摘要
目的研究扶正解毒含药血清(fuzhengjiedu-containing serum,FCS)对镍(nickel,Ni)致癌干预作用的细胞分子机制。方法分别用无菌MEM、不同浓度的NiS及FCS处理16HBE细胞。比较各组细胞存活率以及各组细胞p-ERK、p-P38、p-JNK表达以及NF-κB活性。结果加入NiS各组细胞存活率均显著低于阴性对照组,且NiS浓度越高,细胞存活率越低,差异均具有统计学意义(均P<0.05);NiS+对应抑制剂组以及NiS+FSC中、高剂量组可以下调p-P38以及p-JNK表达量,且剂量越高,下调作用越明显,差异均具有统计学意义(均P<0.05);NiS+对应抑制剂组p-ERK表达量下降(P<0.05)。结论NiS能显著激活p-P38、p-JNK以及NF-κB的表达,不能显著激活p-ERK表达。一定剂量的FCS能明显抑制p-P38、p-JNK表达。
Objective To study the cellular and molecular mechanism of fuzhengjiedu-containing serum （FCS） for intervention of nickel carcinogenesis. Methods 16HBE cells were processed with aseptic MEM, different concentrations of NiS and FCS respectively. The cell survival rate and cells expression ofp-ERK, p-P38 and p-JNK, and NF-KB activity were compared. Results The cell survival rate of groups added NiS were significantly lower than those in the negative control group, and with higher concentration of NiS, the cell survival rate was lower; the difference was statistically significant （P〈0.05）. NiS ＋ corresponding inhibitor group, NiS ＋ FSC （medium dose and high dose） groups could down-regulate p-P38 and p-JNK expression, and the higher dose, the more obvious down-regulation effect; the difference was statistically significant （P 〈0.05）. NiS ＋ corresponding inhibitor group decreased expression of p-ERK （P〈0.05）. Conclusions NiS can activate p-P38, p-JNK and NF-KB expression, but cannot significantly activate p-ERK expression. A certain dose of FCS can inhibit the exlgression of D-P38 and o-JNK.
出处
《临床医学工程》
2014年第3期290-291,共2页
Clinical Medicine & Engineering
基金
惠州市科技计划项目(项目编号:2011Y080)
关键词
扶正解毒含药
镍
致癌
干预
细胞分子机制
Fuzhengjiedu containing
Nickel
Carcinogenesis
Intervention
Cellular and molecular mechanism
