山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2014年
9期
1-3
,共3页
王洪州%邓丽娟%王利民%董发勤
王洪州%鄧麗娟%王利民%董髮勤
왕홍주%산려연%왕이민%동발근
温石棉%代用品纤维%基因表达调控,肿瘤%基因,p16%基因,p53
溫石棉%代用品纖維%基因錶達調控,腫瘤%基因,p16%基因,p53
온석면%대용품섬유%기인표체조공,종류%기인,p16%기인,p53
chrysotile%substitute%tumor gene%genes expression regulation,neoplastic%genes,p16%genes,p53
目的:研究温石棉及其代用纤维对中国仓鼠肺细胞( V79细胞) p16及p53表达的影响,探讨温石棉及其代用纤维的致癌机制。方法将不同种类(四川新康温石棉、陕西陕南温石棉、玻璃纤维、陶瓷纤维、硅灰石、岩棉)及不同浓度(1~10 mg/L)的温石棉及其代用纤维暴露于V79细胞中,并设阴性对照。采用免疫组化SABC法检测V79细胞p16及p53的表达,并进行比较。结果与阴性对照比较,各染毒V79细胞中的抑癌基因p16和p53表达下调,P均<0.05;随着温石棉及其代用纤维暴露浓度的增加,V79细胞p16和p53的表达减弱,其OD值也呈下降趋势(P均<0.05)。结论温石棉及其代用纤维均有不同程度的致癌性;其诱导癌症发生的机制可能与下调抑癌基因p16和p53表达有关。
目的:研究溫石棉及其代用纖維對中國倉鼠肺細胞( V79細胞) p16及p53錶達的影響,探討溫石棉及其代用纖維的緻癌機製。方法將不同種類(四川新康溫石棉、陝西陝南溫石棉、玻璃纖維、陶瓷纖維、硅灰石、巖棉)及不同濃度(1~10 mg/L)的溫石棉及其代用纖維暴露于V79細胞中,併設陰性對照。採用免疫組化SABC法檢測V79細胞p16及p53的錶達,併進行比較。結果與陰性對照比較,各染毒V79細胞中的抑癌基因p16和p53錶達下調,P均<0.05;隨著溫石棉及其代用纖維暴露濃度的增加,V79細胞p16和p53的錶達減弱,其OD值也呈下降趨勢(P均<0.05)。結論溫石棉及其代用纖維均有不同程度的緻癌性;其誘導癌癥髮生的機製可能與下調抑癌基因p16和p53錶達有關。
목적:연구온석면급기대용섬유대중국창서폐세포( V79세포) p16급p53표체적영향,탐토온석면급기대용섬유적치암궤제。방법장불동충류(사천신강온석면、협서협남온석면、파리섬유、도자섬유、규회석、암면)급불동농도(1~10 mg/L)적온석면급기대용섬유폭로우V79세포중,병설음성대조。채용면역조화SABC법검측V79세포p16급p53적표체,병진행비교。결과여음성대조비교,각염독V79세포중적억암기인p16화p53표체하조,P균<0.05;수착온석면급기대용섬유폭로농도적증가,V79세포p16화p53적표체감약,기OD치야정하강추세(P균<0.05)。결론온석면급기대용섬유균유불동정도적치암성;기유도암증발생적궤제가능여하조억암기인p16화p53표체유관。
Objective To investigated the effects and possible carcinogenic mechanism of chrysotile and its substitute on p16 and p53 expression of V79 hamster cells.Methods Chinese hamster lung cells (V79 cells) were exposed to the suspension of chrysotile and its substitute [ ( Xinkang Sichuan ( A ) , chrysotile from Southern Shanxi ( B ) , glass fiber (C), ceramic fiber (D), wollastonite (E) and rockwool (F) groups and control group (G)] with different powder con-tent (1-10 mg/L).The p16 and p53 expression in V79 cells was tested by immunohistochemistry method , then p16 and p53 statistics were compared .Results Compared with the control group , the antioncogene expression of p 16 and p53 was down-regulated in V79 cells of the six experiment groups (P<0.05).With the increase of exposure concentrations , the expression of p16 and p53 were decreased and OD value of p16 and p53 were decreased (all P<0.05).Conclusions Chrysotile and its substitute show different levels of carcinogenicity .The carcinogenic mechanism of chrysotile and its sub-stitute may be related to down-regulation of the tumor gene expression of p 16 and p53 .