陆海波 张清媛 周建华 王 影 鲁海玲.PPAR??激动剂罗格列酮对人乳腺癌细胞生长
抑制及诱导凋亡作用研究[J].,2006,6(2):24-26 |
PPAR??激动剂罗格列酮对人乳腺癌细胞生长
抑制及诱导凋亡作用研究 |
Study on Peroxisome Proliferator- activated Receptor- ??Activation in InhibitingTumor Growth and Inducing Apoptosis in Breast Cancer |
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DOI: |
中文关键词: 氧化酶体激活物增殖受体( PPAR??) 罗格列酮 生长抑制 凋亡 |
英文关键词: Peroxisome proliferator- activated receptor- ?? Rosiglitazone Growth inhibiting Apoptosis |
基金项目:黑龙江省卫生厅医学科研课题资助( 2005- 061) |
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中文摘要: |
目的: 观察氧化酶体激活物增殖受体( PPAR??) 激动剂罗格列酮( ROZ) 在体外激活PPAR?? 后对MCF- 7 细胞的生长抑
制及诱导凋亡作用。方法:MTT 法检测ROZ 对MCF- 7 细胞的生长抑制作用; 集落形成实验观察ROZ 对MCF- 7 细胞集落形成
的影响; 不同浓度ROZ 作用72h, Hoechst33342 染色观察MCF- 7 细胞的形态变化, 流式细胞光度分析术( FCM) 检测凋亡细胞百分
率以及ROZ 对细胞周期的影响; Western blot 方法检测ROZ 对MCF- 7 细胞Bcl- 2、Caspase- 3 表达的影响。结果: ROZ 可呈剂量
依赖性抑制MCF- 7 细胞的生长及集落形成。ROZ 浓度为6 ?? 10- 5M 和3 ?? 10- 4M 时则G1 期细胞数明显增加, S 期相应减少。
Hoechst33342 染色经ROZ 处理的肿瘤细胞染色质呈颗粒状, 且有凋亡小体出现。FCM 检测结果显示, ROZ 作用72h 凋亡细胞数达
22. 05%。Western blot 提示ROZ 可抑制Bcl- 2 表达, 促进Caspase3 表达。结论: ROZ 在体外可抑制MCF- 7 细胞的增殖并诱导其
凋亡, 这可能与其抑制Bcl- 2 表达、促进caspase3 表达有关。提示ROZ 有望成为乳腺癌治疗药或肿瘤治疗的辅助用药, PPAR??
有潜力成为肿瘤治疗的新靶点。 |
英文摘要: |
Objective: To observe the effects of rosiglitazone( ROZ) , a perox isome proliferator- activated receptor- ?? activation, in the
inhibition of tumor growth and inducement apoptosis in breast cancer in vitro. Methods: MTT was used to detect how ROZ inhibited the growth of
MCF- 7, observing ROZ how to influence the colony formation of MCF- 7 by colony formation test. After different concentration of ROZ for 72
hours, the morphologic change ofMCF- 7 was seen by Hoechst33342 dyeing; the apoptosis percentage and cell cycle change were detected by
FCM; the effects of ROZ in the expression of Bcl- 2 and Caspase- 3 of MCF- 7 were evaluated by Western Blotting. Results: Using ROZ to
treat breast cancer, with a dose- dependence, could inhibit cell growth and colony formation of MCF- 7. The number of cells in G1 phase increased
and the number of cells in S phase decreased when the concentration of ROZ was 6?? 10- 5M and 3?? 10- 4M. Through Hoechst33342 dyeing,
there were granulochromatin and apoptotic body in tumor cells after being treated with ROZ for 72 hours, and the number of apoptosis cell
reached 22. 05% by FCM. ROZ inhibited the expression of Bcl- 2 and enhanced the expression of Caspase- 3. Conclusion: ROZ inhibited the
cell proliferation and induced apoptosis in vitro, which may be relative to inhibiting the expression of Bcl- 2 and enhancing the expression of Caspase-
3. These results hint that ROZ is hoped to be the therapeutic drug or aid drug in tumor treatment. PPAR?? has great potentialities to be new
target of tumor treatment. |
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