中国医师进修杂志
中國醫師進脩雜誌
중국의사진수잡지
CHINESE JOURNAL OF POSTGRADUATES OF MEDICINE
2013年
20期
10-13
,共4页
蒋小猛%徐岷%张尤历%焦志军
蔣小猛%徐岷%張尤歷%焦誌軍
장소맹%서민%장우력%초지군
丙戊酸%消化系统肿瘤%细胞增殖%细胞周期
丙戊痠%消化繫統腫瘤%細胞增殖%細胞週期
병무산%소화계통종류%세포증식%세포주기
Valproic acid%Digestive system neoplasms%Cell proliferation%Cell cycle
目的 探讨不同浓度丙戊酸钠对人消化系统肝癌SMMOL/LC-7721细胞株及胰腺癌PaTu8988细胞株细胞增殖和细胞周期的影响.方法 将肝癌SMMOL/LC-7721细胞株及胰腺癌PaTu8988细胞株分别接种于培养板,常规培养于DMEM培养基中,分别用丙戊酸钠干预48 h,根据丙戊酸钠的浓度分为0.2 mmol/L组、1.0 mmol/L组和5.0 mmol/L组；另设对照组,其DMEM培养基中加入等量的二甲亚砜.使用酶联免疫检测仪测定吸光度值,计算抑制率；流式细胞仪检测细胞周期.结果 5.0 mmol/L组肝癌SMMOL/LC-7721细胞株和胰腺癌PaTu8988细胞株吸光度值均明显低于对照组和0.2 mmol/L组(0.569±0.059比0.706±0.033和0.760±0.020,2.068±0.178比2.793±0.144和2.663±0.078),差异有统计学意义(P＜0.05)；1.0 mmol/L组胰腺癌PaTu8988细胞株吸光度值(2.432±0.084)明显低于对照组和0.2 mmol/L组,差异有统计学意义(P＜0.05).随丙戊酸钠浓度升高,肿瘤细胞抑制率逐渐增强,5.0 mmol/L组肝癌SMMOL/LC-7721细胞株和胰腺癌PaTu8988细胞株细胞抑制率分别为23.5％和25.9％.与对照组比较,0.2、1.0、5.0 mmol/L组随丙戊酸钠浓度升高,肝癌SMMOL/LC-7721细胞株G1期细胞比例逐渐增多[(49.25±1.63)％、(65.26±2.34)％、(83.13±1.78)％比(49.22±4.35)％],S期细胞比例逐渐减少[(26.84±2.30)％、(17.76±3.90)％、(3.38±0.65)％比(29.21±2.35)％],细胞周期发生G1期阻滞,差异有统计学意义(P＜0.05).与对照组和0.2 mmol/L组比较,1.0、5.0 mmol/L组胰腺癌PaTu8988细胞株的G2期细胞比例明显增多[(26.80±1.50)％、(36.58±3.78)％比(12.00±4.62)％、(16.54±2.26)％],细胞周期发生G2期阻滞,差异有统计学意义(P＜0.05).结论 丙戊酸钠可显著抑制肝癌SMMOL/LC-7721细胞株及胰腺癌PaTu8988细胞株的细胞增殖,诱导细胞周期阻滞,为临床有前景的抗肿瘤药物.
目的 探討不同濃度丙戊痠鈉對人消化繫統肝癌SMMOL/LC-7721細胞株及胰腺癌PaTu8988細胞株細胞增殖和細胞週期的影響.方法 將肝癌SMMOL/LC-7721細胞株及胰腺癌PaTu8988細胞株分彆接種于培養闆,常規培養于DMEM培養基中,分彆用丙戊痠鈉榦預48 h,根據丙戊痠鈉的濃度分為0.2 mmol/L組、1.0 mmol/L組和5.0 mmol/L組；另設對照組,其DMEM培養基中加入等量的二甲亞砜.使用酶聯免疫檢測儀測定吸光度值,計算抑製率；流式細胞儀檢測細胞週期.結果 5.0 mmol/L組肝癌SMMOL/LC-7721細胞株和胰腺癌PaTu8988細胞株吸光度值均明顯低于對照組和0.2 mmol/L組(0.569±0.059比0.706±0.033和0.760±0.020,2.068±0.178比2.793±0.144和2.663±0.078),差異有統計學意義(P＜0.05)；1.0 mmol/L組胰腺癌PaTu8988細胞株吸光度值(2.432±0.084)明顯低于對照組和0.2 mmol/L組,差異有統計學意義(P＜0.05).隨丙戊痠鈉濃度升高,腫瘤細胞抑製率逐漸增彊,5.0 mmol/L組肝癌SMMOL/LC-7721細胞株和胰腺癌PaTu8988細胞株細胞抑製率分彆為23.5％和25.9％.與對照組比較,0.2、1.0、5.0 mmol/L組隨丙戊痠鈉濃度升高,肝癌SMMOL/LC-7721細胞株G1期細胞比例逐漸增多[(49.25±1.63)％、(65.26±2.34)％、(83.13±1.78)％比(49.22±4.35)％],S期細胞比例逐漸減少[(26.84±2.30)％、(17.76±3.90)％、(3.38±0.65)％比(29.21±2.35)％],細胞週期髮生G1期阻滯,差異有統計學意義(P＜0.05).與對照組和0.2 mmol/L組比較,1.0、5.0 mmol/L組胰腺癌PaTu8988細胞株的G2期細胞比例明顯增多[(26.80±1.50)％、(36.58±3.78)％比(12.00±4.62)％、(16.54±2.26)％],細胞週期髮生G2期阻滯,差異有統計學意義(P＜0.05).結論 丙戊痠鈉可顯著抑製肝癌SMMOL/LC-7721細胞株及胰腺癌PaTu8988細胞株的細胞增殖,誘導細胞週期阻滯,為臨床有前景的抗腫瘤藥物.
