论文部分内容阅读
目的 探讨山莨菪碱对实验性肝损伤的疗效及其作用机制。方法 应用ANIT和CCl4分别诱发大鼠肝内胆汁淤积及小鼠肝损伤的模型 ,使用山莨菪碱治疗后观察、测定给药组与对照组的肝组织病理切片和生化指标、肝组织中的Ca2 + 含量、总抗氧化能力、丙二醛的含量及山莨菪碱对CCl4中毒小鼠戊巴比妥钠睡眠时间的影响。结果 山莨菪碱能明显对抗ANIT和CCl4所致的ALT、ALP、Bil升高和血清Tp下降 (P <0 0 1) ,并且使肝细胞和胆管上皮细胞变性、坏死显著减轻。检测山莨菪碱治疗组肝匀浆Ca2 + 含量为( 15 6 9± 3 2 8) μg/g、丙二醛为 ( 62 9± 17 4)nmol/ml及总抗氧化能力为 ( 3 1 9± 8 5 )U/ml ,CCl4中毒小鼠腹腔注射戊巴比妥钠后的睡眠时间为 ( 13 0 9± 3 5 9)min。提示山莨菪碱能明显减低肝匀浆含量 (P <0 0 5 )、脂质过氧化产物丙二醛含量 ,提高机体总抗氧化能力 (P<0 0 1)且可缩短CCl4中毒小鼠腹腔注射戊巴比妥钠后的睡眠时间 ( P <0 0 1)。结论 山莨菪碱对实验性肝损伤具有保护作用 ,其疗效与茵栀黄注射液和肝炎灵相似 ( P >0 0 5 ) ,其作用机制可能与M受体阻断、Ca2 + 拮抗和抗氧化作用有关
Objective To investigate the effect of anisodamine on experimental liver injury and its mechanism. Methods ANIT and CCl4 were used to induce intrahepatic cholestasis and liver injury in rats respectively. The rats were treated with anisodamine and observed. The pathological sections and biochemical indexes of liver tissue in the treated group and the control group were determined. The levels of Ca2 + Content, total antioxidant capacity, malondialdehyde content and anisodamine on the sleep time of pentobarbital sodium in CCl4-poisoned mice. Results Anisodamine could significantly antagonize the increase of ALT, ALP and Bil and the decrease of serum Tp (P <0.01) caused by ANIT and CCl4, and significantly degeneration and necrosis of hepatocytes and biliary epithelial cells. The content of Ca2 + in the liver homogenates of the treated group was (15 6 9 ± 3 2 8) μg / g, the level of MDA was (62 9 ± 17 4) nmol / ml and the total antioxidant capacity was (3 1 9 ± 8 5) U / ml, CCl4 poisoning mice after intraperitoneal injection of sodium pentobarbital sleep time was (13 0 9 ± 359) min. The results showed that anisodamine could significantly reduce the content of liver homogenate (P <0.05), the content of malondialdehyde (MDA) and increase the total antioxidant capacity (P <0.01) and shorten the abdominal cavity of CCl4-poisoned mice Sleep time after pentobarbital injection (P <0.01). Conclusion Anisodamine has a protective effect on experimental liver injury. The therapeutic effect is similar to that of Yinzhihuang Injection and Hepatitis (P> 0.05), and its mechanism may be related to the blockage of M receptor, Ca2 + antagonism and antioxidation Relevant role