Bauhinia championii alleviates extracellular matrix degradation in IL-1β induced chondrocytes via miRNA-145-5p/TLR4/NF-κB axis

被引:1
作者
Lin, Jiazhong [1 ]
Huang, Yanfeng [2 ]
Lin, Xiang [1 ]
Liu, Weinan [1 ]
Wu, Xiapin [3 ]
Qiu, Hanglin [3 ]
Wang, Rongmao [1 ]
机构
[1] Fujian Univ Tradit Chinese Med, Dept Traumatol & Orthoped, Affiliated Peoples Hosp, Fuzhou 350004, Fujian, Peoples R China
[2] Fujian Univ Tradit Chinese Med, Acad Integrat Med, Fuzhou 350122, Fujian, Peoples R China
[3] Fujian Univ Tradit Chinese Med, Dept Articular Surg, Quanzhou Orthoped Hosp, Quanzhou 362019, Fujian, Peoples R China
关键词
Osteoarthritis; Bauhinia championii; Extracellular matrix; Micro RNA-145; Toll-like receptor4; Nuclear factor-kappa B; SMALL-MOLECULE; OSTEOARTHRITIS; CARTILAGE; MIR-145; PROLIFERATION; INHIBITION; CELLS; INFLAMMATION; ACTIVATION; EXPRESSION;
D O I
10.1016/j.heliyon.2023.e19138
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Bauhinia championii is a herbal medicine used to treat osteoarthritis (OA) in Chinese traditional medicine. However, the molecular mechanisms underlying the therapeutic effects of this medicinal herb against OA have rarely been reported. Given that it has been established that extracellular matrix metabolism plays an important role in the pathogenesis of OA, the present study focused on the effects and mechanisms of Bauhinia championii in the regulation of extracellular matrix metabolism in chondrocytes induced by IL-1 beta. Rat chondrocytes were isolated, cultured and identified in vitro. The CCK-8 method was used to detect the cell viability of Bauhinia championii aqueous extract (BCAE)-treated chondrocytes. The chondrocyte inflammatory and degeneration models were induced by 10 ng/mL IL-1 beta, then chondrocytes were grouped into different groups to evaluate the effect of BCAE on extracellular matrix degradation and the regulation of TLR4/NF-kappa B signaling pathway. Furthermore, whether the regulatory effect of BCAE on TLR4/NF-kappa B signaling pathway is related to miRNA-145-5p was also investigated by cell transfection. We found that BCAE promoted chondrocyte viability in a dose- and time-dependent manner. BCAE delayed chondrocyte degeneration induced by IL-1 beta. BCAE could reduce the degradation of the cartilage extracellular matrix by inhibiting the TLR4/NF-.B signaling pathway. miRNA-145-5p negatively regulated the expression of TLR4 in chondrocytes, while BCAE could upregulate the expression of miRNA-145-5p in chondrocytes induced by IL-1 beta. These results suggest that BCAE upregulates the expression of miRNA-145-5p to inhibit the TLR4/NF-kappa B signaling pathway, thereby alleviating the metabolic imbalance of the extracellular matrix and protecting chondrocytes from degeneration.
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页数:10
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