Effect of butorphanol on lipopolysaccharide-induced chondrocyte injury by regulating SDF-1α/CXCR4 pathway
10.3969/j.issn.1671-7856.2025.08.009
- VernacularTitle:布托啡诺调控SDF-1α/CXCR4通路对脂多糖诱导的软骨细胞损伤的影响
- Author:
Jun FANG
1
;
Ximing LIU
;
Zhen LI
;
Meng YANG
;
Qingyong DONG
Author Information
1. 滕州市中心人民医院麻醉科,山东滕州 277599
- Publication Type:Journal Article
- Keywords:
butorphanol;
SDF-1α/CXCR4 pathway;
lipopolysaccharide;
chondrocyte;
injury
- From:
Chinese Journal of Comparative Medicine
2025;35(8):94-101
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of butorphanol on lipopolysaccharide-induced chondrocyte injury by regulating the stromal cell-derived factor-1α(SDF-1α)/C-X-C chemokine receptor 4(CXCR4)pathway.Methods Human C28/12 chondrocytes were cultured in vitro and assigned to the following groups:control(normal culture),model(100 μmol/L lipopolysaccharide),model+low-dose butorphanol(100 μmol/L lipopolysaccharide+1μmol/L butorphanol),model+medium-dose butorphanol(100 μmol/L lipopolysaccharide+2 μmol/L butorphanol),model+high-dose butorphanol(100 μmol/L lipopolysaccharide+4 μmol/L butorphanol),and model+high-dose butorphanol+NUCC-390(100 μmol/L lipopolysaccharide+4 μmol/L butorphanol+500 nmol/L CXCR4 agonist NUCC-390).Cell viability,interleukin(IL)-6 and tumor necrosis factor-α(TNF-α)levels,apoptosis,and SDF-1α/CXCR4 pathway-related proteins were evaluated by MTT assay,enzyme-linked immunosorbent assay,flow cytometry,and Western blot,respectively.Results Chondrocyte survival rate and Bcl-2 protein expression were decreased while TNF-α,IL-6,apoptosis rate,Bax,Cleaved caspase-3,SDF-1α,and CXCR4 proteins were increased in the model group compared with the control group(P＜0.05).The above indicators were improved in the model+low-,medium-,and high-dose butorphanol groups compared with the model group,while the result for the model+high-dose butorphanol+NUCC-390 group were opposite to those of the model+high-dose butorphanol group.Conclusions Butorphanol may improve lipopolysaccharide-induced chondrocyte injury induced by inhibiting the SDF-1α/CXCR4 signaling pathway.
