Background
Pyroptosis has been implicated in the development of human diseases, including vitiligo. TanshinoneIIA has been confirmed to play anti-vitiligo role. However, whether tanshinoneIIA inhibits vitiligo progression via regulating cell pyroptosis remains unclear.
Conclusion
TanshinoneIIA suppressed melanocyte pyroptosis probably through modulating the ROS/NLRP3 signaling axis, which provides the evidence for therapeutic effect in vitiligo.
Methods
Hydrogen peroxide (H2 O2 )-induced melanocytes were used to mimic vitiligo cell model in vitro. Cell viability was assessed by cell counting kit 8 assay, and reactive oxygen species (ROS) production was detected by DCFH-DA staining. Nod-like receptor protein 3 (NLRP3) expression was detected by quantitative real-time PCR, western blot and immunofluorescence staining. Cell pyroptosis was measured using flow cytometry, and the contents of interleukin-1β and interleukin-18 were determined by ELISA. Besides, the protein levels of apoptosis-associated speck-like protein containing CARD (ASC) and cleaved-Caspase-1 were examined by western blot analysis.
Results
H2 O2 could induce ROS production, NLRP3 expression and pyroptosis in melanocytes. TanshinoneIIA inhibited ROS production, pyroptosis, and the expression of NLRP3, ASC and cleaved-caspase-1 in H2 O2 -induced melanocytes. Compared with the function of ROS inhibitor (NAC), tanshinoneIIA acted as a ROS scavenger to relieve melanocyte pyroptosis. In addition, NLRP3 inhibitor (MCC950) also could aggravate the inhibition effect of tanshinoneIIA on melanocyte pyroptosis.