Background. Yinchen Wuling powder is often used to treat clinical hyperlipidemia, although its mechanism of action remains unclear. In this study, we aimed to investigate the active ingredients found in Yinchen Wuling powder and find its mechanism of action when treating hyperlipidemia, using a combination of network pharmacology, molecular docking, and molecular dynamics simulation approaches. Methods. The TCMSP database was used to obtain the principle active ingredients found in Yinchen Wuling powder and the NCBI and DisGeNet databases were used to obtain the main target genes involved in hyperlipidemia, and the intersectional targets were obtained by EXCEL. We also used Cytoscape 3.7.2 software to construct a “Traditional Chinese Medicine‐Active Ingredient‐Target” network and use STRING platform to conduct “protein‐protein interactional” (PPI) analyses on the intersection targets. Bioconductor software and RX 64 4.0.0 software were then used to perform GO functional enrichment analysis and KEGG pathway enrichment analysis on the targets. Molecular docking of core protein‐ligand interactions was modeled using AutoDock Vina software. A simulation of molecular dynamics was conducted for the optimal core protein‐ligand obtained by molecular docking using Amber18 software. Results. A total of 63 active ingredients were found in Yinchen Wuling powder, corresponding to 175 targets, 508 hyperlipidemia targets, and 55 intersection targets in total. Cytoscape 3.7.2 showed that the key active ingredients were quercetin, isorhamnetin, taxifolin, demethoxycapillarisin, and artepillin A. The PPI network showed that the key proteins involved were AKT1, IL6, VEGFA, and PTGS2. GO enrichment analysis found that genes were enriched primarily in response to oxygen levels and nutrient levels of the vesicular lumen and were associated with membrane rafts. These were mainly enriched in AGE‐RAGE (advanced glycation end products‐receptor for advanced glycation end products) signaling pathway in diabetic complications, fluid shear stress, and atherosclerosis, as well as other pathways. The molecular docking results indicated key binding activity between PTGS2‐quercetin, PTGS2‐isorhamnetin, and PTGS2‐taxifolin. Results from molecular dynamics simulations showed that PTGS2‐quercetin, PTGS2‐isorhamnetin, and PTGS2‐taxifolin bound more stably, and their binding free energies were PTGS2‐quercetin ‐29.5 kcal/mol, PTGS2‐isorhamnetin ‐32 kcal/mol, and PTGS2‐taxifolin ‐32.9 kcal/mol. Conclusion. This study is based on network pharmacology and reveals the potential molecular mechanisms involved in the treatment of hyperlipidemia by Yinchen Wuling powder.

Background: The potential role of the gut microbiome (GM) in heart failure (HF) had recently been revealed. However, the underlying mechanisms of the GM and fecal metabolome in HF have not been characterized. The Dahl salt-sensitive rat model of hypertensive heart failure (H-HF) was used to study the clinical symptoms and characteristics. To elucidate the pathogenesis of HF, we combined 16S rRNA gene sequencing and metabolomics to analyze gut microbial compositions and fecal metabolomic profiles of rats with H-HF. Results: PCoA of beta diversity shown that the gut microbiome composition profiles among the three groups were separated. Gut microbial composition was significantly altered in H-HF rats, the ratio of Firmicutes to Bacteroidetes(F/B) increased and the abundance of Muribaculaceae, Lachnospiraceae, and Lactobacillaceae decreased. Significantly altered levels of 17 genera and 35 metabolites were identified as the potential biomarker of H-HF. Correlation analysis revealed that specific altered genera were strongly correlated with changed fecal metabolites. The reduction in short-chain fatty acids (SCFA)-producing bacteria and trimethylamine N-oxide (TMAO) might be a notable characteristic for H-HF. Conclusions: This is the first study to characterize the fecal microbiome of hypertensive heart failure by integrating 16S rRNA gene sequencing and LC–MS-based metabolomics approaches. Collectively, the results suggesting changes of gut microbiome composition and metabolites are associated with hypertensive heart failure rats.

