Role and Mechanism of GSK3β/Fis1 Signaling Pathway in the Apoptosis of Osteoblast Induced by Methylglyoxal
10.11969/j.issn.1673-548X.2024.06.022
- VernacularTitle:GSK3β/Fis1信号通路在甲基乙二醛诱导成骨细胞凋亡中的作用及机制
- Author:
Panpan DAI
1
;
Hui YU
;
Peng ZHANG
Author Information
1. 317000 浙江省台州医院、台州恩泽医疗中心(集团)恩泽医院
- Keywords:
Diabetic periodontitis;
Methylglyoxal;
Glycogen synthase kinase 3β;
Fission protein 1;
Apoptosis
- From:
Journal of Medical Research
2024;53(6):104-108
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role and mechanism of glycogen synthase kinase 3β(GSK3 β)/fission protein 1(Fis1)signa-ling pathway in the apoptosis of osteoblast induced by methylglyoxal.Methods LiCl was used as GSK3β inhibitor,and the cells were randomly divided into 4groups:control group,MG group,LiCl group,LiCl+MG group.The cell proliferation activity was detected by MTT assays.The cell apoptosis was analyzed by Tunel assays.The protein expression levels of GSK3β and Fis1 were detected by Western blot.Mitochondrial morphology was analyzed by MitoTracker Deep Red.Results MTT assay showed that MG inhibited the proliferation activity of osteoblast.Tunel staining showed that MG induced osteoblast apoptosis.Western blot assay showed that the phosphorylation lev-el of GSK3β decreased and the expression level of Fis1 protein increased after MG treatment.MitoTracker Deep Red staining showed that mitochondrion were fragmented after MG treatment.After the addition of GSK3β inhibitor LiCl,compared with the MG group,the MG-inhibited cell proliferation activity and apoptosis were significantly restored.Meanwhile,the phosphorylation level of GSK3β protein was increased,the expression level of Fis1 protein was decreased,and the mitochondrial morphology was restored.Conclusion MG may pro-mote the increase of mitochondrial division and induce osteoblast apoptosis by regulating GSK3 β/Fis1 signaling pathway.
