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为了研究过氧化酶体增殖物激活受体γ(PPARγ)表达在β-胡萝卜素影响乳腺癌MCF-7细胞活力中所起的作用,采用MTT法测定细胞活力、Western印迹检测细胞中PPARγ的蛋白质水平,用RT-PCR从mRNA水平检测细胞内PPARγ、P21WAF1/CIP1、COX-2和P27表达.研究发现,β-胡萝卜素显著抑制人乳腺癌细胞株MCF-7细胞的生长,β-胡萝卜素对细胞生长的抑制作用呈现出时间和计量依赖关系;β-胡萝卜素能够呈现时间效应地从mRNA和蛋白质水平显著上调PPARγ的表达,β-胡萝卜素能够通过PPARγ调节P21WAF1/CIP1和COX-2 mRNA水平;PPARγ的抑制剂GW9662和抗氧化剂还原型谷胱甘肽(GSH)都能部分阻止由β-胡萝卜素引起的细胞活力下降.研究结果提示,激活PPARγ途径和调制细胞氧化状态是β-胡萝卜素对乳腺癌细胞MCF-7的生长抑制效应原因之一.
In order to study the role of peroxisome proliferator-activated receptor gamma (PPARγ) expression in β-carotene effects on breast cancer MCF-7 cell viability, cell viability was measured by MTT assay, and PPARγ protein in cells was detected by Western blotting. Levels, mRNA expression levels of PPARγ, P21WAF1/CIP1, COX-2, and P27 were measured by RT-PCR. It was found that β-carotene significantly inhibited the growth of human breast cancer cell line MCF-7, β-carotene The inhibitory effect on cell growth showed a time-dependent and quantitative dependence; β-carotene was able to significantly up-regulate the expression of PPARγ from mRNA and protein levels, and β-carotene could regulate P21WAF1/CIP1 and COX-2 mRNA through PPARγ. Levels; PPARγ inhibitor GW9662 and the antioxidant reduced glutathione (GSH) both partially prevented the decrease in cell viability caused by β-carotene. The results suggest that activating the PPARγ pathway and modulating cellular oxidative status is β-carrot One of the factors that inhibit the growth of MCF-7 in breast cancer cells.