CAJ | 학술논문

目的：观察白藜芦醇（RES）诱导 CD34+ CD38- KG -1a 白血病细胞凋亡的效应，初步探讨其作用机制。方法流式细胞术检测急性髓系白血病 KG -1a 细胞 CD34和 CD38的表达。以未加药物为对照，台盼蓝计数检测不同浓度（12.5、25.0、50.0、100、200μmol/ L）RES 对 KG -1a 细胞和外周血单个核细胞增殖的影响。选择KG -1a 细胞抑制率约为50％的 RES 浓度作为后续实验的干预因素。AnnexinV - FITC/ PI 染色流式细胞术检测RES 诱导 KG -1a 细胞的凋亡效应，real - time RT - PCR 检测 RES 对 KG -1a 白血病细胞 Bcl 家族抗凋亡 Bcl -2/Bcl - xl 基因和促凋亡基因 Bid/ Bax 表达的影响，分光光度法检测 RES 对 KG -1a 细胞 Caspase -3活性的影响。结果 KG -1a 细胞中 CD34+ CD38-细胞比例占（90.23±2.57）％。RES 能抑制 KG -1a 白血病细胞生长，呈浓度依赖性。25.0μmol/ L RES 对 KG -1a 细胞的抑制率约为50％，而该浓度对正常单个核细胞增殖无抑制作用。25.0μmol/ L RES 能诱导 KG -1a 细胞发生早期凋亡（ AnnexinV - FITC + PI -）和晚期凋亡（ AnnexinV - FITC +PI +）。25.0μmol/ L RES 作用后的 KG -1a 细胞，抗凋亡基因 Bcl -2和 Bcl - xl 表达下调，促凋亡基因 Bid 和 Bax表达升高，Caspase -3活性增强。结论 RES 能调节 Bcl -2家族，诱导 CD34+ CD38- KG -1a 白血病细胞凋亡。
목적：관찰백려호순（RES）유도 CD34+ CD38- KG -1a 백혈병세포조망적효응，초보탐토기작용궤제。방법류식세포술검측급성수계백혈병 KG -1a 세포 CD34화 CD38적표체。이미가약물위대조，태반람계수검측불동농도（12.5、25.0、50.0、100、200μmol/ L）RES 대 KG -1a 세포화외주혈단개핵세포증식적영향。선택KG -1a 세포억제솔약위50％적 RES 농도작위후속실험적간예인소。AnnexinV - FITC/ PI 염색류식세포술검측RES 유도 KG -1a 세포적조망효응，real - time RT - PCR 검측 RES 대 KG -1a 백혈병세포 Bcl 가족항조망 Bcl -2/Bcl - xl 기인화촉조망기인 Bid/ Bax 표체적영향，분광광도법검측 RES 대 KG -1a 세포 Caspase -3활성적영향。결과 KG -1a 세포중 CD34+ CD38-세포비례점（90.23±2.57）％。RES 능억제 KG -1a 백혈병세포생장，정농도의뢰성。25.0μmol/ L RES 대 KG -1a 세포적억제솔약위50％，이해농도대정상단개핵세포증식무억제작용。25.0μmol/ L RES 능유도 KG -1a 세포발생조기조망（ AnnexinV - FITC + PI -）화만기조망（ AnnexinV - FITC +PI +）。25.0μmol/ L RES 작용후적 KG -1a 세포，항조망기인 Bcl -2화 Bcl - xl 표체하조，촉조망기인 Bid 화 Bax표체승고，Caspase -3활성증강。결론 RES 능조절 Bcl -2가족，유도 CD34+ CD38- KG -1a 백혈병세포조망。
Objective To observe the apoptotic effect of resveratrol on CD34 + CD38 - KG - 1a leukemia cells and to investigate the preliminary mechanism. Methods The expression of CD34 and CD38 on the surface of acute myeloid leukemia(AML)KG - 1a cells was assessed by flow cytometry. The effects of resveratrol at various concentration(12. 5, 25. 0,50. 0,100 and 200 μmol/ L)on the proliferation of KG - 1a cells and peripheral mononuclear cells were analyzed by trypan blue staining. The concentration of resveratrol that could inhibit the proliferation of about 50% KG - 1a was se-lected for subsequent experimental interventions. The changes of apoptosis in KG - 1a cells induced by resveratrol were as-sayed by flow cytometry through the staining of AnnexinV - FITC/ PI. The changes of Bcl - 2 family members,including Bcl - 2,Bcl - xl,Bid and Bax,in KG - 1a cells induced by resveratrol were assayed by real - time RT - PCR. The chan-ges of caspase - 3 in KG - 1a cells induced by resveratrol were assayed by spectrophotometry. Results The CD34 +CD38 - KG - 1a cells accounted for(90. 23 ± 2. 57)% cell count. Resveratrol inhibited the proliferation of KG - 1a leu-kemia cells in a concentration - dependent manner,while resveratrol at 25. 0 μmol/ L could inhibit the proliferation of a-bout 50% KG - 1a leukemia cells without effect on the proliferation of peripheral mononuclear cells. Early apoptosis(An-nexinV - FITC + PI - )and late apoptosis(AnnexinV - FITC + PI + )were induced by resveratrol at 25. 0 μmol/ L in KG -1a cells. Down - regulation of Bcl - 2 and Bcl - xl,with up - regulation of Bid and Bax,and increase caspase - 3 activity in KG - 1a cells were induced by resveratrol at 25. 0 μmol/ L. Conclusion Resveratrol induces apoptosis in KG - 1a cells by regulating the Bcl - 2 family gene expression.