中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2010年
4期
456-458
,共3页
噻唑类/药理学%胃肿瘤/药物疗法%细胞生长过程/药物作用%肿瘤转移
噻唑類/藥理學%胃腫瘤/藥物療法%細胞生長過程/藥物作用%腫瘤轉移
새서류/약이학%위종류/약물요법%세포생장과정/약물작용%종류전이
Thiazoles/PD%Stomach neoplasms/DT%Cell hrowth processes/DE%Neoplasm metastasis
目的 探讨PPARγ合成配体曲格列酮(TGZ)对胃癌细胞生长、黏附及侵袭转移能力的影响,明确PPARγ配体与胃癌的关系.方法 采用免疫荧光细胞化学法检测PPARγ在胃癌细胞株MGC803中的表达,通过MTT比色法检测不同浓度的TGZ对胃癌细胞增殖活性和体外黏附能力的影响.用体外侵袭系统检测TGZ对MGC803胃癌细胞体外侵袭转移和趋化运动能力的影响.结果 PPARγ在胃癌细胞MGC803中主要表达于细胞核;TGZ抑制胃癌细胞的生长活性,且随着配体药物浓度的升高,胃癌细胞增殖逐渐降低,呈剂量依赖趋势;当TGZ浓度为0.1、1.0及10 μmol/L时,细胞侵袭及运动抑制率分别为8.79%、31.31%、51.42%及28.29%、4.27%、59.27%,与对照组比较差异有统计学意义(P<0.05);当TGZ浓度为10μmol/L时,细胞黏附能力为0.32±0.03,与对照(0.52±0.04)相比差异有统计学意义(P<0.05).结论 人胃癌细胞MGC803表达功能性PPARγ蛋白;TGZ不同程度抑制MGC803细胞的生长、黏附和侵袭,其作用机制还有待于研究.
目的 探討PPARγ閤成配體麯格列酮(TGZ)對胃癌細胞生長、黏附及侵襲轉移能力的影響,明確PPARγ配體與胃癌的關繫.方法 採用免疫熒光細胞化學法檢測PPARγ在胃癌細胞株MGC803中的錶達,通過MTT比色法檢測不同濃度的TGZ對胃癌細胞增殖活性和體外黏附能力的影響.用體外侵襲繫統檢測TGZ對MGC803胃癌細胞體外侵襲轉移和趨化運動能力的影響.結果 PPARγ在胃癌細胞MGC803中主要錶達于細胞覈;TGZ抑製胃癌細胞的生長活性,且隨著配體藥物濃度的升高,胃癌細胞增殖逐漸降低,呈劑量依賴趨勢;噹TGZ濃度為0.1、1.0及10 μmol/L時,細胞侵襲及運動抑製率分彆為8.79%、31.31%、51.42%及28.29%、4.27%、59.27%,與對照組比較差異有統計學意義(P<0.05);噹TGZ濃度為10μmol/L時,細胞黏附能力為0.32±0.03,與對照(0.52±0.04)相比差異有統計學意義(P<0.05).結論 人胃癌細胞MGC803錶達功能性PPARγ蛋白;TGZ不同程度抑製MGC803細胞的生長、黏附和侵襲,其作用機製還有待于研究.
목적 탐토PPARγ합성배체곡격렬동(TGZ)대위암세포생장、점부급침습전이능력적영향,명학PPARγ배체여위암적관계.방법 채용면역형광세포화학법검측PPARγ재위암세포주MGC803중적표체,통과MTT비색법검측불동농도적TGZ대위암세포증식활성화체외점부능력적영향.용체외침습계통검측TGZ대MGC803위암세포체외침습전이화추화운동능력적영향.결과 PPARγ재위암세포MGC803중주요표체우세포핵;TGZ억제위암세포적생장활성,차수착배체약물농도적승고,위암세포증식축점강저,정제량의뢰추세;당TGZ농도위0.1、1.0급10 μmol/L시,세포침습급운동억제솔분별위8.79%、31.31%、51.42%급28.29%、4.27%、59.27%,여대조조비교차이유통계학의의(P<0.05);당TGZ농도위10μmol/L시,세포점부능력위0.32±0.03,여대조(0.52±0.04)상비차이유통계학의의(P<0.05).결론 인위암세포MGC803표체공능성PPARγ단백;TGZ불동정도억제MGC803세포적생장、점부화침습,기작용궤제환유대우연구.
Objective To study the effect of PPARγ ligand troglitazone (TGZ) on invasion and metastasis of gastric cancer cells, and investigate the relationship of PPARγ ligand with gastric cancer.Methods The expression of PPARγ in gastric cancer cell line MGC803 were detected by immunofluorescence cytochemistry method. The effect of different density TGZ on proliferation activity and adhesion of gastric cancer cell were detected by MTT chromatometry. The effect of different ligands on invasion and metastasis of gastric cancer cell MGC803 were detected by invasion system in vitro. Results The expression of PPARγ mainly located in cell nucleus. TGZ inhibited the proliferation of gastric cancer cell, decreased cell adhesion, locomotory capacity and invasion to matrigel, which had time and dose-dependent relationship.When treatment with 0. 1,1.0 and 10μ mol/ L TGZ, inhibition ratio of invasion and metastasis of cell was 8.79% ,31.31% ,51.42% and 28.29% ,4. 27% ,59. 27% respectively, which had statistical significance compared with control group( P <0. 05). When treatment was 10μ mol/L TGZ, cell adhesion was 0. 32 ±0. 03, it was statistically significant higher than that in control group (0. 52 ± 0. 04, P < 0. 05 ). Conclusion Human gastric cancer cell line MGC803 expressed functional PPARγ protein. TGZ inhibited adhesion and invasion of MGC803 cell on ECM at different degree, the effect of combination of two ligands was evident, which mechanism of action needed to be further investigated.
