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Abstract Aim This study aimed to find a more sensitive and systematic behavioral evaluation protocol to evaluate the cognitive impairment in rats with heart failure (HF). Methods and results An HF rat model was built by ligating the left anterior descending coronary artery. The cardiac function and structure were detected using echocardiography. Myocardial histopathological changes were observed by nitro blue tetrazolium and hematoxylin–eosin staining. The cognitive functions were evaluated using the acquisition task, probe trial, reversal test, and matching‐to‐sample test of the Morris water maze. In the probe trial, the number of times the rats in the model group crossed the platform site significantly decreased compared with that in the sham group. In the reversal test, the average latency was significantly longer in the sham group compared with the model group in the first trial but was shorter in the second and third trials. In the matching‐to‐sample test, the average latency of Trial1 increased significantly in the model group compared with the sham group, while no obvious difference was observed in Trial2. Therefore, the difference in the average latency between Trial1 and Trial2 of the model group was significantly larger. Conclusions The cognitive impairment in rats with HF mainly reflected in the long‐term and working memory, spatial learning, and reversal learning ability. The probe trial and reversal test in the water maze may be more sensitive and preferred to evaluate cognitive function after HF. These findings would provide a brief evaluation protocol for further studies on the relationship between cognitive function and HF.

Wenxin Granule (WXKL) is a traditional Chinese medicine used for treatment of myocardial infarction (MI) and arrhythmias. However, the genomic pathological mechanisms of MI and mechanisms of WXKL are largely unknown. This study aims to investigate a comprehensive miRNA expression profile, and the predicted correlation pathways to be targeted by differentially expressed miRNAs in MI, and mechanisms of WXKL from a gene level. MI rat model was established by a coronary artery ligation surgery. miRNA expression microarrays were performed and the data were deposited in Gene Expression Omnibus (GEO number GSE95855). And, pathway analysis was performed by using the DIANA-miRPath v3.0 online tool. The expressions of miR-1, miR-133, Cx43, and Cx45 were detected by quantitative real-time PCR. It was found that 35 differentially expressed miRNAs and 23 predicted pathways, including miR-1, miR-133, and gap junction pathway, are involved in the pathogenesis of MI. And, WXKL increased the expressions of miR-1 and miR-133, while also increased the mRNA levels of Cx43 and Cx45, and, especially, recovered the Cx43/Cx45 ratio near to normal level. The results suggest that regulatory effects on miR-1, miR-133, Cx43, and Cx45 might be a possible mechanism of WXKL in the treatment of MI at the gene level.