绿茶多酚改善环孢素A抑制血管舒张的作用

目的 观察绿茶多酚(GTP)对环孢素A(CsA)抑制血管舒张作用的改善,并探讨其机制.方法 将30只SD大鼠随机平均分为3组:CsA组、对照组和CsA+GTP组.建模5周后,检测体质量、肾功能:血尿素氮(BUN)、肌酐(Cre);并取胸主动脉环,观察乙酰胆碱(Ach)诱发的血管舒张反应、左旋硝基精氨酸甲酯(L-NAME)和吲哚美辛预处理对舒张反应的影响、去内皮细胞的血管舒张反应.并检测血管组织一氧化氮(NO)水平.结果 实验5周后,CsA组大鼠体质量(253.2±8.1)g低于对照组(292.1±9.5)g;CsA+GTP组体质量(287.9±9.7)g高于CsA组;CsA组BUN、Cre含量高于对照组;CsA+GTP组BUN、Cre低于CsA组;差异均有统计学意义(P<0.05).CsA组大鼠Ach引起的动脉环的最大舒张度为(42.5±4.3)%,低于对照组的(81.2±7.6)%和CsA+GTP组的(70.1±6.5)%,差异有统计学意义(P<0.05).用L-NAME预处理后,CsA组和CsA+GTP组动脉环的舒张幅度分别为(40.3±3.7)%和(45.8±4.2)%,均低于对照组的(79.4±6.8)%;用吲哚美辛预处理后对照组和CsA+GTP组的舒张反应高于CsA组;差异均有统计学意义(P<0.05).去内皮细胞的各组血管中,血管舒张反应被明显抑制,各组血管的舒张百分比差异无统计学意义(P>0.05).CsA组大鼠血管组织中NO含量显著低于对照组和CsA+GTP组,差异有统计学意义(P<0.05).结论 CsA可导致血管组织NO水平下降,引起NO介导的内皮依赖性血管舒张功能异常.应用绿茶多酚后,则升高其血管组织中NO水平,改善内皮依赖性的血管舒张功能.

Alleviation effect of green tea polyphenols on cyclosporine A-induced inhibition of vasodilation

Objective To observe the alleviation effect of green tea polyphenols (GTP) on cyclosporine A (CsA)-induced inhibition of vasodilation, and to study the underlying mechanism. Methods Thirty SD rats were randomly divided into three groups: CsA group, control group and CsA + GTP group. Five weeks after the treatment, the body weight, kidney function (BUN, Cr) of the rats were measured. Then thoracic aorta rings were mounted on a bath system, and the Ach-induced vasodilation, the effect of L-NAME and indomethacin pretreatment on the vasodilation and the denuded vasodilation were evaluated. The contents of nitric oxide (NO) in the vascular tissues were measured. Results Five weeks later, the body weight of the rats in CsA group (253.2 ±8.1) g was lighter than that in control group (292.1 ±9.5) g (P < 0.05);the body weight in CsA + GTP group (287.9 ± 9.7) g was heavier than that in CsA group ( P < 0.05);The levels of BUN and Cr in CsA group were higher than in control group (P <0.05);The levels of BUN and Cr in CsA + GTP group were lower than in CsA group (P <0.05). The maximal response for Achinduced vasodilation in CsA group was (42.5 ±4.3)% , significantly lower than (81.2 ±7. 6)% in control group and (70.1 ± 6.5) % in CsA + GTP group (both/P < 0.05). After pretreatment with L-NAME, the vasodilation in CsA group and CsA + GTP group was (40.3 ±3.7)% and (45.8 ±4.2)% respectively, lower than in control group (79. 4 ± 6. 8)% ;After pretreatment with indomethacin, the vasodilation in control group and CsA + GTP group was higher than in CsA group (both P < 0.05). The vasodilation in the denuded groups was inhibited, but there was no significant difference between groups (P>0.05). In CsA group, the content of NO in vascular tissues was lower than that in control group and CsA + GTP group (both P < 0.05). Conclusion CsA might decrease the NO content in vascular tissues and induce abnormal endothelium-dependent vasodilation which is mediated by NO. The administration of GTP could increase the NO content and alleviate the CsA-induced inhibition of the endothelium-dependent vasodilation.