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目的:研究温郁金醚提物中新二萜类化合物C对由脂多糖(LPS)诱导胃上皮细胞炎症因子释放的影响及作用机制。方法:不同浓度的温郁金二萜类化合物C在不同的时间,体外作用于人胃癌SGC-7901细胞,用MTT法检测其对SGC-7901细胞的生长抑制率;用ELISA检测炎症因子IL-1β、IL-2的分泌;RT-PCR检测两种炎症因子mRNA转录情况;Western Blot方法检测p38、JNK、ERK蛋白量的表达变化。结果:温郁金二萜类化合物C在10μg/mL浓度以内、LPS在10ng/mL以内对SGC-7901增殖无影响;二萜类化合物C能显著性抑制由LPS诱导的炎症因子IL-1β释放(P<0.01),促进抑炎因子IL-2的释放(P<0.01);RT-PCR检测的结果与之相同;温郁金二萜类化合物C抑制MAPK通路中P38、JNK、ERK蛋白的表达。结论:温郁金二萜类化合物C能抑制由脂多糖诱导胃癌细胞炎症因子的释放,其作用机制可能与其抑制细胞内MAPK通路有关。
Objective: To study the effect of new diterpene C on the release of inflammatory cytokines in gastric epithelial cells induced by lipopolysaccharide (LPS) and its mechanism. Methods: Different concentrations of diterpene C in different concentrations of different concentrations of human gastric cancer SGC-7901 cells at different times, with MTT assay SGC-7901 cell growth inhibition rate; using ELISA detection of inflammatory cytokines IL-1β, IL-2 secretion; RT-PCR detection of two inflammatory cytokines mRNA transcription; Western Blot detection of p38, JNK, ERK protein expression changes. Results: The diterpenoid C at 10μg / mL had no effect on the proliferation of SGC-7901 with LPS at 10ng / mL. Diterpene C significantly inhibited the release of IL-1β by LPS (P (P <0.01). The result of RT-PCR assay was the same as that of the control. The results showed that the diterpenoids C inhibited the expression of P38, JNK and ERK in MAPK pathway. Conclusion: Diclosporin C can inhibit the release of inflammatory cytokines in gastric cancer cells induced by lipopolysaccharide, and its mechanism may be related to the inhibition of intracellular MAPK pathway.