Icariin interferes with TDP43-induced inflammatory factor secretion and inhibits the JNK and p38 MAPK signaling pathway in vitro

IntroductionTo investigate the molecular mechanism of icariin (ICA) intervention in TDP-43 mediated chondrocyte lesions of osteoarthritis.Material and methodsHC-α chondrocytes were transfected with TDP-43 lentiviruses to generate TDP-43-overexpressing chondrocytes and treated with 5 μg/mL icariin. The level of TDP-43, JNK, p38 MAPK and relative factors were detected by Western blotting assays. TNF-α and IL-1β in the supernatant were determined by ELISA.ResultsCompared with the HC-α group, TDP-43 expression was significantly increased in the TDP-43-HC-α group and was not significantly different that of the HC-α+ICA group. However, TDP-43 expression in the TDP-43-HC-α+ICA group was significantly lower than that in the TDP-43-HC-α group. ELISA showed that the secretion of TNF-α and IL-1β in the supernatant of the TDP-43-HC-α group was significantly increased (PConclusionsIcariin could interfere with TDP-43-induced secretion of inflammatory factors, inhibit JNK/p38 MAPK signaling. Our findings provided a new theoretical basis for the treatment of osteoarthritis.