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目的以顺铂为主的非小细胞肺癌化疗方案不断更新,目前研究旨在寻求疗效的放大及毒副作用的缩小。黄腐酚被证明有抗癌及保护正常细胞的作用。本实验主要探讨黄腐酚的不同给药方式对顺铂诱导人非小细胞肺癌细胞株H1650凋亡的影响。方法采用CCK-8法检测黄腐酚、顺铂单用及先用低浓度黄腐酚干预,后补入顺铂对H1650细胞增殖的影响;使用流式细胞术分别分析先用黄腐酚后用顺铂、先用顺铂再补入黄腐酚2种干预方式对H1650细胞凋亡率或存活率的影响。结果 CCK-8检测结果显示,2μmol/L黄腐酚干预H1650细胞48h后,继续给予20、40和80μmol/L顺铂干预24h,抑制细胞增殖率分别为(13.16±1.06)%、(19.14±1.67)%和(28.17±2.79)%,均低于同浓度顺铂单纯干预24h组的(18.96±3.02)%、(23.28±1.43)%和(39.79±3.44)%,P<0.05。流式细胞术检测结果显示,10、20和40μmol/L顺铂干预细胞24h后,继续给予7[(85.66±3.19)%、(74.62±2.98)%和(59.55±2.70)%]或14μmol/L[(82.04±2.88)%、(76.50±3.11)%和(61.76±3.01)%]黄腐酚干预24h,其细胞存活率明显高于同浓度顺铂单纯干预48h组的(72.60±2.69)%、(56.98±3.80)%和(44.15±2.01)%,P<0.05。3μmol/L黄腐酚干预细胞24h,弃培养液,更换10、20和40μmol/L顺铂再干预24h,其细胞凋亡率分别为(29.79±3.78)%、(30.53±3.89)%和(39.48±4.98)%,明显高于顺铂单纯干预24h组的(17.21±3.01)%、(14.53±2.99)%和(18.88±4.20)%,P<0.05。结论黄腐酚直接有效保护顺铂对H1650细胞的杀伤,但低浓度黄腐酚的前期干预间接提高了顺铂对H1650细胞的凋亡率。
The purpose of cisplatin-based non-small cell lung cancer chemotherapy program is constantly updated, the current study aims to seek the efficacy of amplification and side effects reduced. Xanthohumol has been shown to have anti-cancer effects and to protect normal cells. This experiment mainly explore the different dosage of xanthohumol on cisplatin-induced human non-small cell lung cancer cell line H1650 apoptosis. Methods CCK-8 method was used to detect the effects of xanthohumol, cisplatin alone and with low concentrations of xanthohumol before intervention with cisplatin on the proliferation of H1650 cells. Flow cytometry was used to analyze the effects of xanthohumol With cisplatin, first with cisplatin and then into two kinds of intervention of xanthohumol on H1650 cell apoptosis rate or survival rate. Results The results of CCK-8 showed that intervention of 2 μmol / L xanthohumol for 48 h resulted in an increase of 13.16 ± 1.06% (19.14 ± 10.6)% for cells treated with 20, 40 and 80 μmol / L cisplatin for 24 h 1.67% and 28.17 ± 2.79%, respectively, which were all lower than that of the 24 h group (18.96 ± 3.02), (23.28 ± 1.43)% and (39.79 ± 3.44)%, respectively. The results of flow cytometry showed that after treated with 10, 20 and 40 μmol / L cisplatin for 24 h, the cells were continuously treated with 7 (85.66 ± 3.19)%, (74.62 ± 2.98)% and (59.55 ± 2.70)%] (82.04 ± 2.88)%, (76.50 ± 3.11)%, and (61.76 ± 3.01)%, respectively. The cell viability of xanthohumol was significantly higher than that of the cells treated with cisplatin for 48 h (72.60 ± 2.69) (56.98 ± 3.80)% and (44.15 ± 2.01)%, P <0.05.3μmol / L xanthohumol intervention cells 24h, discarded culture medium, and then replaced by 10, 20 and 40μmol / (29.79 ± 3.78)%, (30.53 ± 3.89)% and (39.48 ± 4.98)%, respectively, which were significantly higher than that of the 24 h (17.21 ± 3.01)%, (14.53 ± 2.99)% and ± 4.20)%, P <0.05. Conclusion Xanthohumol directly protects H1650 cells against cisplatin, but pretreatment with low concentrations of xanthohumol indirectly increases the apoptosis rate of H1650 cells.