Effect of emodin on gut microbiota of rats with acute kidney failure / 中国中药杂志

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.

Relationship Between Cardiac Troponin Ⅰ Autoantibody and Left Ventricular Remodeling in Patients With Acute Myocardial Infarction / 中国循环杂志

Objectives: To analyze the relationship between cardiac troponin I autoantibody (cTnIAAb) and left ventricular remodeling in patients with acute myocardial infarction (AMI). Methods: A total of 131 AMI patients were enrolled. Serum levels of cTnIAAb were measured by ELISA. Echocardiography was examined at the onset of AMI and 1 year follow-up evaluation. Taking left ventricular end systolic volume (LVESV) increasing>15% as left ventricular remodeling, 2-classified logistic stepwise regression analysis was conducted to screen 12 risk factors related to left ventricular remodeling. Results: 23/131(17.6%) patients were with positive cTnIAAb and 82.4% with negative cTnIAAb. 49 patients lost contact and in the rest 91 patients, 21.1% were with positive cTnIAAb. Clinical information was similar between cTnIAAb positive and negative patients upon admission, P>0.05; echocardiography showed that 28 (42.2%) patients had LVESV increasing>15% by 1 year follow-up study whom including 10 (52.6%) patients with cTnIAAb positive and 18 (25.4%) negative. 2-classified logistic stepwise regression analysis indicated that BNP peak and positive cTnIAAb were the risk factors for left ventricular remodeling (OR=1.001, 95% CI 1.001-1.002) and (OR=3.552, 95% CI 1.148-10.989), both P=0.028. Conclusions: Serum cTnIAAb was positive in part of AMI patients which was related to increased risk of left ventricular remodeling; cTnIAAb might be involved in pathophysiological process of left ventricular remodeling in AMI patients.