摘要
目的观察β-榄香烯对食管内镜下黏膜下剥离术(Endoscopic submucosal dissection,ESD)后成纤维细胞的抑制作用,并研究其作用机制是否与凋亡有关。方法将成纤维细胞分为对照组(常规培养)、低、中、高剂量实验组(100,200,400μg·mL^-1β-榄香烯)。给药24 h后,用细胞增殖毒性检测(Cell Counting Kit-8,CCK-8)法检测细胞生长抑制率,用流式细胞术检测细胞凋亡率;用蛋白质印迹法检测对照组和中剂量实验组的磷酸化细胞外信号调节激酶1/2(p-ERK1/2)、磷酸化P38(p-P38)蛋白表达。结果给药24 h后,对照组、低、中、高剂量实验组的细胞生长抑制率分别为0,(24.39±6.64)%,(63.40±6.27)%,(95.01±2.83)%;细胞凋亡率分别为(1.34±0.08)%,(1.12±0.07)%,(32.33±0.63)%,(32.01±1.18)%,3个实验组分别与对照组比较,差异均有统计学意义(均P<0.001)。对照组、中剂量实验组的p-ERK1/2蛋白相对表达量分别为1.92±0.45,0.80±0.50;p-P38蛋白相对表达量分别为1.44±0.16,1.89±0.48,差异均有统计学意义(均P<0.05)。结论β-榄香烯对食管ESD术后的成纤维细胞具有抑制生长的作用,其机制与调节凋亡相关蛋白的表达从而诱导凋亡有关。
Objective To investigate the inhibitory effect of β-elemene on fibroblasts after esophageal endoscopic submucosal dissection(ESD),and to study whether its mechanism is involved in apoptosis.Methods Fibroblasts were assigned to control group(routine treatment)and test-L,-M,-H group(100,200,400μg·mL^-1 β-elemene).After fibroblasts were interfered for 24 hours,the growth inhibition rate of cells was detected by cell counting kit-8(CCK-8),the apoptosis rate was detected by flow cytometry;The expression levels of phosphorylated extracellular signal-regulated protein kinases 1/2(p-ERK1/2)protein and phosphorylated P38(p-P38)protein in the control group and the test-M group were detected by Western blot.Results After fibroblasts were treated for 24 hours,the inhibition rates of cells in control group and test-L,-M,-H group were 0,(24.39±6.64)%,(63.40±6.27)%,(95.01±2.83)%,respectively;the apoptosis rates were(1.34±0.08)%,(1.12±0.07)%,(32.33±0.63)%,(32.01±1.18)%,respectively.There were statistically significant differences between the test-L,-M,-H group and the control group(all P<0.001).The relative expression levels of p-ERK1/2 protein in control group and test-M group were 1.92±0.45,0.80±0.50,respectively;The relative expression levels of p-P38 protein were 1.44±0.16,1.89±0.48,respectively.There were statistically significant differences in the above indicators between the two groups(P<0.05).Conclusion β-elemene can inhibit the growth of fibroblasts after esophageal ESD,and the mechanism was associated with apoptosis through regulating the expression of apoptosis proteins.
作者
蔡宝壤
洪才发
胡俊
房太勇
CAI Bao-rang;HONG Cai-fa;HU Jun;FANG Tai-yong(Department of Gastroenterology,The Second Affiliated Hospital of Fujian Medical University,Quanzhou 362000,Fujian Province,China)
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2020年第20期3310-3312,3316,共4页
The Chinese Journal of Clinical Pharmacology
基金
泉州市高层次人才科技计划基金资助项目(2017Z013)。