论文部分内容阅读
目的研究２，４，６三硝基氯苯（ｐｉｃｒｙｌｃｈｌｏｒｉｄｅ，ＰＣｌ）致迟发型变态（ＤＴＨ）反应ＰＣｌＤＴＨ诱导肝损伤过程中Ｃａ２＋的参与机制及钙拮抗剂的影响。方法将ＰＣｌ导致的ＤＴＨ反应导入肝脏诱发肝损伤，原子吸收分光光度法测定损伤后不同时间肝组织Ｃａ２＋含量，攻击前１ｈ及后８ｈ２次口服给予５０ｍｇ·ｋｇ－１钙拮抗剂硝苯吡啶或维拉帕米，观察血清谷丙转氨酶（ＡＬＴ）水平及肝组织Ｃａ２＋含量与对照组的差异。结果ＰＣｌ肝穿刺攻击后６ｈ肝组织Ｃａ２＋含量开始上升，１８ｈ达峰值，３６ｈ恢复正常；钙拮抗剂在保护肝损伤的同时降低了血清ＡＬＴ水平，且两者呈线性相关。结论Ｃａ２＋参与了该肝损伤过程，钙拮抗剂的降钙作用与其对该肝损伤的保护作用相关。
Objective To investigate the mechanism of delayed Ca2 + -induced delayed-type metamorphosis (DTH) induced by 2,4,6-trichloro-chlorphenylamine (PCl) and the effect of calcium antagonists on PCl-DTH-induced hepatic injury. Methods DTH induced by PCl was induced into liver to induce liver injury. Atomic absorption spectrophotometry was used to determine the content of Ca2 + in liver tissue at different time points after injury. Oral administration of 50 mg · kg-1 nifedipine or Laparib, observe the level of serum alanine aminotransferase (ALT) and liver tissue Ca2 + content difference with the control group. Results The content of Ca2 + in liver tissue began to rise at 6h after PCl liver puncture and peaked at 18h, and returned to normal at 36h. Calcium antagonist decreased serum ALT level while protecting liver injury, and both of them were linearly correlated. Conclusion Ca2 + is involved in the process of liver injury. The calcium-lowering effect of calcium antagonists is related to its protective effect on liver injury.