中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
Chinese Journal of Experimental Surgery
2015年
9期
2092-2095
,共4页
陈玲%宋佳%孙巧%彭维恒%黄徐英%任立权%陈继革
陳玲%宋佳%孫巧%彭維恆%黃徐英%任立權%陳繼革
진령%송가%손교%팽유항%황서영%임립권%진계혁
竹节参皂苷Ⅴ%PC-12细胞%淀粉样前体蛋白样蛋白-1%去整合素-金属蛋白酶-17%基因表达
竹節參皂苷Ⅴ%PC-12細胞%澱粉樣前體蛋白樣蛋白-1%去整閤素-金屬蛋白酶-17%基因錶達
죽절삼조감Ⅴ%PC-12세포%정분양전체단백양단백-1%거정합소-금속단백매-17%기인표체
Chikusetsusaponin Ⅴ%PC-12 cells%Amyloid precursor-like protein 1%A disinte-grin and metalloproteinase domain 17%Gene expression
目的 观察竹节参皂苷Ⅴ对损伤的PC-12细胞的修复作用以及对淀粉样前体蛋白样蛋白-1(APLP-1)和去整合素-金属蛋白酶-17(ADAM-17)基因表达的影响.方法 利用β-淀粉样蛋白25-35(Aβ25-35)诱导制备PC-12细胞损伤模型,噻唑蓝(MTT)法测定竹节参皂苷Ⅴ对受损PC-12细胞增殖活力的恢复作用,实时荧光定量聚合酶链反应(FQ-PCR)测定竹节参皂苷Ⅴ对PC-12细胞中APLP-1、ADAM-17基因表达的影响.结果 终质量浓度为15 μmol/L的Aβ25-35在作用于PC-12细胞12、24、48 h时,对细胞增殖的抑制率分别为13.15％、22.80％和9.80％,与空白组比较差异有统计学意义(P＜0.05).在Aβ25-35诱导的细胞损伤模型(24h)的基础上,竹节参皂苷Ⅴ作用6、12、18、24h时PC-12细胞的增殖率与模型组比较分别增高5.53％、7.74％ (P＜0.05)、9.60％(P＜0.01)和2.07％.模型组中PC-12细胞中APLP-1基因的相对表达量较空白组明显上调,ADAM-17基因的相对表达量则明显下调;竹节参皂苷Ⅴ给药组中APLP-1基因的相对表达量相对模型组明显下调,而ADAM-17基因明显上调.结论 竹节参皂苷Ⅴ对Aβ25-35诱导损伤的PC-12细胞有修复作用,推测是通过下调APLP-1的相对表达量,使淀粉样前体蛋白(APP)低量表达,并上调ADAM-17基因的相对表达量,使APP朝着非Aβ生成途径降解的方式来修复损伤的PC-12细胞.
目的 觀察竹節參皂苷Ⅴ對損傷的PC-12細胞的脩複作用以及對澱粉樣前體蛋白樣蛋白-1(APLP-1)和去整閤素-金屬蛋白酶-17(ADAM-17)基因錶達的影響.方法 利用β-澱粉樣蛋白25-35(Aβ25-35)誘導製備PC-12細胞損傷模型,噻唑藍(MTT)法測定竹節參皂苷Ⅴ對受損PC-12細胞增殖活力的恢複作用,實時熒光定量聚閤酶鏈反應(FQ-PCR)測定竹節參皂苷Ⅴ對PC-12細胞中APLP-1、ADAM-17基因錶達的影響.結果 終質量濃度為15 μmol/L的Aβ25-35在作用于PC-12細胞12、24、48 h時,對細胞增殖的抑製率分彆為13.15％、22.80％和9.80％,與空白組比較差異有統計學意義(P＜0.05).在Aβ25-35誘導的細胞損傷模型(24h)的基礎上,竹節參皂苷Ⅴ作用6、12、18、24h時PC-12細胞的增殖率與模型組比較分彆增高5.53％、7.74％ (P＜0.05)、9.60％(P＜0.01)和2.07％.模型組中PC-12細胞中APLP-1基因的相對錶達量較空白組明顯上調,ADAM-17基因的相對錶達量則明顯下調;竹節參皂苷Ⅴ給藥組中APLP-1基因的相對錶達量相對模型組明顯下調,而ADAM-17基因明顯上調.結論 竹節參皂苷Ⅴ對Aβ25-35誘導損傷的PC-12細胞有脩複作用,推測是通過下調APLP-1的相對錶達量,使澱粉樣前體蛋白(APP)低量錶達,併上調ADAM-17基因的相對錶達量,使APP朝著非Aβ生成途徑降解的方式來脩複損傷的PC-12細胞.
