Abstract
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.
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.
Conclusion:
TanshinoneIIA suppressed melanocyte pyroptosis probably through modulating the ROS/NLRP3 signaling axis, which provides the evidence for therapeutic effect in vitiligo.
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