中文摘要：

目的：研究辣椒素对胶质瘤细胞的影响及其作用机制.方法：U251细胞常规培养,不同浓度的辣椒素作用于U251细胞,MTT法检测细胞存活率;然后将U251细胞分为正常对照组、辣椒素组、3-甲基腺嘌呤（3-MA）组、辣椒素＋3-MA组,免疫荧光显色检测Smac蛋白的表达,RT-PCR检测beclin 1和Smac的mRNA表达水平,免疫印迹检测procaspase-3蛋白的表达.结果：MTT结果显示,辣椒素浓度在100 μmol/L时,U251细胞的存活减少,之后再增加辣椒素的浓度,细胞的存活几乎不变.免疫荧光显色结果显示,在辣椒素＋ 3-MA组中,Smac蛋白的表达与正常对照组、辣椒素组、3-MA组相比,其荧光强度显著增强.RT-PCR结果显示,在辣椒素＋3-MA组中,beclin 1的mRNA表达与正常对照组、辣椒素组、3-MA组相比,其表达量显著降低,而Smac的mRNA表达量升高.免疫印迹结果显示,在辣椒素＋ 3-MA组中,procaspase-3的表达与正常对照组、辣椒素组、3-MA组相比,其表达量显著降低.结论：辣椒素能够诱导胶质瘤U251细胞的凋亡.抑制自噬能够促进辣椒素的促凋亡作用,这种作用主要是通过促进Smac释放到细胞质中,从而激活caspase-3实现的.

英文摘要：

Objective： To study the effects and mechanisms of capsaicine on glioma ceils. Methods： U251 cells were cultured routinely. Different concentrations of capsaicine acted on U251 cells, and cell survival was detected by MTT. Then the U251 cells were divided into 4 groups., normal control group, capsaicine group, 3-MA group, capsaicine ＋ 3-MA group. The expressions of Smac were observed by immunofluorescence. The levels of beclin 1 and Smac mRNA were detected by RT-PCR, and the expressions of procaspase-3 were detected by Western blotting. Results： MTT results showed that the survival rate of U251 cells was decreased at the 100 t~mol/L of capsaicine, and the cell survival rate remained unchanged although the concentration of capsaicine was increasing. Immunofluorescence result showed that the fluorescence intensity of Smac was enhanced in the capsaicine＋3-MA group compared with the normal control group, the capsaicine group and 3-MA group. RT- PCR results showed the expression of beclin 1 mRNA was reduced and the expression of Smac mRNA was increased in the capsaicine＋ 3-MA group compared with normal control group. Compared with the capsaicine group and 3-MA group, the expression of beclin 1 rnRNA was decreased while the expression of Smac mRNA was increased. Western blotting results showed that the expression of procaspase-3 was reduced in the capsaicine＋ 3-MA group compared with normal control group, capsaicine group and 3-MA group. Conclusion： Capsaicine could induce the apoptosis of U2 51 cells, and inhibited autophagy could promote apoptosis of capsaicine, which is realized by activating caspase-3 through promoting Smac to release into the cytoplasm.