PM2.5对AngⅡ诱导人脐静脉内皮细胞凋亡的研究(1)
【摘要】 目的：研究PM2.5和AngⅡ的共同干预下，人脐静脉血管内皮细胞的凋亡率及可能的凋亡机制。方法：体外培养人脐静脉内皮细胞株，分别以不同浓度PM2.5、AngⅡ、PM2.5+AngⅡ处理24、48 h，CCK-8法检测细胞活性，流式细胞术检测细胞凋亡率，Western blot法检测凋亡相关蛋白p-AKT的表达变化。结果：48 h CCK-8结果显示，PM2.5在100.00、200.00、800.00 μg/mL时、AngⅡ在20.00 μmol/L时与对应组别的PM2.5+AngⅡ组比较，差异均有统计学意义(P<0.05)。进一步的流式结果显示，48 h时PM2.5+AngⅡ组凋亡率与单PM2.5或AngⅡ处理比较，差异均有统计学意义(P<0.01，P<0.001)。Western Blot结果显示，PM2.5+AngⅡ处理比单PM2.5或单AngⅡ处理后P-AKT的表达量下调，差异均有统计学意义(P<0.005)。结论：本研究表明体外实验中，PM2.5对AngⅡ诱导血管内皮细胞凋亡具有促进作用，并可能通过PI3K/Akt/eNOS信号通路来实现。
【关键词】 细颗粒物 AngⅡ P-AKT 人脐静脉内皮细胞 凋亡
Effect of PM2.5 on Apoptosis of Human Umbilical Vein Endothelial Cells Induced by AngⅡ/LI Gang， DENG Yuting， CHEN Dongmei. //Medical Innovation of China， 2020， 17(04)： 00-006
[Abstract] Objective： To study the apoptosis rate and possible apoptosis mechanism of Human Umbilical Vein Endothelial Cells (HUVEC) under the co-intervention of PM2.5 and AngⅡ. Method： HUVEC were treated with different concentrations of PM2.5， AngⅡand PM2.5 + AngⅡ for 24 and 48 h. The cell activity was detected by CCK-8 assay and the apoptosis rate was detected by flow cytometry (FCM). The expression of apoptosis-related protein p-AKT was detected by Western blot. Result： The results of CCK-8 showed that there were significant differences between PM2.5 at 100.00， 200.00， 800.00 μg/mL and AngⅡ at 20.00 μmol/L and PM2.5 + AngⅡ (P<0.05). The further results of FCM showed that there were differences significantly between PM2.5 with AngⅡ and single PM2.5 or single AngⅡ treatment group in the apoptosis rate (P<0.01， P<0.001). The results of Western Blot showed that the expression of p-AKT in PM2.5 with AngⅡ treatment group was significantly lower than that in single PM2.5 or single AngⅡ treatment group (P<0.005). Conclusion： This study shows that in vitro experiments， PM2.5 can promote the apoptosis effect of AngⅡ to HUVEC. It may be achieved through PI3K/Akt/eNOS signaling pathway.
[Key words] PM2.5 AngⅡ P-AKT Human umbilical vein endothelial cells Apoptosis
First-author’s address： School of Basic Medicine， Shenyang Medical College， Shenyang 110034， China
doi：10.3969/j.issn.1674-4985.2020.04.001
近些年，隨着我国城市化进程的加快，大气污染备受关注。其中，颗粒物对人体健康有着严重的危害性[1]。根据粒径大小，大气颗粒物被分成总悬浮颗粒物(total suspended particles，TSP)、可吸入颗粒物(inhalable particles，PM10)、细颗粒物(fine partieles，PM2.5)和超细颗粒物(ultrafine particles，UFP)四类。其中PM 2.5粒直径小、表面积大，吸附的重金属和有毒物质较多，在大气中停留时间长、输送距离远，且可直接到达终末肺泡，在呼吸系统中易于溶解吸收，对人体健康危害最为严重。大量流行病学研究表明PM2.5能增加人体呼吸和心血管系统疾病的发生率，有调查显示雾霾天医院住院人数明显增加，其中主要是以呼吸和心血管系统疾病患者常见[2-3]。血管内皮细胞损伤可引起心血管疾病的发生，这是心血管疾病的一个重要病因[4-5]。而血管内皮细胞损伤的一个重要因素就是血管组织局部RAS系统激活，AngⅡ(血管紧张素Ⅱ)作为该系统的活性肽，当其与受体AT1R结合后对血管内皮细胞功能及结构发挥损害作用。文献[6]表明AngⅡ可诱导血管内皮细胞凋亡，同时也有研究表明暴露于PM2.5中，内皮细胞的AngⅡ浓度能够增加[7]。但并未见PM2.5对AngⅡ诱导血管内皮细胞凋亡作用的相关文献报道，因此通过本实验来探究大气污染物PM2.5与AngⅡ及血管内皮细胞凋亡的相关性，为进一步探究大气污染对心血管疾病的发生机制提供依据，现报道如下。, 百拇医药(李岗 邓宇亭 陈冬梅)
