Redox-mediated mitochondrial collapse drives intrinsic apoptotic signaling in ELT3 cells response to apigenin

Information from the abstract

Uterine leiomyoma is the most common benign gynecological tumor and a major cause of abnormal uterine bleeding, pelvic pain, and infertility. Although apigenin (API) exhibits antioxidant, antiproliferative, and anticancer activities, its mechanism of action in uterine leiomyoma, particularly the involvement of oxidative stress-mediated mitochondrial apoptosis, remains unclear. This study investigated the role of oxidative stress in API-induced apoptosis using rat uterine leiomyoma ELT3 cells. Cells were treated with 50 and 100 µM API for 48 h. Oxidative stress was assessed by measuring reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione reductase (GR) activity. Mitochondrial membrane potential (ΔΨm), cell proliferation, lactate dehydrogenase (LDH) release, and apoptosis-related gene and protein expression were also evaluated. API significantly increased ROS and MDA levels while decreasing GR activity, indicating oxidative stress. These changes were accompanied by ΔΨm collapse, reduced cell proliferation, increased LDH release, upregulation of p53, Bax, caspase-3, and caspase-9, and downregulation of Bcl-2, indicating activation of the intrinsic mitochondrial apoptotic pathway. These findings demonstrate that API induces intrinsic mitochondrial apoptosis through oxidative stress-mediated mechanisms, providing mechanistic evidence for its cytotoxic effects and supporting its potential as a phytochemical candidate for uterine leiomyoma treatment.

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Related topics: Flavonoids in Medical Research · Mitochondrial Function and Pathology · Cell death mechanisms and regulation