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目的评价红芪多糖-1(HPS-1)对人肺癌A549细胞氧自由基(ROS)、谷胱甘肽(GST)、总超氧化物歧化酶(T-SOD)、总抗氧化能力(T-AOC)、硫氧还蛋白还原酶(Trx R)以及脂肪酸过氧化代谢产物丙二醛(MDA)表达的影响。方法人肺腺癌A549细胞经低、中、高(50 mg/L、100 mg/L、200 mg/L)不同剂量HPS-1处理不同时间后,MTT法检测细胞细胞增殖情况,流式细胞术检测细胞凋亡情况,化学荧光法检测细胞内ROS,比色法检测细胞上清液中GSH、T-SOD、T-AOC、Trx R、MDA水平。结果不同剂量HPS-1均具有抑制人肺腺癌A549细胞增殖的作用,且具有时间、剂量依赖性(P<0.05)。不同剂量HPS-1具有诱导人肺腺癌A549细胞凋亡的作用,且具有时间、剂量依赖性(P<0.05)。HPS-1可促进人肺腺癌A549细胞ROS、MDA的上调(P<0.05),随着作用时间的延长,上调作用降低;可促进GSH、T-SOD、T-AOC、Trx R的下调(P<0.05),随着HPS-1干预时间的延长,下调作用降低。结论 HPS-1具有抑制人肺腺癌A549细胞增殖、诱导人肺腺癌A549细胞凋亡的作用。机制可能与其调控人肺腺癌A549细胞氧化/抗氧化能力比例的作用有关。
Objective To evaluate the effects of HPS-1 on the expressions of oxygen free radicals (ROS), glutathione (GST), total superoxide dismutase (T-SOD), total antioxidant capacity -AOC), thioredoxin reductase (TrxR) and the malondialdehyde (MDA), a metabolite of fatty acids. Methods Human lung adenocarcinoma A549 cells were treated with different doses of HPS-1 (50 mg / L, 100 mg / L, 200 mg / L) for different time. MTT assay was used to detect cell proliferation. Flow cytometry The cell apoptosis was detected by chemical method. The intracellular ROS was detected by chemiluminescence method. The levels of GSH, T-SOD, T-AOC, Trx R and MDA in the cell supernatant were detected by colorimetric assay. Results Different doses of HPS-1 could inhibit the proliferation of human lung adenocarcinoma A549 cells in a time-and dose-dependent manner (P <0.05). Different doses of HPS-1 can induce the apoptosis of human lung adenocarcinoma A549 cells in a time-and dose-dependent manner (P <0.05). HPS-1 promoted the up-regulation of ROS and MDA in human lung adenocarcinoma A549 cells (P <0.05), and downregulated with the prolongation of action time. HPS-1 promoted the down-regulation of GSH, T-SOD, T-AOC and Trx R P <0.05). With the prolongation of HPS-1 intervention, the down-regulation effect decreased. Conclusion HPS-1 can inhibit the proliferation of human lung adenocarcinoma A549 cells and induce the apoptosis of human lung adenocarcinoma A549 cells. Mechanism may be related to its role in regulating the ratio of oxidative / anti-oxidative capacity of human lung adenocarcinoma A549 cells.