Abstract: Zhang Jiaan, Zhou Bingrong, Hu Yanyan, Wu Wei, Yin Huibin, Zhang Qian, Guo Xianfei, Luo Dan. Department of Dermatology and Venereology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China Corresponding author: Luo Dan, Email: daniluo2011@gmail.com 【Abstract】 Objective To evaluate the effect of miRNA-23a silencing on ultraviolet B （UVB）-induced chronic photodamage to fibroblasts. Methods Fibroblasts from human foreskin were divided into four groups: blank control group receiving untreated, UVB group receiving UVB irradiation only, miRNA-23a group transfected with a miRNA-23a antagomir, UVB + miRNA-23a group receiving transfection with miRNA-23a antagomir followed by UVB irradiation. UVB irradiation was carried out once a day for five consecutive days at a dose of 10 mJ/cm2. Three days after the last irradiation, SA-β-galactosidase staining was performed to detect senescent cells, flow cytometry to analyze cell cycle, and real-time PCR and Western blot to measure the mRNA and protein expressions of p53, p16 and p21, respectively. Results Both the percentage of β-galactosidase-positive cells and proportion of G1-phase cells were significantly higher in the UVB group than in the UVB + miRNA-23a group （（94.60 ± 2.58）% vs. （48.18 ± 3.70）%, （85.06 ± 1.52）% vs. （57.48 ± 2.01）%, both P < 0.05）. Significant differences were observed in the mRNA and protein expressions of p53, p16 and p21 between the UVB group and UVB + miRNA-23a group （all P < 0.05）. Conclusions The silencing of miRNA-23a may suppress UVB-induced chronic photodamage, which is likely to be associated with the inhibition of senescence-associated downstream signaling molecules.

Key words: Ultraviolet rays, Fibroblasts, MicroRNAs, Cell aging