:: Volume 20, Issue 1 (1-2022) ::
Int J Radiat Res 2022, 20(1): 1-7 Back to browse issues page
Lycium barbarum polysaccharide inhibits the mitochondrial pathway of apoptosis in mouse bone marrow mononuclear cells after radiation injury
H. Huang, Y. Wang, L. Zhang, F.Q. Hu, J. Li, H. Pang
Department of Nuclear Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China , phua1973@163.com
Abstract:   (1532 Views)
Background: Lycium barbarum is a traditional Chinese medicine. Its pharmacological effects mainly rely on a component called Lycium barbarum polysaccharide (LBP). The present study aims to explore the mechanism by which LBP reduces radiation damage in X-ray-irradiated cultured mouse bone marrow mononuclear cells (BMNCs) and the potential involvement of apoptosis. Materials and Methods: Mouse BMNCs were cultured in vitro and exposed to radiation. After 24 hours of LBP treatment, BMNCs viability was detected by cck-8 method, apoptosis rate was examined by Flow cytometry (FCM), Mitochondrial membrane potential (MMP) fluorescence was detected by JC-1, and the expression of mitochondrial pathway-associated protein was measured by immunoblotting. Results: LBP significantly increased BMNCs viability and reduced the apoptosis rate of radiation-exposed BMNCs 24 h after treatment compared to the non-treated control group. In a mitochondrial membrane potential fluorescence assay, LBP reduced the radiation-induced decrease in mitochondrial membrane potential. Western blot analysis further proved this point, where LBP inhibited the release of cytochrome C from mitochondria and also inhibited the expression of caspase 9 and other mitochondrial-related proteins. Conclusions: The mechanism of LBP action in radiation-exposed mouse BMNCs cells seems to involve inhibition of the mitochondrial apoptosis pathway.
Keywords: Lycium barbarum polysaccharide, radiation, apoptosis, in vitro.
Full-Text [PDF 2267 kb]   (920 Downloads)    
Type of Study: Original Research | Subject: Radiobiology

XML     Print

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
Volume 20, Issue 1 (1-2022) Back to browse issues page