Key Laboratory of Pu-er Tea Science, Ministry of Education, Yunnan Agricultural University, Kunming, China.
College of Science, Yunnan Agricultural University, Kunming, China.
Skin Res Technol. 2023 Mar;29(3):e13303. doi: 10.1111/srt.13303.
Skin photoaging is the damage caused by excessive exposure to ultraviolet (UV) irradiation. We investigated the effect of adenosine triphosphate (ATP) supplementation on UVB-induced photoaging in HaCaT cells and its potential molecular mechanism.
The toxicity of ATP on HaCaT cells was examined by the MTT assay. The effects of ATP supplementation on the viability and apoptosis of HaCaT cells were determined by crystal-violet staining and flow cytometry, respectively. Cellular and mitochondrial ROS were stained using fluorescent dyes. Expression of Bax, B-cell lymphoma (Bcl)-2, sirtuin (SIRT)3, and superoxide dismutase (SOD)2 was measured via western blotting.
ATP (1, 2 mM) exerted no toxic effect on the normal growth of HaCaT cells. UVB irradiation caused the apoptosis of HaCaT cells, and ATP supplementation inhibited the apoptosis induced by UVB significantly, as verified by expression of Bax and Bcl-2. UVB exposure resulted in accumulation of cellular and mitochondrial reactive oxygen species (ROS), but ATP supplementation suppressed these increases. Expression of SIRT3 and SOD2 was decreased upon exposure to UVB irradiation but, under ATP supplementation, expression of SIRT3 and SOD2 was reversed, which was consistent with the reduction in ROS level observed in ATP-treated HaCaT cells after exposure to UVB irradiation.
ATP supplementation can suppress UVB irradiation-induced photoaging in HaCaT cells via upregulation of expression of SIRT3 and SOD2.
皮肤光老化是过度暴露于紫外线(UV)照射引起的损伤。我们研究了三磷酸腺苷(ATP)补充对 HaCaT 细胞中 UVB 诱导的光老化的影响及其潜在的分子机制。
通过 MTT 法检测 ATP 对 HaCaT 细胞的毒性。通过结晶紫染色和流式细胞术分别测定 ATP 补充对 HaCaT 细胞活力和凋亡的影响。使用荧光染料染色细胞和线粒体 ROS。通过 Western blot 测定 Bax、B 细胞淋巴瘤(Bcl)-2、沉默调节蛋白(SIRT)3 和超氧化物歧化酶(SOD)2 的表达。
ATP(1、2 mM)对 HaCaT 细胞的正常生长没有毒性作用。UVB 照射导致 HaCaT 细胞凋亡,ATP 补充显著抑制 UVB 诱导的凋亡,这通过 Bax 和 Bcl-2 的表达得到验证。UVB 暴露导致细胞和线粒体活性氧(ROS)积累,但 ATP 补充抑制了这些增加。SIRT3 和 SOD2 的表达在暴露于 UVB 照射后降低,但在 ATP 补充下,SIRT3 和 SOD2 的表达得到逆转,这与观察到的在 ATP 处理的 HaCaT 细胞中暴露于 UVB 照射后 ROS 水平降低一致。
ATP 补充可通过上调 SIRT3 和 SOD2 的表达抑制 HaCaT 细胞中 UVB 照射诱导的光老化。