CAJ | 학술논문

目的评价异丙酚对多西紫杉醇致转染Cx32宫颈癌Hela细胞毒作用的影响.方法将转染Cx32的宫颈癌HeLa细胞用高密度接种法(1×l05个/ml)和低密度接种法(500个/ml)获得生长融合和生长未融合细胞,加入多西环素培养48 h后,采用随机数字表法,将两种方法获得的细胞各分为5组(n=8):空白对照组(C组)；多西紫杉醇组(D组)加入多西紫杉醇5 nmol/L；多西紫杉醇+脂肪乳组(D+I组)加入多西紫杉醇5 nmol/L及脂肪乳10 μg/ml；多西紫杉醇+18-α-GA组(D+18-α-GA组)加入多西紫杉醇5 nmol/L及18-α-GA 10 μmol/L;多西紫杉醇+异丙酚组(D+P组)加入多西紫杉醇5nmol/L及异丙酚2.8 μg/ml.18-α-GA、脂肪乳及异丙酚于多西紫杉醇之前加入,18-α-GA单独的作用时间为lh,后两者均为2h.3种药物与多西紫杉醇共同的作用时间均为2h.采用标准细胞集落形成分析法计算细胞集落形成率.结果高密度接种法处理的D组细胞集落形成率比低密度接种法处理的D组明显降低(P＜0.05).在高密度接种法处理的细胞中,与C组比较,其余各组细胞集落形成率降低(P＜0.05)；与D组和D+I组比较,D+18-α-GA组和D+P组细胞集落形成率升高(P＜0.05)；D组和D+I组间上述指标差异无统计学意义(P＞0.05).在低密度接种法处理的细胞中,与C组比较,其余各组细胞集落形成率降低(P＜0.05)；其余各组间上述指标比较差异无统计学意义(P＞0.05).结论异丙酚可减弱多西紫杉醇对转染Cx32宫颈癌HeLa细胞毒作用,其作用机制与抑制细胞缝隙连接功能有关.
목적 평개이병분대다서자삼순치전염Cx32궁경암Hela세포독작용적영향.방법 장전염Cx32적궁경암HeLa세포용고밀도접충법(1×l05개/ml)화저밀도접충법(500개/ml)획득생장융합화생장미융합세포,가입다서배소배양48 h후,채용수궤수자표법,장량충방법획득적세포각분위5조(n=8):공백대조조(C조)；다서자삼순조(D조)가입다서자삼순5 nmol/L；다서자삼순+지방유조(D+I조)가입다서자삼순5 nmol/L급지방유10 μg/ml；다서자삼순+18-α-GA조(D+18-α-GA조)가입다서자삼순5 nmol/L급18-α-GA 10 μmol/L;다서자삼순+이병분조(D+P조)가입다서자삼순5nmol/L급이병분2.8 μg/ml.18-α-GA、지방유급이병분우다서자삼순지전가입,18-α-GA단독적작용시간위lh,후량자균위2h.3충약물여다서자삼순공동적작용시간균위2h.채용표준세포집락형성분석법계산세포집락형성솔.결과 고밀도접충법처리적D조세포집락형성솔비저밀도접충법처리적D조명현강저(P＜0.05).재고밀도접충법처리적세포중,여C조비교,기여각조세포집락형성솔강저(P＜0.05)；여D조화D+I조비교,D+18-α-GA조화D+P조세포집락형성솔승고(P＜0.05)；D조화D+I조간상술지표차이무통계학의의(P＞0.05).재저밀도접충법처리적세포중,여C조비교,기여각조세포집락형성솔강저(P＜0.05)；기여각조간상술지표비교차이무통계학의의(P＞0.05).결론 이병분가감약다서자삼순대전염Cx32궁경암HeLa세포독작용,기작용궤제여억제세포봉극련접공능유관.
Objective To evaluate the effect of propofol on docetaxel-induced toxicity to cervical cancer Hela cells transfected with Cx32 plasmid.Methods Cervical cancer Hela cells transfected with Cx32 plasmid were seeded at two different densities and induced to express Cx32 by incubation with doxycycline for 48 h.The cells at high density were seeded at 1 × 105 cells/ml such that the cells would be confluent at the time of docetaxel exposure.The cells at low density were seeded at 500 cells/ml and the cells did not attach at the density.Each type of cells obtained was randomly divided into 5 groups (n =8 each):control group (group C),docetaxel group (group D),docetaxel + intralipid group (group D + I),docetaxel + 18-α-GA group (D + 18-α-GA),and docetaxel +propofol group (group D + P).Groups D,D + I,D + 18-α-GA and D + P were exposed to 5 nmol/L docetaxel,5 nmol/L docetaxel + 10μg/ml intralipid,5 nmol/L docetaxel + 10 μmol/L 18-α-GA,and 5 nmol/L docetaxel +2.8 μg/ml propofol,respectively.18-α-GA,intralipid and propofol were added prior to docetaxel,and the action time for 18-α-GA alone was 1 h and for intralipid or propofol alone 2 h.The time for coaction between the three drugs and docetaxel was 2 h.Cell survival was determined by a standard colony-forming assay.Results The colony formation rate of the cells seeded at high density in group D was significantly lower than that of the cells seeded at low density in group D (P ＜ 0.05).For the cells seeded at high density,the colony formation rate was significantly decreased in the other groups when compared with group C (P ＜ 0.05).The colony formation rate was significantly higher in groups D + 18-α-GA and D + P than in groups D and D + I (P ＜ 0.05).There was no significant difference in the colony formation rate between groups D and D + I (P ＞ 0.05).For the cells seeded at low density,the colony formation rate was significantly decreased in the other groups when compared with group C (P ＜ 0.05) and there was no significant difference in the colony formation rate between D,D + I,D + 18-α-GA and D + P groups (P ＞ 0.05).Conclusion Propofol can attenuate docetaxel-induced toxicity to Hela cells transfected with Cx32 plasmid and inhibition of gap junction function is involved in the mechanism.