RETRACTED: Tripterine alleviates LPS-induced inflammatory injury by up-regulation of miR-146a in HaCaT cells (Retracted Article)

Background: Corticosteroid-dependent dermatitis (CDD) is an inflammation caused by long-term repeated inappropriate external use of corticosteroids. Tripterine is a natural product from the root of Tripterygium wilfordii Hook.f. This study aimed to explore the effect and mechanism of tripterine on LPS-induced inflammatory injury in HaCaT cells. Methods: In this study, different concentrations (0, 1, 2, 3 and 4 mu M) of tripterine and 10 mu M of LPS were used to treat HaCaT cells. The expression of miR-146a was altered by transfection. Cell viability, apoptosis, and the release of pro-inflammatory cytokines (IL-6 and TNF-alpha) were detected by CCK-8, flow cytometry analysis, qRT-PCR and ELISA, respectively. The expression levels of apoptosis-related and JNK/NF-kappa B-related proteins were tested by western blotting. Results: We found that 3 and 4 mu M of tripterine significantly decreased cell viability. Tripterine alleviated LPS-induced reduction of cell viability, increase of apoptosis and the release of IL-6 and TNF-alpha in HaCaT cells. miR-146a was down-regulated by LPS exposure, while tripterine attenuated this impact. Further, inhibition of miR-146a abolished the protective effect of tripterine on cell damage triggered by LPS. Finally, tripterine deactivated JNK and NF-kappa B pathways through up-regulation of miR-146a. Conclusion: These results demonstrated that tripterine could attenuate LPS-induced inflammatory injury and deactivate JNK and NF-kappa B pathways by up-regulation of miR-146a. This study will provide a theoretical basis for further study of tripterine in CDD.