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Baicalein induces human osteosarcoma cell line MG-63 apoptosis via ROS-induced BNIP3 expression
Fangfan Ye1, Honghan Wang, Lusi Zhang
1Department of Anesthesiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Hunan, China, ye-cathy@126.com.
Abstract:
Baicalein, a flavonoid compound, is one of the active constituents of the root of Scutellariae Radix. Its antitumor effects have attracted widespread attention worldwide. One of its major functions is to induce the apoptosis of tumor cells, but the antitumor mechanism is currently unclear. In the present study, we found that baicalein increased MG-63 cell mortality in a dose-dependent manner. Meanwhile, baicalein activated apoptosis through induced intracellular reactive oxygen species (ROS) generation, and that ROS scavenger N-acetyl-cysteine (NAC), glutathione (GSH), and superoxide dismutase (SOD) apparently inhibited intracellular ROS production, consequently attenuating the baicalein-induced apoptosis. Baicalein also induce the mitochondrial fragmentation which precedes the cell apoptosis. This morphological alteration is accompanied by an increase in the expression of the protein BNIP3 as well as Mul1 and Drp1. Furthermore, we show that the inhibition of BNIP3 expression can inhibit cell apoptosis by baicalein treatment. Taken together, our results bring the evidence of a mechanism that links apoptosis and ROS-induced BNIP3 expression in MG-63 cells with bacalein treatment and suggest that baicalein has a good potential as an anti-osteosarcoma drug.
Insights
Baicalein, a flavonoid, induces apoptosis in osteosarcoma cells by increasing reactive oxygen species (ROS) and BNIP3 expression. This mechanism highlights baicalein
Area of Science:
- Molecular Biology
- Cell Biology
- Pharmacology
Background:
- Baicalein, a flavonoid from Scutellariae Radix, exhibits antitumor properties.
- Its role in inducing tumor cell apoptosis is recognized, but the precise mechanism remains unclear.
- Osteosarcoma remains a significant challenge in oncology.
Purpose of the Study:
- To elucidate the antitumor mechanism of baicalein in MG-63 osteosarcoma cells.
- To investigate the role of reactive oxygen species (ROS) and BNIP3 in baicalein-induced apoptosis.
Main Methods:
- MG-63 cells were treated with varying concentrations of baicalein.
- Intracellular ROS generation was measured, and ROS scavengers (NAC, GSH, SOD) were used.
- Mitochondrial morphology, BNIP3, Mul1, and Drp1 protein expression were analyzed.
Main Results:
- Baicalein increased MG-63 cell mortality and induced apoptosis in a dose-dependent manner.
- Apoptosis was mediated by increased intracellular ROS, which was attenuated by ROS scavengers.
- Baicalein induced mitochondrial fragmentation and increased BNIP3, Mul1, and Drp1 expression; inhibiting BNIP3 reduced apoptosis.
Conclusions:
- Baicalein induces apoptosis in MG-63 cells via ROS generation and subsequent BNIP3 upregulation.
- The findings reveal a mechanism linking ROS-induced BNIP3 expression to baicalein-mediated apoptosis.
- Baicalein shows potential as an anti-osteosarcoma therapeutic agent.
