KGF‐2 ameliorates UVB‐triggered skin photodamage in mice by attenuating DNA damage and inflammatory response and mitochondrial dysfunction

Abstract

AbstractBackgroundLong‐term exposure to UVB induces DNA damage, inflammatory response, mitochondrial dysfunction, and apoptosis in skin cells, thus causing skin photodamage. Research has demonstrated the noteworthy antioxidant, anti‐inflammatory, DNA repair, and mitochondrial protective properties of keratinocyte growth factor‐2 (KGF‐2).MethodsTo examine the impact of KGF‐2 on UVB‐triggered skin photodamage in mice, hair‐removed mice were initially exposed under UVB radiation and subsequently treated with KGF‐2 hydrogel and repeated for 6 days. On day 7, the assessment of histopathological alterations, inflammation, DNA damage, mitochondrial function, and apoptosis in mouse skin was assessed.ResultsIt was found that KGF‐2 could effectively relieve cutaneous photodamage symptoms and inhibit epidermal proliferation in mice. Meanwhile, KGF‐2 was found to significantly reduce DNA damage, attenuate the inflammatory response, and inhibit the mitochondria‐mediated intrinsic apoptotic pathway in the UVB‐exposed mouse skin photodamage model.ConclusionTo summarize, our results indicated that KGF‐2 reduces the severity of mouse skin photodamage caused by UVB rays by attenuating DNA damage and the inflammatory response, besides inhibiting the mitochondria‐mediated intrinsic apoptosis pathway.