首页|姜黄素抑制甲基硝基亚硝基胍诱导胃黏膜上皮细胞上皮间质转化

姜黄素抑制甲基硝基亚硝基胍诱导胃黏膜上皮细胞上皮间质转化

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  • 国家科技期刊平台
  • NETL
  • NSTL
  • 万方数据
目的 探讨姜黄素(Cur)对甲基硝基亚硝基胍(MNNG)诱导胃黏膜上皮细胞(GES-1)上皮间质转化(EMT)的抑制作用及其机制。方法 将GES-1分为对照组、MNNG处理组(MNNG浓度为20pmol/L，该处理组获得的稳定传代细胞为MC1细胞)、Cur处理组(Cur浓度为20μmol/L)、MNNG+Cur组(该处理组获得的稳定传代细胞为MC2细胞)。采用噻唑蓝(MTT)法评价不同浓度姜黄素对GES-1细胞增殖的影响;光学显微镜观察Cur干预对MNNG诱导的胃黏膜上皮细胞的细胞形态及生长情况的影响;划痕愈合法检测细胞的迁移能力;Western Blot及免疫荧光检测PTEN、Vimentin表达。结果 MTT结果显示在5～20 μmol/L浓度范围内姜黄素对GES-1细胞生长增殖无影响，较大浓度姜黄素作用后GES-1细胞增殖受到抑制。MNNG可诱导GES-1细胞发生EMT转化过程，Cur对MNNG诱导GES-1细胞EMT形态学变化有明显影响。通过划痕修复试验显示，与MC1细胞比较，MC2细胞在48、72 h的划痕愈合速度慢(P＜0。05);Western Blot、免疫荧光试验显示，与MNNG处理组比较，MNNG+Cur组PTEN表达上调;MNNG+Cur组、Cur组间质标志物Vimentin表达下调，差异均有统计学意义(P＜0。05);EMT转化稳定传代后的MC1细胞中PTEN表达明显低于MC2细胞(P＜0。05)。结论 Cur可以抑制MNNG诱导的GES-1细胞EMT进程，其机制可能与PTEN介导的相关信号通路有关。
Curcumin Inhibits Epithelial-Mesenchymal Transition in Human Gastric Epithelial Cells Induced by N-methyl-N'-nitro-N-nitrosoguanidine
Objective To explore the inhibitory effect and underlying mechanism of curcumin(Cur)on epithelial-mesenchymal transition(EMT)in human gastric epithelial cells(GES-1)induced by N-methyl-N'-nitro-N-nitrosoguanidine(MNNG).Methods The GES-1 cells were divided into the control group,the MNNG treatment group(the concentration of MNNG action was 20 µmol/L,the stably passaged cells obtained in this group were used as MC1 cells),the curcumin treatment group(the concentration of Curcumin action was 20 µmol/L),and the MNNG+curcumin group(the stably passaged cells obtained in this group were used as MC2 cells).The impact of various concentrations of curcumin on GES-1 cell proliferation was assessed using the MTT assay.The influence of curcumin intervention on the morphology and growth of MNNG-induced gastric mucosal epithelial cells was observed under an optical microscope.Cell migration ability was evaluated using the scratch healing method.The expression levels of PTEN and Vimentin were detected by Western Blot and immunofluorescence assays.Results MTT assay results indicated that curcumin concentrations ranging from 5-20 µmol/L showed no significant impact on GES-1 cell growth and proliferation.However,higher concentrations of curcumin were found to inhibit the proliferation of GES-1 cells.MNNG was observed to induce EMT in GES-1 cells,and curcumin significantly affected the morphological changes associated with MNNG-induced EMT.The scratch repair assay revealed that compared with the MC1 cells,the scratch healing speed of MC2 cells exhibited a significant deceleration at 48 h and 72 h(P＜0.05).Subsequent Western Blot and immunofluorescence analyses unveiled that compared with the MNNG group,PTEN expression was up-regulated in the MNNG+curcumin group and the expression of the mesenchymal marker Vimentin was down-regulated in the MNNG+curcumin group and the curcumin treatment group(P＜0.05).PTEN expression in EMT-transformed MC1 cells was significantly lower than that in MC2 cells(P＜0.05).Conclusion Curcumin could inhibit the MNNG-induced EMT process in GES-1 cells,and the mechanism might be related to the relevant signaling pathway mediated by PTEN.

curcuminepithelial-mesenchymal transitiongastric cancerphosphatase and tensin homolog deleted on chromosome tenChinese herbal extracts

贾婷婷、万学婷、潘秋如、覃月凤、强占荣

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桂林医学院临桂临床医学院(广西 541000)

桂林医学院第二附属医院消化内科(广西 541100)

姜黄素 上皮间质转化 胃癌 人第10号染色体缺失的磷酸酶及张力蛋白同源基因 中药提取物

广西自然科学基金项目桂林市科技开发项目桂林医学院中青年教职工科研能力提升项目

2022GXNSFAA10300720210227-8-42018glmcy091

2024

10.7661/j.cjim.20240301.036

中国中西医结合杂志
中国中西医结合学会 中国中医科学院

中国中西医结合杂志

CSTPCD北大核心
影响因子：2.149
ISSN：1003-5370
年,卷(期)：2024.44(9)