Yang Jianhua, Yan Yao, Liu Huibin, Wang Jianhua, Hu Junping
Department of Pharmacy, The First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang Uyghur Autonomous Region 830011, P.R. China.
Department of Pharmacy, The Affiliated Tumor Hospital, Xinjiang Medical University, Urumqi, Xinjiang Uyghur Autonomous Region 830011, P.R. China.
Mol Med Rep. 2015 Aug;12(2):2301-6. doi: 10.3892/mmr.2015.3630. Epub 2015 Apr 16.
To investigate the protective effects of acteoside against apoptosis induced by X-ray radiation in human skin fibroblasts (HSFs), the cells were divided into the following groups: Control group; X-ray radiation group; acteoside group, in which the confluent cells were preincubated with 50 μg/ml acteoside for 2 h followed by radiation; and positive control group, in which the cells were preincubated with 50 μg/ml paeoniflorin followed by radiation. For the radiation, HSF cells preincubated with acteoside or paeoniflorin were exposed to X-ray beams at a dose-rate of 3 Gy/min (16 Gy in total). Cell viability, apoptosis and intracellular alteration of redox were monitored by MTT and flow cytometry. Compared with the radiation group, the number of cells arrested at the G0/G1 phase was significantly reduced in the acteoside and paeoniflorin groups, respectively (P<0.05). X-ray radiation induced marked apoptosis in HSF cells and acteoside reversed this effect. Compared with the radiation group, the generation of intracellular reactive oxygen species (ROS) was abrogated by pre-incubation with acteoside or paeoniflorin (P<0.05). In addition, the upregulation of pro-caspase-3 induced by radiation was reversed by acteoside or paeoniflorin. Radiation could induce upregulation of Bax and downregulation of Bcl-2; however, it was reversed completely after administration of acteoside or paeoniflorin. Furthermore, the enhanced expression of ERK and JNK induced by radiation was reversed by acteoside or paeoniflorin. Acteoside could protect the cells from X-ray induced damage through enhancing the scavenging activity of ROS, decreasing the Bax/Bcl-2 ratio and downregulating the activity of procaspase-3, as well as modulating the mitogen-activated protein kinase signaling pathways.
为研究毛蕊花糖苷对X射线辐射诱导人皮肤成纤维细胞（HSFs）凋亡的保护作用，将细胞分为以下几组：对照组；X射线辐射组；毛蕊花糖苷组，即汇合细胞先用50μg/ml毛蕊花糖苷预孵育2小时，然后进行辐射；阳性对照组，即细胞先用50μg/ml芍药苷预孵育，然后进行辐射。对于辐射，用毛蕊花糖苷或芍药苷预孵育的HSF细胞以3Gy/min的剂量率（总共16Gy）暴露于X射线束。通过MTT和流式细胞术监测细胞活力、凋亡和细胞内氧化还原变化。与辐射组相比，毛蕊花糖苷组和芍药苷组中停滞在G0/G1期的细胞数量分别显著减少（P<0.05）。X射线辐射诱导HSF细胞明显凋亡，而毛蕊花糖苷可逆转这种作用。与辐射组相比，用毛蕊花糖苷或芍药苷预孵育可消除细胞内活性氧（ROS）的产生（P<0.05）。此外，毛蕊花糖苷或芍药苷可逆转辐射诱导的前半胱天冬酶-3上调。辐射可诱导Bax上调和Bcl-2下调；然而，给予毛蕊花糖苷或芍药苷后可完全逆转。此外，毛蕊花糖苷或芍药苷可逆转辐射诱导的ERK和JNK表达增强。毛蕊花糖苷可通过增强ROS清除活性、降低Bax/Bcl-2比值、下调前半胱天冬酶-3活性以及调节丝裂原活化蛋白激酶信号通路来保护细胞免受X射线诱导的损伤。
