苦参苍术颗粒对大肠杆菌感染肉鸡肝组织胆固醇代谢的调节作用

Regulation of Kushen-cangzhu Granules on Hepatic Cholesterol Metabolism in Broilers Infected with Escherichia coli

旨在探究苦参苍术颗粒是否通过调节肝组织胆固醇代谢,改善致病性大肠杆菌诱导的肉鸡肝组织胆固醇合成异常。将40只21日龄白羽肉鸡随机分为空白对照组、模型对照组、苦参苍术低剂量组、中剂量组和高剂量组,每组8只。模型对照组和苦参苍术组分别胸部肌肉注射0.7 mL致病性大肠杆菌菌液(8.37×10^(8)CFU·mL^(-1)),苦参苍术组在接种菌液24 h后,在饮水中分别添加不同剂量的苦参苍术颗粒(低剂量组:3.6 g·L^(-1),中剂量组:5.5 g·L^(-1),高剂量组:7.3 g·L^(-1)),自由饮水,连用7 d。试验结束,所有试验肉鸡处死,收集血液,采集组织样品,称体重和各器官重;采用石蜡切片技术观察肝组织形态变化;检测血清和肝组织中总胆固醇(total cholesterol,TCH)、甘油三酯(hepatic triglyceride,TG)、高密度脂蛋白胆固醇(high-density lipoprotein-cholesterol,HDL-C)、低密度脂蛋白胆固醇(low-density lipoprotein cholesterol,LDL-C)含量的变化;采用RT-qPCR检测肝组织中胆固醇代谢相关基因的变化。结果显示,与空白对照组相比,模型对照组肉鸡体重显著降低,肝脏指数和血清TG含量显著增加(P<0.05),肝小叶中央静脉周围和肝血窦内有炎性细胞浸润,肝细胞排列紊乱,同时肝组织中TG含量以及SREBP裂解激活蛋白(SREBP cleavage activating protein,SCAP)mRNA相对表达量也显著降低(P<0.05);和模型对照组相比,低剂量组显著增加了肉鸡体重和肝中LDL-C含量(P<0.05),降低了肝脏指数和血清中TG含量(P<0.05),且肝组织形态结构得到改善;和模型对照组相比,中剂量组显著升高了肝HDL-C、LDL-C含量及LDL-C/HDL-C的比值(P<0.05),3羟基3甲基戊二酸单酰辅酶A还原酶(3-hydroxy-3-methylglutaryl coenzyme A reductase,HMGCR)、调节元件结合蛋白2(sterol regulator element-binding protein-2,SREBP2)、SCAP mRNA相对表达量也显著提高(P<0.05)。和模型对照组相比,高剂量组显著降低了血清中TG含量(P<0.05),显著增加肝中LDL-C含量(P<0.05),同时显著增加了LDL-C/HDL-C比值(P<0.05)。综上所述,苦参苍术颗粒可通过调节肉鸡肝组织胆固醇代谢,缓解大肠杆菌感染所致的肝组织胆固醇合成异常。

The aim of this experiment was to investigate whether kushen-cangzhu(Sophora flavescens Ait.and Atractylodes Lancea)granules could improve the abnormal cholesterol synthesis induced by Escherichia coli(E.coli)through regulating liver cholesterol metabolism in broilers.Forty 21 days old white-feathered broilers were randomly divided into 5 groups(8 in each group):Blank control group,model control group,low-,medium-and high-dose of kushen-cangzhu groups.The model control group and different doses of kushen-cangzhu groups were intramuscular thoracic injection treated with pathogenic E.coli bacterial solution for 0.7 mL(8.37×10^(8) CFU·mL^(-1)).After inoculating pathogenic E.coli bacterial solution for 24 h,different doses of kushen-cangzhu granules(low-dose group:3.6 g·L^(-1),medium-dose group:5.5 g·L^(-1),high-dose group:7.3 g·L^(-1))were supplemented in drinking water for chickens in low-,medium-and high-dose groups,respectively,and the trail lasted for 7 days.At the end of the experiment,all the broilers were slaughtered,body and organs were weighed,blood and tissue samples were collected.The morphological changes of liver were observed by hematoxylin-eosin(HE)staining.The levels of serum and liver total cholesterol(TCH),hepatic triglyceride(TG),high-density lipoprotein-cholesterol(HDL-C)and low-density lipoprotein cholesterol(LDL-C)were detected,RT-qPCR was used to detect the expression of cholesterol metabolism-related genes in liver.The results showed that,compared with the blank control group,the broilers in the model control group had significantly lower body weight,higher liver index and serum TG content(P<0.05),while infiltrated inflammatory cells in the central vein and the hepatic sinusoid and disordered hepatocyte was observed in model control group.TG and SCAP mRNA expression was significantly lower(P<0.05)in liver of model control group compared with blank control group.Compared with the model control group,the body weight and liver LDL-C content was significantly increased in the low-dose group(P<0.05),while the liver index and serum TG content were significantly decreased(P<0.05),and the hepatic morphological structure was at a better state.The HDL-C,LDL-C and the LDL-C/HDL-C ratio in liver were significantly increased in the medium-dose group compared with model control group.Meanwhile,the mRNA expression of HMGCR,SREBP2 and SCAP was significantly enhanced(P<0.05)in medium-dose group than model control group.In the high-dose group,the serum TG concentration was significantly reduced(P<0.05)but hepatic LDL-C was significantly increased(P<0.05),and the ratio of LDL-C/HDL-C was significantly raised(P<0.05)compared with the model control group.In conclusion,the liver abnormal synthesis of cholesterol in broilers induced by E.coli was alleviated by kushen-cangzhu granules through regulating cholesterol metabolic pathway.