목적 관찰죽절삼조감Ⅴ대손상적PC-12세포적수복작용이급대정분양전체단백양단백-1(APLP-1)화거정합소-금속단백매-17(ADAM-17)기인표체적영향.방법 이용β-정분양단백25-35(Aβ25-35)유도제비PC-12세포손상모형,새서람(MTT)법측정죽절삼조감Ⅴ대수손PC-12세포증식활력적회복작용,실시형광정량취합매련반응(FQ-PCR)측정죽절삼조감Ⅴ대PC-12세포중APLP-1、ADAM-17기인표체적영향.결과 종질량농도위15 μmol/L적Aβ25-35재작용우PC-12세포12、24、48 h시,대세포증식적억제솔분별위13.15％、22.80％화9.80％,여공백조비교차이유통계학의의(P＜0.05).재Aβ25-35유도적세포손상모형(24h)적기출상,죽절삼조감Ⅴ작용6、12、18、24h시PC-12세포적증식솔여모형조비교분별증고5.53％、7.74％ (P＜0.05)、9.60％(P＜0.01)화2.07％.모형조중PC-12세포중APLP-1기인적상대표체량교공백조명현상조,ADAM-17기인적상대표체량칙명현하조;죽절삼조감Ⅴ급약조중APLP-1기인적상대표체량상대모형조명현하조,이ADAM-17기인명현상조.결론 죽절삼조감Ⅴ대Aβ25-35유도손상적PC-12세포유수복작용,추측시통과하조APLP-1적상대표체량,사정분양전체단백(APP)저량표체,병상조ADAM-17기인적상대표체량,사APP조착비Aβ생성도경강해적방식래수복손상적PC-12세포.
Objective To explore the effect of chikusetsusaponin Ⅴ on the repair of the injured PC-12 cell line and the expression of Amyloid precursor-like protein 1 (APLP-1) and A disintegrin and metalloproteinase domain 17 (ADAM-17).Methods PC-12 cell injury model was induce by Amyloid beta 25-35 (Aβ25-35).Methyl thiazol tetrazolium (MTT) was applied to analyze the repair effect of chikusetsusaponin Ⅴ on damaged proliferation of PC-12 cell line,while real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) was used to assay the influence of chikusetsusaponin Ⅴ on the expression of APLP-1 and ADAM-17.Results Aβ25-35 (15 μmol/L) inhibited proliferation of PC-12 cells by 13.15％,22.80％ and 9.80％ respectively at 12,24,and 48 h after treatment,which had significant difference compared to control group.Chikusetsusaponin Ⅴ could protect PC-12 cell line against the cytotoxicity of Aβ25-35 through increasing cell proliferation by 5.53％,7.74％ (P ＜ 0.05),9.60％ (P ＜0.01) and 2.07％ at 6,12,18 and 24 h time points,respectively.The expression level of APLP-1 gene in model groups was obviously higher than that in control groups,while ADAM-17 gene was obviously lower than the control.Moreover,APLP-1 gene expression in PC12 cell line treated with chikusetsusaponin Ⅴ was strikingly down-regulated,while ADAM-17 gene was up-regulated.Conclusion It is indicated that chikusetsusaponin Ⅴ could repair the proliferation of PC-12 cell line injured by Aβ25-35 through down-regulating the APLP-1 gene and up-regulating ADAM-17 gene.
