Bcl-2 signaling pathway.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.