总丹酚酸对过氧化氢诱导内皮细胞损伤的抑制作用(英文)

目的　研究总丹酚酸对过氧化氢 (H2 O2 )诱导血管内皮细胞损伤的影响。方法　培养的人脐静脉内皮细胞 ,用MTT法测定内皮细胞的存活率。用碘化丙啶 (PI)染色和TUNEL法测定H2 O2 诱导内皮细胞的凋亡作用。用荧光法测定半胱天冬酶 (cas pase) 3的活性。用Fura 2 /AM测定内皮细胞内游离钙离子浓度 ([Ca2 + ] i)。结果　 1 0 0 μmol·L-1 H2 O2可使内皮细胞的存活率下降 40 .2 % ,提前 1h给予总丹酚酸 1 0和 1 0 0mg·L-1 使存活率分别增加8.4%和2 8.6 %。 1 0 0 μmol·L-1 H2 O2 还可引起内皮细胞的凋亡 ,PI染色的结果显示 ,H2 O2 处理内皮细胞 1 8h后 ,凋亡率从 (7.1 %± 0 .7) %升至 (38.1±4.0 ) %。总丹酚酸 1 0 0mg·L-1 提前处理内皮细胞1h,可使内皮细胞凋亡率降至 (1 3 .6± 0 .8) %。TUNEL方法检测结果显示 ,H2 O2 处理内皮细胞后 ,TUNEL染色阳性的细胞从 (3 .0± 0 .8) %升至 (30 .5±2 .9) % ,总丹酚酸 1 0 0mg·L-1 可使TUNEL阳性细胞率降至 (1 9.0± 3 .7) %。此外 ,H2 O2 处理细胞后 ,内皮细胞半胱天冬酶 3的活性增加 1 76% ,[Ca2 + ] i 升高 1 0 1 % ,而总丹酚酸可以抑制H2 O2 引起的半胱天冬酶 3活性的增加和 [Ca2 + ] i 升高。结论　总丹酚酸对H2 O2 引起的内皮细胞损伤具有明显的抑制作

Inhibitory effect of salvianolic acids on endothelial cells damage induced by hydrogen peroxide

AIM To elucidate the mechanism of actions of salvianolic acids on cardiovascular system. METHODS The viability of cultured human umbilical vein endothelial cells(HUVEC) was measured by MTT assay. Apoptosis was assessed by propidium iodide (PI) staining and TUNEL assay. Caspase-3 activity and [Ca2+]i in HUVEC were measured by fluorescent assays. RESULTSThe results showed that the viability of HUVEC treated with 100 μmol*L-1 H2O2 for 8 h decreased by 40.2%. Salvianolic acids 10 and 100 mg*L-1 increased the viability of H2O2-treated cells by 8.4% and 28.6%, respectively. The apoptotic rate of HUVEC tested by PI staining increased from (7.1±0.7)% to (38.1±4.0)%after 18 h of treatment with H2O2. Salvianolic acids 100 mg*L-1 reduced the apoptotic rate to (13.6±0.8)%. Under the same condition tested by TUNEL assay, the number of TUNEL-positive cells increased from (3.0±0.8)% to (30.5±2.9)%. Salvianolic acids 10 and 100 mg*L-1 reduced the number to (21.5±2.4)% and (19.0±3.7)%, respectively. In addition, H2O2 increased caspase-3 activity in HUVEC by 176% and the [Ca2+]i by 101%. Salvianolic acids inhibited elevation of caspase-3 activity and [Ca2+]i induced by H2O2. CONCLUSION Salvianolic acids have protective effect on endothelial cells against damage induced by H2O2.