白细胞介素-2对缺氧/复氧心肌细胞[Ca^(2+)]_i的作用

Effect of interleukin-2 on intracellular calcium levels in rat ventricular myocytes during anoxia and reoxygenation

目的 :观察白细胞介素 - 2 (IL - 2 )对心肌细胞在缺氧 /复氧过程中电刺激诱导的 [Ca2 + ]i 的作用。方法 :采用酶解分离成年大鼠心室肌细胞化学缺氧模型 ,以Fura - 2 /AM为钙探针 ,用细胞内双波长钙荧光系统检测心肌 [Ca2 + ]i 的变化。结果 :①缺氧 /复氧过程中 ,缺氧 5min时 ,心肌 [Ca2 + ]i 幅度降低、舒张末期 [Ca2 + ]i 升高 ,[Ca2 + ]i 达峰时间 (TTP)延长 ,恢复时间 (RT)延长。复氧 10min后 ,心肌 [Ca2 + ]i 幅度、舒张末期 [Ca2 + ]i、TTP及RT逐渐回复 ,但不能完全恢复到对照水平 ;②在缺氧期间加入IL - 2 (2× 10 5U/L) ,复氧期间 [Ca2 + ]i 各参数回复减慢 ;③用κ-阿片受体拮抗剂nor-BNI(10 -8mol/L)预处理后 ,缺氧 +IL - 2对复氧时 [Ca2 + ]i 作用的影响被减弱 ,而δ -阿片受体拮抗剂纳曲吲哚 (10 -6mol/L)预处理则无此作用。结论 :缺氧时同时存在IL - 2 ,可加剧复氧时心肌 [Ca2 + ]i 的变化 ,其机制可能是IL - 2通过心肌κ-阿片受体而发挥作用。

AIM: To investigate the effect of interleukin-2 (IL-2) on the intracellular calcium in electrically stimulated adult rat ventricular myocytes during anoxia and reoxygenation. METHODS: The isolated cardiac ventricular myocytes were exposed to 5 min anoxia followed by 10 min reoxygenation. Chemical anoxia was introduced by Krebs-Henseleit (K-H) solution containing 10 -3 mol/L sodium dithionite. The spectrofluorometric method was used to verify intracellular calcium transient with fura-2/AM as calcium fluorescence probe. RESULTS: It was shown that during anoxia, the amplitude of Ca 2+ transient was decreased, diastolic [Ca 2+ ] i, time to peak and time to relaxation of Ca 2+ transient were increased. All the parameters were got back but did not returned to the pre-anoxia level during reoxygenation. IL-2 at 2×10 5 U/L administrated during anoxia aggravated the effect of rexoxygenation on [Ca 2+ ] i transient. Pretreatment with a specific κ opioid antagonist, nor-BNI (10 -8 mol/L), abolished the effect induced by IL-2 during anoxia on the [Ca 2+ ] i transients, whereas specific δ opioid antagonist, naltrindole (10 -6 mol/L), did not cancel the effect. CONCLUSION: It is concluded that administration of IL-2 during anoxia aggravated the effect of reoxygenation on the [Ca 2+ ] i transients of isolated ventricular myocytes, which was mediated by cardiac κ opioid receptor pathway.