Meihan Liu1, Jingzhe Zhang2, Wanguo Liu2, Wenjun Wang3. 1. Department of Ultrasonography, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China. 2. Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China. 3. Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin, China. Electronic address: wangwenjun0053@sina.com.
Abstract
BACKGROUND: Osteoarthritis (OA) is a kind of degenerative disease characterized by the degeneration of the articular cartilage. Salidroside (SAL) is an active component of Rhodiola rosea L., which exhibits diverse pharmacological effects in different diseases. However, the effects of SAL on OA remain largely unclear. The study aimed to investigate the roles of SAL in lipopolysaccharides (LPS)-induced inflammatory injury in murine ATDC5 chondrocyte cells. METHODS: LPS induced ATDC5 cell injury model was constructed by determining cell viability, apoptosis, apoptosis-associated factors as well as inflammatory cytokines expressions and concentrations. Then, the various concentrations of SAL were used to treat ATDC5 cells, and the effect of SAL on LPS-induce inflammatory injury was detected. After treatment with SAL, the expression level of miR-145 was measured by qRT-PCR. Subsequently, miR-145 inhibitor and corresponding control were transfected into ATDC5 cells to explore the influences of miR-145 in LPS-induce inflammatory injury. Besides, the key signaling pathways of NF-κB and p38MAPK were analyzed by using western blot. RESULTS: LPS inhibited cell viability, induced apoptosis, activated cleaved-caspase-3/-9 expression, as well as increased IL-6, MCP-1 and TNF-α expressions and secretions in ATDC5 cells. SAL significantly alleviated LPS-induced inflammatory injury. Meanwhile, the expression of miR-145 was up-regulated by SAL. The protective effect of SAL on LPS-induced injury was obviously reversed by miR-145 inhibition. Furthermore, SAL inactivated NF-κB and p38MAPK signaling pathways by regulating miR-145. CONCLUSIONS: These findings suggested that SAL could protect ATDC5 cells against LPS-induced injury via up-regulation of miR-145 in ATDC5 chondrocyte cells.
BACKGROUND:Osteoarthritis (OA) is a kind of degenerative disease characterized by the degeneration of the articular cartilage. Salidroside (SAL) is an active component of Rhodiola rosea L., which exhibits diverse pharmacological effects in different diseases. However, the effects of SAL on OA remain largely unclear. The study aimed to investigate the roles of SAL in lipopolysaccharides (LPS)-induced inflammatory injury in murine ATDC5 chondrocyte cells. METHODS:LPS induced ATDC5 cell injury model was constructed by determining cell viability, apoptosis, apoptosis-associated factors as well as inflammatory cytokines expressions and concentrations. Then, the various concentrations of SAL were used to treat ATDC5 cells, and the effect of SAL on LPS-induce inflammatory injury was detected. After treatment with SAL, the expression level of miR-145 was measured by qRT-PCR. Subsequently, miR-145 inhibitor and corresponding control were transfected into ATDC5 cells to explore the influences of miR-145 in LPS-induce inflammatory injury. Besides, the key signaling pathways of NF-κB and p38MAPK were analyzed by using western blot. RESULTS:LPS inhibited cell viability, induced apoptosis, activated cleaved-caspase-3/-9 expression, as well as increased IL-6, MCP-1 and TNF-α expressions and secretions in ATDC5 cells. SAL significantly alleviated LPS-induced inflammatory injury. Meanwhile, the expression of miR-145 was up-regulated by SAL. The protective effect of SAL on LPS-induced injury was obviously reversed by miR-145 inhibition. Furthermore, SAL inactivated NF-κB and p38MAPK signaling pathways by regulating miR-145. CONCLUSIONS: These findings suggested that SAL could protect ATDC5 cells against LPS-induced injury via up-regulation of miR-145 in ATDC5 chondrocyte cells.
Authors: Yi Han; Su-Cheng Mu; Jian-Li Wang; Wei Wei; Ming Zhu; Shi-Lin Du; Min Min; Yun-Jie Xu; Zhen-Ju Song; Chao-Yang Tong Journal: World J Emerg Med Date: 2021