青葙子苷A对AHNP诱导肝损伤的保护作用研究

Protective Effects of Celosin-A on the AHNP-induced Liver Injury

为研究青葙子苷A对大鼠急性出血性坏死性胰腺炎(AHNP)诱导肝损伤的治疗作用及其初步作用机制,应用逆行胰胆管术注射牛磺胆酸钠(TAC)复制了AHNP试验动物模型,将其分为假手术组(A组)、AHNP生理盐水对照组(B组)、AHNP青葙子苷A高、低剂量治疗组(C、D组)和AHNP奥曲肽治疗组(阳性药物对照,E组)。各组试验动物手术后6 h处死,测定腹水量,运用比色法检测其血清淀粉酶含量,ELISA法测定肝组织中TNF-α含量,HE染色观察其肝组织病理变化,透射电镜观察肝脏卵圆细胞形态变化,Western-Blot检测肝组织中细胞核转录因子(NF-кB)蛋白的表达情况。结果表明,与A组比较,AHNP生理盐水对照组(B组)大鼠肝组织中腹水量、血清淀粉酶含量、TNF-α含量明显升高,NF-кB蛋白表达明显增强;青葙子苷A治疗组(C、D组)和奥曲肽治疗组(E组)肝组织中腹水量、血清淀粉酶含量、TNF-α含量及NF-кB蛋白表达均较B组显著(P<0.05)降低。说明青葙子苷A对AHNP诱导的肝损伤有显著的保护作用,其机制可能是通过抑制胰弹性蛋白酶的分泌与激活,抑制NF-кB表达,降低炎症反应,从而减轻肝损伤。

The therapeutical effect of Celosin-A on liver injury of rats caused by acute hemorrhagic necrotizing pancreatitis （AHNP） were investigated and the potential mechanism of AHNP animal was studied by injecting TAC with retrograde cholangiopancreatography divided into five groups including sham operation group （A）,AHNP saline control group（B group）,treatment group in high and low dosage of Celosin-A （C and D group）,AHNP control group treated with Octreotide （E group,positive drug control）.All aninals in each group were executed after 6h of surgery and measured its volume of ascites,content of serum amylase,TNF-α content in liver tissue with colorimetry and ELSIA method.The liver pathological changes were observed by HE dye.The hepatic oval cells morphology was observed under transmission electron microscope.The expression of NF-κB were detected by Westeen-Blot method.The results showed that the volume of ascites,content of serum amylase and TNF-α in AHNP saline control group （B group） were obviously higher than those in group A.The expression of NF-κB was obviously strengthened.Compared with AHNP saline control group （B group） the volume of ascites,content of serum amylase and TNF-α,NF-κB expression-in group C,D and E were all significantly lower （P〈0.05）.It is indicated that the Celosin-A had significant protective effect on AHNP-induced liver injury.Liver injury might be alleviated through inhabiting the activation and secretion of pancreatic elastase to inhabit the expression of NF-κB and reduce inflammation.