摘要
目的 观察金属硫蛋白 (metallothionein ,MT)对同型半胱氨酸损伤血管内皮细胞的拮抗作用。方法 人血管内皮细胞培养 ;自动生化分析仪测乳酸脱氢酶 (LDH)漏出量 ;10 9Cd 血红素饱和法测细胞MT含量 ;台盼蓝排除法计算细胞存活率。结果 同型半胱氨酰 (Hcy) (0 1～ 1 0mmol·L-1)呈浓度依赖性地增加细胞LDH漏出和降低细胞存活率。外源给予MT 5× 10 -8μmol·L-1可呈剂量依赖性的抑制Hcy引起的血管内皮细胞损伤 ,5× 10 -8mol·L-1MT与1 0mmol·L-1Hcy共同孵育组较单纯Hcy孵育组血管内皮细胞LDH漏出降低 2 7 1% (P <0 0 5 ) ,细胞存活增加 6 %(P <0 0 5 )。凝血酶预孵育可诱导培养的血管内皮细胞MT生成 ,其含量较对照组增加 32 5 % (P <0 0 1)。凝血酶诱导内源性MT生成亦明显抑制Hcy引起的血管内皮细胞损伤 ,10 0 0U·L-1凝血酶与Hcy共同孵育组较单纯Hcy孵育组血管内皮细胞LDH漏出降低 46 % (P <0 0 1) ;细胞存活率升高 8% (P <0 0 5 )。
AIM To observe the antagonistic effect of metallothionein (MT) against homocysteine (Hcy) induced endothelial cell injury. METHODS Human vascular endothelial cells (VECs) were cultured. LDH leakage of VECs and content of MT in VECs were measured. The viabilities of VECs were calculated by trypan blue exclusion. RESULTS Hcy not only increased LDH leakage of cultured VECs but also decreased the viabilities of cultured VECs in dose dependent manner. Exogenous MT (5×10 -8 mol·L -1 ) could inhibit Hcy induced VECs injury in dose dependent manner. LDH leakage in MT(5×10 -8 mol·L -1 ) plus Hcy (1 0 mmol·L -1 ) group decreased by 27 1%( P <0 05), whereas the viabilities of VECs increased by 6% ( P <0 05), compared with Hcy group. MT production of cultured VECs was induced by preincubation of thrombin. MT content (in 1 000 U·L -1 thrombin induced cells) increased by 32 5%( P <0 01) compared with control. LDH leakage of cultured VECs in thrombin plus Hcy group decreased by 46%( P <0 01), and the viabilities of cultured VECs increased by 8% ( P <0 05), compared with Hcy alone group. CONCLUSION Whether administration of exogenous MT or induction of endogenous MT formation can diminish Hcy induced VECs injury.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2000年第4期394-396,共3页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助课题 !No 39730 2 2 0