Background: Traditional Chinese medicine (TCM) is the health care system developed with the help of clinical trials that are based ideally on the scientific model of regulation.Objective: This systematic health care system relies on some specific unique theories and practical experiences to treat and cure diseases, thus enhancing the public’s health.Review Methodology: The current review covers the available literature from 2000 to 2021. The data was collected from journals research articles, published books, thesis, and electronic databases, search engines such as Google Scholar, Elsevier, EBSCO, PMC, PubMed, ScienceDirect, Willey Online Library, Springer Link, and CNKI) searching key terms, cardiovascular disease, traditional Chinese medicines, natural products, and bioactive compounds. Full-length articles and abstracts were screened for the collection of information included in the paper.Results: Clinical trials on the TCM and basic research carried out on its mechanism and nature have led to the application and development of the perfect design of the research techniques, for example, twofold striking in acupuncture that aid in overcoming the limitations and resistances in integrating and applicability of these experiences and trials into the pre-existing biomedical models. Furthermore, TCM has also been utilized from ancient times to treat heart diseases in Asia, particularly in China, and is now used by people in many other areas. Cardiovascular disease (CVD) is mainly developed by oxidative stress. Hence antioxidants can be beneficial in treating this particular disease. TCM has a wide variety of antioxidant components.Conclusion: The current review article summarizes the underlying therapeutic property of TCM and its mechanism. It also overviews the evidence of the mechanism of TCM action in CVD prevention by controlling oxidative stress and its signaling pathway.

Objective: To investigate the relationship between heart failure (HF) and gut microbiota-mediated energy metabolism, and to explore the role of Shenfu Injection in this process.Materials and methods: In this study, Adriamycin-induced chronic heart failure (CHF) rat model was used and randomly divided into the blank control group (Normal, n = 9), HF control group (Model, n = 12), Shenfu Injection treatment group (SFI, n = 9), and positive drug control group (TMZ, n = 9). The changes in gut microbiota structure were analyzed by 16S rRNA high-throughput sequencing, the content of short-chain fatty acids (SCFAs) was detected by targeted metabolomics technology, and cardiac function and energy metabolism-related indicators were evaluated.Results: Myocardial energy metabolism in HF rats was disordered, characterized by reduced fatty acid oxidation, enhanced anaerobic glycolysis of glucose, mitochondrial damage, and decreased ATP content; The gut microbiota of HF rats was imbalanced, with a reduction in beneficial bacteria, an increase in conditional pathogenic bacteria, and impaired intestinal barrier function; Both Shenfu Injection and trimetazidine improved myocardial energy metabolism and cardiac function, but Shenfu Injection was more significant in regulating gut microbiota and improving intestinal health; The production of SCFAs from the gut microbiota of HF rats increased, which may be closely related to myocardial energy metabolism; SCFAs-producing bacteria Akkermansia and Blautia played a key role in the development of HF, and their abundance was positively correlated with SCFAs content.Conclusion: Shenfu Injection in treating HF may improve myocardial energy metabolism and intestinal health by regulating gut microbiota, especially the abundance of SCFAs-producing bacteria Akkermansia and Blautia, thereby exerting therapeutic effects. This provides theoretical support for treatment strategies based on gut microbiota.

Background: Sini Decoction (SND), a classic Chinese medicine prescription, has been proved to have a good effect on heart failure (HF), whereas its underlying mechanism is still unclear. In order to explore the therapeutic mechanism of SND, we combined with 16S rRNA gene sequencing to analyze the composition of gut microflora in rats with HF. Material and methods: Twenty Sprague–Dawley (SD) rats were divided into four groups (n = 5): normal group, model group, SND treatment group (SNT group), and metoprolol (Met) treatment group (Meto group). All the rats except the normal group were intraperitoneally injected with doxorubicin (concentration 2 mg/mL, dose 0.15 mL/100 g) once a week to induce HF. After successfully modeling, SND and Met were gavaged to rats, respectively. After the treatment period, blood was collected for hematological analyses, myocardial tissue and colon tissues were collected for Hematoxylin–Eosin (H&E) staining, and mucosal scrapings were collected for Illumina Miseq high-throughput sequencing. Results: Echocardiographic results suggested that both left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) in Model rats decreased compared with normal rats. The results of H&E staining showed that compared with the model group, the structures of myocardial tissue and colon tissue in the SNT group and Meto group showed a recovery trend. Alpha results showed that the model group had higher species diversity and richness compared with the normal group. After treatment, the richness and diversity of intestinal bacteria in the SNT group were significantly restored, and Met also showed the effect of adjusting bacterial diversity, but its effect on bacterial richness was not ideal. At the Family level, we found that the number of several bacteria associated with HF in the model group increased significantly. Excitingly, SND and Met had shown positive effects in restoring these HF-associated bacteria. Similarly, the results of Linear discriminant analysis (LDA) showed that both SND and Met could reduce the accumulation of bacteria in the model group caused by HF. Conclusion: Collectively, SND can improve HF by regulating the intestinal flora. This will provide new ideas for the clinical treatment of patients with HF.