Abstract: WANG Ying*, CHEN Xu, JU Mei, JIANG Peng-shuang, GUO Xin-yun, XIA Li-jun, JIANG Jing, CHEN Kun, GU Heng, ZHOU Zhi-hai. *General Hospital of Tianjin Medical University, Tianjin 300052, China Corresponding authors: CHEN Xu, Email: chenxuxusong@yahoo.com.cn; ZHOU Zhi-hai, Email: zhouzh65@sohu.com 【Abstract】 Objective To study the regulatory effect of chronic ultraviolet （UV） radiation on the expressions of three regulatory elements involved in the cross-talk between apoptosis and autophagy （including Bax, Bcl-2 and Beclin-1）, as well as cysteine-containing aspartate-specific protease 3 （caspase 3） in keratinocytes of mouse skin. Methods Thirty healthy Kunming mice at 6-8 weeks of age were included in this study, and randomly divided into two groups with the ratio of female to male mice being 1 ∶ 1 in each group: chronic UV damage group （n = 20） receiving sunlight simulator UV radiation, and control group （n = 10） receiving no radiation. The irradiation was performed on the back of mice once a day for 5 consecutive days per week, and lasted for 9 weeks. The dose of irradiation began at one minimal erythema dose （UVB: 0.07 J/cm2, UVA: 0.7 J/cm2）, and increased by 0.5 minimal erythema dose per week, with the total dose of UVB and UVA being 9.45 J/cm2 and 94.5 J/cm2 respectively. Skin samples were resected from the back of these mice before and at 9 weeks after the beginning of the radiation. Skin damage was evaluated by histological observation, specific chemical staining and epidermal thickness measurement. Immunohistochemistry was conducted to detect the expressions of Bax, Bcl-2, caspase 3 and Beclin-1 in epidermal keratinocytes. Paired t test and Wilcoxon signed rank test were carried out for statistical analysis. Results After UV irradiation, the mice showed an obvious increase in epidermal thickness. Histological examination and specific staining for collagen and elastic fibers both revealed a histological change characteristic of chronic UV damage in the mice receiving UV radiation. In the chronic UV damage group, the average immunoreactivity intensity distribution index （IRIDI） was statistically increased for Beclin-1, caspase 3 and Bax in the skin sample （2.70 vs. 0.30, 3.30 vs. 0.25, 3.35 vs. 0.35, Z = 4.034, 4.001, 3.970, respectively, all P < 0.05）, but remained unchanged for Bcl-2 （0.25 vs. 0.25, Z = 0, P > 0.05） at 9 weeks after the radiation compared with that before radiation. No significant changes were observed in the control group for the expression intensity of Beclin-1, caspase 3, Bax or Bcl-2 during the 9 weeks （Z = 0, 0.577, 0, 0.577, respectively, all P > 0.05）. Conclusions Chronic UV irridiation shows no obvious effect on the expression of Bcl-2, but can up-regulate the expression of Beclin-1 and Bax, both of which may be involved in the cross-talk between apoptosis and autophagy in chronic UV radiation-induced skin damage. 【Key words】 Ultraviolet rays; Keratinocyte; bcl-2-Associated X protein; Caspase 3; Beclin-1

Key words: Sun protection factor, Beclin-1, Caspase-3