1. Tanshinone IIA Ameliorates Inflammation Response in Osteoarthritis via Inhibition of miR-155/FOXO3 Axis
- Author
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Hui Xiong, Lin-Hui Li, Li-Ming Tan, Yu-Xing Guo, Zhi Tang, Wang-Yang Li, Wen-Bing Luo, Biao Zhou, Dan Liu, Li-Guo Zhu, and Xiaolong Lu
- Subjects
Lipopolysaccharides ,Cell Survival ,Interleukin-1beta ,Primary Cell Culture ,Apoptosis ,Inflammation ,miR-155 ,chemistry.chemical_compound ,Chondrocytes ,Annexin ,Osteoarthritis ,medicine ,Humans ,MTT assay ,Propidium iodide ,3' Untranslated Regions ,Pharmacology ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,business.industry ,Anti-Inflammatory Agents, Non-Steroidal ,Forkhead Box Protein O3 ,Interleukin ,General Medicine ,MicroRNAs ,chemistry ,Abietanes ,Cancer research ,Tumor necrosis factor alpha ,medicine.symptom ,business - Abstract
Background: Osteoarthritis (OA) is the most common joint disorder characterized by degeneration of the articular cartilage and joint destruction with an associated risk of mobility disability in elderly people. Although a lot of achievements have been made, OA is still regarded as an incurable disease. Therefore, the pathological mechanisms and novel therapeutic strategies of OA need more investigation. Methods: MTT assay was conducted to measure the viability of chondrocytes after LPS treatment. Cell apoptosis was analyzed by annexin V/propidium iodide labeling. ELISA was used to determine the concentrations of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the culture supernatant of chondrocytes. The expression level of miR-155, IL-1β, FOXO3, TNF-α, IL-6, caspase-3, and caspase-9 in chondrocytes was analyzed by RT-qPCR or Western blot. Results: We found that LPS led to inflammatory responses, cell apoptosis, and increased miR-155 expression in human articular chondrocytes. Tanshinone IIA could inhibit LPS-induced inflammation and cell apoptosis of chondrocytes via regulating the expression of miR-155 and FOXO3. miR-155 directly targeted the 3′-UTR of FOXO3 to regulate its expression. Conclusions: Taken together, our data suggest tanshinone IIA ameliorates inflammation response in OA via inhibition of the miR-155/FOXO3 axis, and provide some evidences that tanshinone IIA could be designed and developed as a new promising clinical therapeutic drug for OA patients.
- Published
- 2021
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