被撤回的出版物: Piperine alleviates lipopolysaccharide-induced inflammatory injury by down-regulating microRNA-127 in murine chondrogenic ATDC5 cells (Retracted article. See vol. 149, 2022)

Background: This study aimed to investigate whether piperine has anti-inflammatory activities in lipopolysaccharide (LPS)-induced inflammatory injury of murine chondrogenic ATDC5 cells and to explore the potential mechanisms. Methods: ATDC5 cells were pretreated with piperine and then stimulated by LPS for 12 h. Cell Counting Kit-8 (CCK-8) and flow cytometry were used to assess cell viability and apoptosis, respectively. qRT-PCR, enzymelinked immuno sorbent assay (ELISA) and western blotting were used to detect the expression levels of inflammatory cytokines, microRNA-127 (miR-127) and MyD88, as well as key factors involved in nuclear factor kappa B (NF-kappa B) and p38-mitogen activated protein kinase (p38MAPK) signaling pathways, respectively. Results: Piperine exerted anti-inflammatory effects on LPS-stimulated ATDC5 cells. Piperine reduced the expression of miR-127 in ATDC5 cells. Up-regulation of miR-127 aggravated LPS-induced inflammatory injury. Down-regulation of miR-127 had opposite effects. Moreover, miR-127 up-regulated MyD88 expression and overexpression of MyD88 also aggravated LPS-induced cell inflammatory injury. Further research found that overexpression of MyD88 activated NF-kappa B and p38MAPK signaling pathways in ATDC5 cells, while knockdown of MyD88 inhibited the activation of these two pathways. Conclusion: This study demonstrates the anti-inflammatory effects of piperine on LPS-stimulated ATDC5 cells. The anti-inflammatory properties of piperine are mediated by down-regulating miR-127 and MyD88 expression and then inhibiting NF-kappa B and p38MAPK signaling pathways activation. Our findings may provide a theoretical basis for further research the clinical treatment of osteoarthritis (OA) by using piperine.