摘要
目的探讨SERCA抑制剂抑制结肠癌细胞株SW480生长的作用机制,为结肠癌治疗提供实验依据。方法(1)应用Ca^2+荧光指示剂Fura-2检测细胞内Ca^2+的浓度。(2)MTT法检测细胞抑制率。结果毒胡萝卜素(Tg)可使SW480细胞内Ca^2+水平由(133.26±5.17,197.46±4.62)明显升高到(436.63±5.21,766.41±3.12),差异有统计学意义(P〈0.05);毒胡萝卜素(Tg)对人结肠癌细胞株SW480的抑制率随浓度(10~50μmol/L)的提高而增高,由(10.67±5.28)%至(31.46±7.21)%,抑制率差异有统计学意义(P〈0.05);毒胡萝卜素(Tg)与W7合用时,这种效应则受到抑制。结论随着毒胡萝卜紊(Tg)浓度的增大,细胞内钙浓度同步上升;同时毒胡萝卜素(Tg)对该细胞株的抑制率增高。但其所诱导的细胞抑制具体钙信号途径还有待进一步研究。
Objective To investigate the mechanism of Thapsigargin in the proliferation of SW480 and provide experimental basis for development of anti-signaling therapy for patients with colon cancer by detection of intracellular calcium concentration in Thapsigargininduced human colon cell line SW480,. Methods Level of [Ca^2+] was measured by fluorescence measurement with fura-2/AM, a fluorescent index of calcium. The suppression rate of SW480 ceils was calculated by MTT assay. Results Thapsigargin promoted the levels of [Ca^2+] from ( 133.26±5.17,197.46±4. 62)to(436. 63±5.21,766. 41±3.12 ), and inereased the suppression rate from ( 10.67±5.28) to ( 31.46±7.21 ). When W7 was combined used with Thapsigargin, no significant changes were found in the levels of [Ca^2+] and increment of the suppression rate. Conclusion Thapsigargin might promote the proliferation of SW480 cells and lead to apoptosis, but the signaling pathway still remain to be studied.
出处
《中国医师杂志》
CAS
2009年第3期334-335,共2页
Journal of Chinese Physician