实用医学杂志
實用醫學雜誌
실용의학잡지
THE JOURNAL OF PRACTICAL MEDICINE
2014年
11期
1712-1715
,共4页
二氢杨梅素%HepG2%肝癌细胞%生长抑制%凋亡
二氫楊梅素%HepG2%肝癌細胞%生長抑製%凋亡
이경양매소%HepG2%간암세포%생장억제%조망
Dihydromyricetin%HepG2%Liver Cancer Cell%Proliferation%Apoptosis
目的：探讨二氢杨梅素对人类肝癌细胞株HepG2的抑制生长和诱导凋亡作用及其机制。方法：采用四甲基噻唑蓝比色法测试二氢杨梅素对细胞死亡率和细胞增殖活力的影响，并计算半抑制浓度IC50；通过HE荧光染色法和Annexin V-PI 流式细胞术分别观察和分析二氢杨梅素对肝癌细胞HepG2各个细胞周期的影响，最后利用Western 印迹法对与细胞周期和凋亡相关的蛋白群p34cdc-2、CyclinB1、Bcl-2和PARP 在二氢杨梅素作用前后的表达量进行研究。结果：肝癌细胞HepG2的细胞死亡率随着二氢杨梅素溶液浓度的升高而升高，IC50值为（35．22±1．56）μmol / L，且呈现良好量效关系；二氢杨梅素对肝癌细胞HepG2各个细胞周期均有显著影响，其中G2/ M 期细胞比率剧增、S 期细胞比率大幅降低，而G0/ G1期细胞比率则呈指数级减少，与阴性对照组比较，差异具统计学意义（P ＜0．05）；p34cdc-2蛋白的表达量未见变化，CyclinB1蛋白的表达量剧增，Bcl-2蛋白的表达量大幅下降，而PARP 蛋白则因发生水解而表达量有所减少。结论：二氢杨梅素对人类肝癌细胞株HepG2具显著的抑制生长和诱导凋亡的药理作用，其作用机制是通过线粒体信号转导途径，激活含半胱氨酸的天冬氨酸蛋白水解酶Caspase-3，进而参与细胞凋亡。
目的：探討二氫楊梅素對人類肝癌細胞株HepG2的抑製生長和誘導凋亡作用及其機製。方法：採用四甲基噻唑藍比色法測試二氫楊梅素對細胞死亡率和細胞增殖活力的影響，併計算半抑製濃度IC50；通過HE熒光染色法和Annexin V-PI 流式細胞術分彆觀察和分析二氫楊梅素對肝癌細胞HepG2各箇細胞週期的影響，最後利用Western 印跡法對與細胞週期和凋亡相關的蛋白群p34cdc-2、CyclinB1、Bcl-2和PARP 在二氫楊梅素作用前後的錶達量進行研究。結果：肝癌細胞HepG2的細胞死亡率隨著二氫楊梅素溶液濃度的升高而升高，IC50值為（35．22±1．56）μmol / L，且呈現良好量效關繫；二氫楊梅素對肝癌細胞HepG2各箇細胞週期均有顯著影響，其中G2/ M 期細胞比率劇增、S 期細胞比率大幅降低，而G0/ G1期細胞比率則呈指數級減少，與陰性對照組比較，差異具統計學意義（P ＜0．05）；p34cdc-2蛋白的錶達量未見變化，CyclinB1蛋白的錶達量劇增，Bcl-2蛋白的錶達量大幅下降，而PARP 蛋白則因髮生水解而錶達量有所減少。結論：二氫楊梅素對人類肝癌細胞株HepG2具顯著的抑製生長和誘導凋亡的藥理作用，其作用機製是通過線粒體信號轉導途徑，激活含半胱氨痠的天鼕氨痠蛋白水解酶Caspase-3，進而參與細胞凋亡。
목적：탐토이경양매소대인류간암세포주HepG2적억제생장화유도조망작용급기궤제。방법：채용사갑기새서람비색법측시이경양매소대세포사망솔화세포증식활력적영향，병계산반억제농도IC50；통과HE형광염색법화Annexin V-PI 류식세포술분별관찰화분석이경양매소대간암세포HepG2각개세포주기적영향，최후이용Western 인적법대여세포주기화조망상관적단백군p34cdc-2、CyclinB1、Bcl-2화PARP 재이경양매소작용전후적표체량진행연구。결과：간암세포HepG2적세포사망솔수착이경양매소용액농도적승고이승고，IC50치위（35．22±1．56）μmol / L，차정현량호량효관계；이경양매소대간암세포HepG2각개세포주기균유현저영향，기중G2/ M 기세포비솔극증、S 기세포비솔대폭강저，이G0/ G1기세포비솔칙정지수급감소，여음성대조조비교，차이구통계학의의（P ＜0．05）；p34cdc-2단백적표체량미견변화，CyclinB1단백적표체량극증，Bcl-2단백적표체량대폭하강，이PARP 단백칙인발생수해이표체량유소감소。결론：이경양매소대인류간암세포주HepG2구현저적억제생장화유도조망적약리작용，기작용궤제시통과선립체신호전도도경，격활함반광안산적천동안산단백수해매Caspase-3，진이삼여세포조망。
Objective To discuss the proliferation inhibition, apoptosis-inducing effects and the mechanism of dihydromyricetin on human liver cancer HepG2. Methods The effects of dihydromyricetin on cell death rate and proliferation in light of MTT test were examined and IC50 was calculated. The effects of dihydromyricetin on liver cancer HepG2 in different cell cycles were observed and analyzed in light of HE fluorescent staining method and Annexin V-PI flow cytometry (FCM). The protein expressions of p34cdc-2、CyclinB1、Bcl-2 and PARP which were related to the cell cycle and apoptosis before and after the use of dihydromyricetin were determined in light of Western blotting. Results The death rate of liver cancer HepG2 were increased with the increasing of dihydromyricetin concentration. The IC50 read (35.22 ± 1.56)μmol/L and displayed dose-response relationship. Dihydromyricetin had significant impacts on liver cancer HepG2 in different cell cycles, the proportion of G2/M cells rose dramatically and that of S cells lowered sharply and that of G0/G1 cell decreased exponentially.The difference was of statistical significance compared with the control group (P < 0.05). Conclusion Dihydromyricetin has distinct medical effects on inhibiting the growth and inducing the apoptosis of liver cancer HepG2. The mechanism is to activate Caspase-3,thus engaged in apoptosis in light of signal transduction of the mitochondrion.
