Oral submucous fibrosis (OSF) is a collagen deposition disorder with a relatively high potential for malignant transformation. Astaxanthin (AST) is a marine-derived carotenoid and is known for its powerful antioxidant capacity. However, whether AST can ameliorate OSF has not been reported. The aim of this study was to explore whether AST could improve OSF by regulating the epithelial injury and the underlying mechanism. The results showed that AST significantly protected against arecoline-induced OSF. AST alleviated oral epithelial barrier injury by upregulating ZO-1 and Occludin. It also inhibited EMT by regulating the protein levels of E-cadherin, N-cadherin and Snail. Additionally, AST entered mitochondria and protected the mitochondrial homeostasis in arecoline-induced HOKs. Therefore, our study concludes that AST improved the oral epithelial barrier function by regulating mitochondrial homeostasis in epithelial cells to alleviate OSF. These results imply that AST may be developed as a therapeutic agent or a functional food for OSF. • Astaxanthin was firstly used to against arecoline-treated OSF rats. • Astaxanthin reversed mitochondrial dysfunction in arecoline-induced HOKs. • Astaxanthin protected oral epithelial barrier damage in arecoline-induced HOKs. • Astaxanthin could be a potential therapy for OSF.
Peng et al. (Thu,) studied this question.