Astragaloside exerts anti-photoaging effects in UVB-induced premature senescence of rat dermal fibroblasts through enhanced autophagy

Background Astragalus membranaceus is a fundamental herb in Traditional Chinese Medicine and has attracted significant attention due to its anti-inflammatory, and longevity effects. However, its anti-photoaging property remains to be defined. Autophagy plays important roles in regulating cell homeostasis and aging processes. Whether regulation of autophagy could be an efficient way for anti-photoaging is still unclear. Objective: To investigate the effects and the possible mechanism of astragaloside on anti-photoaging in UVB-induced photoaging cell model. Methods: Primary rat dermal fibroblasts were prepared by repeated exposures to UVB irradiation. The expression levels of cytokines and signal molecules were determined by RT-PCR and western blot. SA-beta-gal staining was performed to indicate senescence level. Intracellular reactive oxygen species and mitochondrial membrane potential were monitored by fluorescent probes DCFH-DA and JC-1. The cell viability was determined using Cell Counting Kit-8. Results: Astragaloside increases the expression of collagen-I (Col1) downregulated by UVB. UVB-induced oxidative stress and photoaging could be inhibited by astragaloside. The degradation of Col1 caused by UVB irradiation through activated ERK and p38 signals could be suppressed by astragaloside. Importantly, autophagy was induced by astragaloside. Col1 could be further accumulated by chloroquine but decreased by 3-methyladenine in photoaged cell after treatment of astragaloside. Conclusion: Autophagy play essential roles, at least partially, in modulating the formation and degradation of Col1 in photoaging cell model. Astragaloside increases the accumulation of Col1 and protects UVB-induced photoaging cells through not only ERIC and p38 inhibition but also autophagy activation, indicating the potential application of astragaloside for anti-photoaging therapy.