浙江临床医学
浙江臨床醫學
절강림상의학
ZHEJIANG CLINICAL MEDICAL JOURNAL
2015年
3期
349-350,351
,共3页
彭环庆%彭志允%谢维宁%张志坚%唐钟祥%林辉文
彭環慶%彭誌允%謝維寧%張誌堅%唐鐘祥%林輝文
팽배경%팽지윤%사유저%장지견%당종상%림휘문
丹参酮ⅡA%慢性心力衰竭%血管内皮细胞%DNA损伤
丹參酮ⅡA%慢性心力衰竭%血管內皮細胞%DNA損傷
단삼동ⅡA%만성심력쇠갈%혈관내피세포%DNA손상
TanshinoneⅡA%Chronic heart failure%Vascular endothelial cell%DNA damage
目的:研究丹参酮ⅡA(TanⅡA)对慢性心力衰竭(CHF)患者血清损伤后的血管内皮细胞(VEC)的影响,探讨丹参酮ⅡA治疗CHF的作用机制。方法利用15%的CHF患者血清损伤正常培养的人脐静脉内皮细胞(CRL-1730),用不同浓度的TanⅡA(10、20、40μg/ml)作用于损伤后的细胞24 h,检测VEC的活性及细胞 DNA 的损伤;并检测细胞培养上清液中VEC损伤标志物循环内皮细胞数(CEC)、血管性假血友病因子(vWF)及血栓调节蛋白(TM)的水平变化。结果与健康对照组比较,模型组VEC细胞活性下降(P<0.05),尾部DNA%、彗星长及尾矩均上升(P<0.05),CEC、vWF及TM水平均上升(P<0.05);与模型组比较,20μg/ml和40μg/ml的TanⅡA能增加内皮细胞的活性(P<0.05);减轻DNA的损伤(P<0.01);3个浓度的TanⅡA均可以减少CEC数(P<0.05);20μg/ml和40μg/ml的TanⅡA可降低 vWF水平(P<0.05);40μg/ml的TanⅡA可降低TM水平(P<0.05)。结论 TanⅡA能通过减轻CHF患者血清对内皮细胞的DNA损伤保护VEC,这可能是TanⅡA治疗CHF的作用机制之一。
目的:研究丹參酮ⅡA(TanⅡA)對慢性心力衰竭(CHF)患者血清損傷後的血管內皮細胞(VEC)的影響,探討丹參酮ⅡA治療CHF的作用機製。方法利用15%的CHF患者血清損傷正常培養的人臍靜脈內皮細胞(CRL-1730),用不同濃度的TanⅡA(10、20、40μg/ml)作用于損傷後的細胞24 h,檢測VEC的活性及細胞 DNA 的損傷;併檢測細胞培養上清液中VEC損傷標誌物循環內皮細胞數(CEC)、血管性假血友病因子(vWF)及血栓調節蛋白(TM)的水平變化。結果與健康對照組比較,模型組VEC細胞活性下降(P<0.05),尾部DNA%、彗星長及尾矩均上升(P<0.05),CEC、vWF及TM水平均上升(P<0.05);與模型組比較,20μg/ml和40μg/ml的TanⅡA能增加內皮細胞的活性(P<0.05);減輕DNA的損傷(P<0.01);3箇濃度的TanⅡA均可以減少CEC數(P<0.05);20μg/ml和40μg/ml的TanⅡA可降低 vWF水平(P<0.05);40μg/ml的TanⅡA可降低TM水平(P<0.05)。結論 TanⅡA能通過減輕CHF患者血清對內皮細胞的DNA損傷保護VEC,這可能是TanⅡA治療CHF的作用機製之一。
목적:연구단삼동ⅡA(TanⅡA)대만성심력쇠갈(CHF)환자혈청손상후적혈관내피세포(VEC)적영향,탐토단삼동ⅡA치료CHF적작용궤제。방법이용15%적CHF환자혈청손상정상배양적인제정맥내피세포(CRL-1730),용불동농도적TanⅡA(10、20、40μg/ml)작용우손상후적세포24 h,검측VEC적활성급세포 DNA 적손상;병검측세포배양상청액중VEC손상표지물순배내피세포수(CEC)、혈관성가혈우병인자(vWF)급혈전조절단백(TM)적수평변화。결과여건강대조조비교,모형조VEC세포활성하강(P<0.05),미부DNA%、혜성장급미구균상승(P<0.05),CEC、vWF급TM수평균상승(P<0.05);여모형조비교,20μg/ml화40μg/ml적TanⅡA능증가내피세포적활성(P<0.05);감경DNA적손상(P<0.01);3개농도적TanⅡA균가이감소CEC수(P<0.05);20μg/ml화40μg/ml적TanⅡA가강저 vWF수평(P<0.05);40μg/ml적TanⅡA가강저TM수평(P<0.05)。결론 TanⅡA능통과감경CHF환자혈청대내피세포적DNA손상보호VEC,저가능시TanⅡA치료CHF적작용궤제지일。
Objective To study the effect of tanshinoneⅡA(TanⅡA)on the vascular endothelial cell(VEC)injury induced by the serum of the patients with chronic heart failure(CHF),and to explore the mechanism of action further. Methods The human umbilicus vein endothelial cells(CRL-1730)were injured by the 15% serum of the patients with CHF,then treated with different concentrations of TanⅡA(10μg/ml,20 μg/ml,40 μg/ml)for 24hours.The activity and the DNA damage of the VEC were determined.The level of the circulating endothelial cells(CEC),von willebrand factor(vWF)and thrombomodulin(TM)in the supernatant were also determined. Results Compare to the healthy control group,the activity of the VEC in the model group was decreasesd(P<0. 05),the percentage of tail DNA,tail extent and the olive tail moment were increased(P<0.05),the level of the CEC,VWF and TM were increased(P<0.05). Compare to the model group,20μg/ml and 40μg/ml TanⅡA can increase the activity of the VEC(P<0.05),reduce the cell DNA damage (P<0.05),all the three dose of TanⅡA can decrease the level of CEC,and 20μg/ml and 40μg/ml TanⅡA can decrease the level of vWF (P<0.05),and only the 40μg/ml TanⅡA can decrease the level of TM(P<0.05). Conclusion TanⅡA has a protective effect on the VEC by reducing the damage of the cell DNA maybe one of the mechanism in treating CHF.