【关键词】 细颗粒物 AngⅡ P-AKT 人脐静脉内皮细胞 凋亡
Effect of PM2.5 on Apoptosis of Human Umbilical Vein Endothelial Cells Induced by AngⅡ/LI Gang， DENG Yuting， CHEN Dongmei. //Medical Innovation of China， 2020， 17(04)： 00-006
[Abstract] Objective： To study the apoptosis rate and possible apoptosis mechanism of Human Umbilical Vein Endothelial Cells (HUVEC) under the co-intervention of PM2.5 and AngⅡ. Method： HUVEC were treated with different concentrations of PM2.5， AngⅡand PM2.5 + AngⅡ for 24 and 48 h. The cell activity was detected by CCK-8 assay and the apoptosis rate was detected by flow cytometry (FCM). The expression of apoptosis-related protein p-AKT was detected by Western blot. Result： The results of CCK-8 showed that there were significant differences between PM2.5 at 100.00， 200.00， 800.00 μg/mL and AngⅡ at 20.00 μmol/L and PM2.5 + AngⅡ (P<0.05). The further results of FCM showed that there were differences significantly between PM2.5 with AngⅡ and single PM2.5 or single AngⅡ treatment group in the apoptosis rate (P<0.01， P<0.001). The results of Western Blot showed that the expression of p-AKT in PM2.5 with AngⅡ treatment group was significantly lower than that in single PM2.5 or single AngⅡ treatment group (P<0.005). Conclusion： This study shows that in vitro experiments， PM2.5 can promote the apoptosis effect of AngⅡ to HUVEC. It may be achieved through PI3K/Akt/eNOS signaling pathway.
[Key words] PM2.5 AngⅡ P-AKT Human umbilical vein endothelial cells Apoptosis
First-author’s address： School of Basic Medicine， Shenyang Medical College， Shenyang 110034， China
doi：10.3969/j.issn.1674-4985.2020.04.001
近些年，隨着我国城市化进程的加快，大气污染备受关注。其中，颗粒物对人体健康有着严重的危害性[1]。根据粒径大小，大气颗粒物被分成总悬浮颗粒物(total suspended particles，TSP)、可吸入颗粒物(inhalable particles，PM10)、细颗粒物(fine partieles，PM2.5)和超细颗粒物(ultrafine particles，UFP)四类。其中PM 2.5粒直径小、表面积大，吸附的重金属和有毒物质较多，在大气中停留时间长、输送距离远，且可直接到达终末肺泡，在呼吸系统中易于溶解吸收，对人体健康危害最为严重。大量流行病学研究表明PM2.5能增加人体呼吸和心血管系统疾病的发生率，有调查显示雾霾天医院住院人数明显增加，其中主要是以呼吸和心血管系统疾病患者常见[2-3]。血管内皮细胞损伤可引起心血管疾病的发生，这是心血管疾病的一个重要病因[4-5]。而血管内皮细胞损伤的一个重要因素就是血管组织局部RAS系统激活，AngⅡ(血管紧张素Ⅱ)作为该系统的活性肽，当其与受体AT1R结合后对血管内皮细胞功能及结构发挥损害作用。文献[6]表明AngⅡ可诱导血管内皮细胞凋亡，同时也有研究表明暴露于PM2.5中，内皮细胞的AngⅡ浓度能够增加[7]。但并未见PM2.5对AngⅡ诱导血管内皮细胞凋亡作用的相关文献报道，因此通过本实验来探究大气污染物PM2.5与AngⅡ及血管内皮细胞凋亡的相关性，为进一步探究大气污染对心血管疾病的发生机制提供依据，现报道如下。, 百拇医药(李岗 邓宇亭 陈冬梅)