Sun Jiang, Luo Jing-Wen, Yao Wen-Jie, Luo Xiao-Ting, Su Chen-Lin, Wei Ying-Hui
College of Pharmaceutical Science,Zhejiang Chinese Medical University Hangzhou 311402,China.
Zhongguo Zhong Yao Za Zhi. 2019 Feb;44(4):758-764. doi: 10.19540/j.cnki.cjcmm.20181105.002.
The aim of this paper was to investigate the effect of emodin on gut microbiota in acute kidney injury rats( AKI). Rats were randomly divided into several groups: normal group,model group,low-dose of emodin group( 10 mg·kg(-1)),medium-dose of emodin group( 25 mg·kg(-1)),high-dose of emodin group( 50 mg·kg(-1)) and control group( 5 mg·kg(-1) of benazepril hydrochloride).The AKI model rats were established by intraperitoneal injection of small dose of gentamicin sulfate for 7 days. Two hours after intraperitoneal injection,except for the normal group and the model group,the other groups were given corresponding doses of drugs for 15 days. The serum levels of serum creatinine( SCr),urea nitrogen( BUN),plasma endotoxin level,24 h urinary protein and D-lactate in the plasma were determined by sarcosine oxidase,urease method,tal reagent method,bromo cresol chloroform method and double antibody sandwich enzyme-linked immunoadsorbent assay,respectively. Gut microbial communities were assayed by fluorescent quantitative PCR methods. HE staining was used to detect the pathological changes of the kidneys. Compared with the normal group,there were significant differences in body weight,urinary protein( UTP),bacterial endotoxin,urea nitrogen,creatinine,D-lactate in the plasma and four bacterial contents in the model group( P<0. 05). The urinary protein,urea nitrogen,D-lactate,creatinine and plasma bacterial endotoxin in control group and each emodin group were lower than those in model group,especially for high-dose of emodin( P<0. 01). Moreover,pathology resolution in high-dose emodin was better than other groups. Except for low-dose of emodin group,qRT-PCR data suggested that the amounts of Escherichia coli and Enterococcus in medication administration group were increased,while the amounts of Lactobacilli and Bifidobacterium were reduced compared with model group( P<0. 05),especially for high-dose of emodin( P<0. 01). There is a clear imbalance of gut microbiota in rats with AKI. Emodin could regulate the imbalance of gut microbiota,which might be one of the mechanisms of its effects on AKI rats.
本文旨在研究大黄素对急性肾损伤大鼠(AKI)肠道微生物群的影响。将大鼠随机分为正常组、模型组、大黄素低剂量组(10 mg·kg⁻¹)、大黄素中剂量组(25 mg·kg⁻¹)、大黄素高剂量组(50 mg·kg⁻¹)和对照组(5 mg·kg⁻¹盐酸贝那普利)。通过腹腔注射小剂量硫酸庆大霉素7天建立AKI模型大鼠。腹腔注射2小时后,除正常组和模型组外,其他组给予相应剂量药物,持续15天。分别采用肌氨酸氧化酶法、脲酶法、鲎试剂法、溴甲酚氯仿法和双抗体夹心酶联免疫吸附测定法测定血浆中血清肌酐(SCr)、尿素氮(BUN)、血浆内毒素水平、24小时尿蛋白和D-乳酸水平。采用荧光定量PCR方法检测肠道微生物群落。用苏木精-伊红(HE)染色检测肾脏的病理变化。与正常组相比,模型组大鼠体重、尿蛋白(UTP)、细菌内毒素、尿素氮、肌酐、血浆D-乳酸及四种细菌含量差异有统计学意义(P<0.05)。对照组和各大黄素组的尿蛋白、尿素氮、D-乳酸、肌酐及血浆细菌内毒素均低于模型组,尤其是大黄素高剂量组(P<0.01)。此外,大黄素高剂量组的病理恢复情况优于其他组。除大黄素低剂量组外,qRT-PCR数据表明,给药组大肠杆菌和肠球菌数量较模型组增加,而乳酸杆菌和双歧杆菌数量减少(P<0.05),尤其是大黄素高剂量组(P<0.01)。AKI大鼠存在明显的肠道微生物群失衡。大黄素可调节肠道微生物群失衡,这可能是其对AKI大鼠发挥作用的机制之一。