Mechanism of alpha-mangostin improving apoptosis and inflammatory response in rat chondrocytes
- VernacularTitle:α-倒捻子素改善大鼠软骨细胞的凋亡和炎症反应的作用机制
- Author:
Xiao-yuan MENG
1
;
Meng-yu AN
1
;
Zhi-gang WANG
1
;
Le MA
1
Author Information
- Publication Type:Journal Article
- Keywords: alpha-mangostin; BDNF/PI3K/Akt signaling pathway; macrophage polarization; chondrocytes; apoptosis; inflammatory response
- From: Journal of Regional Anatomy and Operative Surgery 2025;34(9):759-764
- CountryChina
- Language:Chinese
- Abstract: Objective To explore the effects of alpha-mangostin(α-MG)on the in vitro osteoarthritis(OA)in rat chondrocytes induced by lipopolysaccharide(LPS)and the M1 polarization of macrophages.Methods An in vitro OA model of rat chondrocytes was induced by LPS.Both rat chondrocytes and macrophages were divided into the control group(normal culture),LPS group(stimulated with 1 μg/mL LPS for 24 hours),LPS+α-MG group(stimulated with 40 μmol/L α-MG combined with 1 μg/mL LPS for 24 hours),LPS+α-MG si-NC group(transfected with 70 μg/mL si-NC and stimulated with 40 μmol/L α-MG and 1 μg/mL LPS for 24 hours),and LPS+α-MG+si-BDNF group(transfected with 70 μg/mL si-BDNF and stimulated with 40 μmol/L α-MG and 1 μg/mL LPS for 24 hours).CCK-8 assay was used to detect the proliferative viability of chondrocytes and macrophages in each group,and flow cytometry was used to detect the apoptosis of chondrocytes and the polarization of macrophages.ELISA was used to detect the levels of interleukin(IL)-1β,IL-6,and tumor necrosis factor(TNF)-α of chondrocytes in each group.Western blot was used to detect the expression of BDNF,PI3K,and Akt in chondrocytes and macrophages.Results In chondrocytes,compared with the control group,the LPS group had decreased cell proliferation rate,increased cell apoptosis rate,down-regulated expression of BDNF,PI3K and Akt proteins,and up-regulated levels of IL-1β,IL-6 and TNF-α(P<0.05);compared with the LPS group,the LPS+α-MG group showed increased cell proliferation rate,decreased cell apoptosis rate,up-regulated expression of BDNF,PI3K and Akt proteins,and down-regulated levels of IL-1β,IL-6 and TNF-α(P<0.05);compared with the LPS+α-MG+si-NC group,the LPS+α-MG si-BDNF group demonstrated decreased cell proliferation rate,increased cell apoptosis rate,down-regulated expression of BDNF,PI3K and Akt proteins,and increased levels of IL-1β,IL-6 and TNF-α(P<0.05).In macrophages,compared with the control group,the LPS group had decreased cell proliferation rate,increased proportion of M1 cells,and down-regulated expression of BDNF,PI3K and Akt proteins(P<0.05);compared with the LPS group,the LPS+α-MG group showed increased cell proliferation rate,decreased proportion of M1 cells,and up-regulated expression of BDNF,PI3K and Akt proteins(P<0.05);compared with the LPS+α-MG+si-NC group,the LPS+α-MG+si-BDNF group showed decreased cell proliferation rate,increased proportion of M1 cells,and down-regulated expression of BDNF,PI3K and Akt proteins(P<0.05).Conclusion α-MG inhibits the M1 polarization of macrophages to improve the apoptosis and inflammation of rat chondrocytes by activating the BDNF/PI3K/Akt signaling pathway.