목적 탐토불동농도병무산납대인소화계통간암SMMOL/LC-7721세포주급이선암PaTu8988세포주세포증식화세포주기적영향.방법 장간암SMMOL/LC-7721세포주급이선암PaTu8988세포주분별접충우배양판,상규배양우DMEM배양기중,분별용병무산납간예48 h,근거병무산납적농도분위0.2 mmol/L조、1.0 mmol/L조화5.0 mmol/L조；령설대조조,기DMEM배양기중가입등량적이갑아풍.사용매련면역검측의측정흡광도치,계산억제솔；류식세포의검측세포주기.결과 5.0 mmol/L조간암SMMOL/LC-7721세포주화이선암PaTu8988세포주흡광도치균명현저우대조조화0.2 mmol/L조(0.569±0.059비0.706±0.033화0.760±0.020,2.068±0.178비2.793±0.144화2.663±0.078),차이유통계학의의(P＜0.05)；1.0 mmol/L조이선암PaTu8988세포주흡광도치(2.432±0.084)명현저우대조조화0.2 mmol/L조,차이유통계학의의(P＜0.05).수병무산납농도승고,종류세포억제솔축점증강,5.0 mmol/L조간암SMMOL/LC-7721세포주화이선암PaTu8988세포주세포억제솔분별위23.5％화25.9％.여대조조비교,0.2、1.0、5.0 mmol/L조수병무산납농도승고,간암SMMOL/LC-7721세포주G1기세포비례축점증다[(49.25±1.63)％、(65.26±2.34)％、(83.13±1.78)％비(49.22±4.35)％],S기세포비례축점감소[(26.84±2.30)％、(17.76±3.90)％、(3.38±0.65)％비(29.21±2.35)％],세포주기발생G1기조체,차이유통계학의의(P＜0.05).여대조조화0.2 mmol/L조비교,1.0、5.0 mmol/L조이선암PaTu8988세포주적G2기세포비례명현증다[(26.80±1.50)％、(36.58±3.78)％비(12.00±4.62)％、(16.54±2.26)％],세포주기발생G2기조체,차이유통계학의의(P＜0.05).결론 병무산납가현저억제간암SMMOL/LC-7721세포주급이선암PaTu8988세포주적세포증식,유도세포주기조체,위림상유전경적항종류약물.
Objective To investigate the effect of sodium valproate in suppression of cell proliferation and arrest of cell cycle of in human hepatoma cell line SMMOL/LC-7721 and pancreatic cancer cell line PaTu8988.Methods Hepatoma cell line SMMOL/LC-7721 and pancreatic cancer cell line PaTu8988 were inoculated on the culture plate,cultured in the DMEM medium,they were intervened with sodium valproate in concentration of 0.2 mmol/L (0.2 mmol/L group),1.0 mmol/L (1.0 mmol/L group),5.0 mmol/L (5.0 mmol/L group) and dimethyl sulfoxide (control group) for 48 h respectively.Absorbance was measured by enzymelinked immunosorbentassay equipment,and inhibition ratio was calculated.Cell cycle was detected by flow cytometry.Results The absorbance of hepatoma cell line SMMOL/LC-7721 and pancreatic cancer cell line PaTu8988 in 5.0 mmol/L group were significantly lower than those in control group and 0.2 mmol/L group (0.569 ±0.059 vs.0.706 ±0.033 and 0.760 ±0.020,2.068 ±0.178 vs.2.793 ±0.144 and 2.663 ± 0.078,P ＜ 0.05),the absorbance of pancreatic cancer cell line PaTu8988 in 1.0 mmol/L group (2.432 ± 0.084) was significantly lower than that in control group and 0.2 mmol/L group (P ＜ 0.05).With the sodium valproate concentration increased,inhibition rate of tumor cell increased gradually,the inhibition rate of hepatoma cell line SMMOL/LC-7721 and pancreatic cancer cell line PaTu8988 in 5.0 mmol/L group was 23.5％ and 25.9％ respectively.Compared with control group,with the sodium valproate concentration increased in 0.2,1.0,5.0 mmol/L group,the proportion of G1 phase cell increased gradually in hepatoma cell line SMMOL/LC-7721 [(49.25 ± 1.63)％,(65.26 ± 2.34)％,(83.13 ± 1.78)％ vs.(49.22 ± 4.35)％],the proportion of S phase cell decreased gradually [(26.84 ± 2.30)％,(17.76 ± 3.90)％,(3.38 ± 0.65)％ vs.(29.21 ± 2.35)％],cell cycle showed G1 phase arrest,there was significant difference (P ＜ 0.05).Compared with control group and 0.2 mmol/L group,the proportion of G2 phase cell increased in pancreatic cancer cell line PaTu8988 in 1.0 and 5.0 mmol/L group [(26.80 ± 1.50)％,(36.58 ± 3.78)％ vs.(12.00 ± 4.62)％,(16.54 ± 2.26)％],cell cycleshowed G2 phase arrest,there was significant difference (P ＜ 0.05).Conclusion Sodium valproate mightsignificantly suppress the cell proliferation in hepatoma cell line SMMOL/LC-7721 and pancreatic cancercell line PaTu8988 and induce cell cycle arrest,it is clinically promising antitumor drug.
