Cardiotoxicity of doxorubicin (DOX) has gained increasing attention in clinical application. Fuzhengkangfu (FZK) decoction, a traditional Chinese herbal formula of replenishing Qi strengthening spleen, has been used to treat various cardiovascular diseases. However, the chemical composition, the protective effects of FZK, and the underlying mechanisms are yet unclear. In this study, an high-performance liquid chromatography−mass spectrometry (HPLC−MS) analytical method was established for the structural identification of constituents in FZK extracts. Target prediction and enrichment analysis of the identified ingredients were performed. The cell viability was measured via (3-[4,5dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) (MTT) assay. The protective effects of FZK on cell survival, mitochondrial membrane potential, intracellular calcium homeostasis, and cell apoptosis were detected. The level of relevant proteins was measured by Western blot. The effect of FZK on the antitumor activity of DOX was evaluated in HeLa cells. A total of 42 major chemical constituents were identified in FZK extracts by HPLC−MS. A comprehensive target prediction of these constituents retrieved 46 pathways, of which several key pathways were related to mitochondrial dysfunction, including metabolic pathways and calcium signaling pathways. Furthermore, FZK ameliorated DOX-induced H9C2 cell apoptosis and increased the Bcl-2/Bax ratio. Also, it moderated the loss of mitochondrial membrane potential and reduced the intracellular calcium overload, which are the major targets of DOX-induced injury. These results confirmed that FZK ameliorates DOX-induced cardiotoxicity via antiapoptotic and mitochondrial protection but does not affect the antitumor activity of DOX.

Myocardial hypertrophy plays an essential role in the structural remodeling of the heart and the progression to heart failure (HF). There is an urgent need to understand the mechanisms underlying cardiac hypertrophy and to develop treatments for early intervention. Dangshen Erling decoction (DSELD) is a clinically used formula in Chinese medicine for treating coronary heart disease in patients with HF. However, the mechanism by which DSELD produces its cardioprotective effects remains largely unknown. This study explored the effects of DSELD on myocardial hypotrophy both in vitro and in vivo. In vitro studies indicated that DSELD significantly (p < 0.05) reduced the cross-sectional area of the myocardium and reduced elevated lactate dehydrogenase (LDH), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 levels in the induced H9C2 cell model to study inflammation. In vivo experiments revealed that DSELD restores cardiac function and significantly reduces myocardial fibrosis in isoproterenol (ISO)-induced HF mouse model (p < 0.05). In addition, DSELD downregulated the expression of several inflammatory cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte CSF (G-CSF), IL-1α, IL-1β, IL-3, IL-5, IL-7, IL-12, IL-13, and TNF-α in HF (p < 0.05). Further analysis of the cardiac tissue demonstrated that DSELD produces its anti-inflammatory effects via the Toll-like receptor (TLR)4 signaling pathway. The expression of TLR4 downstream proteins such as matrix metalloproteinase-9 (MMP9) and myeloid differentiation factor-88 (MyD88) was among the regulated targets. In conclusion, these observations suggest that DSELD exerts antihypertrophic effects by alleviating the inflammatory injury via the TLR4 signaling pathway in HF and thus holds promising therapeutic potentials.

Background Radiofrequency ablation in patients with atrial fibrillation (AF) is effective but hampered by pulmonary veins reconnection because of insufficient lesions. High power shorter duration ablation (HPSD) was seen to increase efficacy and safety. This analysis aimed to evaluate the clinical benefits of HPSD in patients with AF. Methods The Medline, PubMed, Embase, and the Cochrane Library databases were searched for studies comparing HPSD and Low power longer duration (LPLD) ablation. Results A total of seven trials with 2023 patients were included in the analysis. Pooled analyses demonstrated that HPSD showed a benefit of first‐pass pulmonary vein isolation (PVI) [risk ratio (RR): 1.27; 95% confidence interval (CI): 1.18‐1.37, P < .001]. HPSD could reduce recurrence of atrial arrhythmias (RR: 0.70; 95% CI: 0.50‐0.98, P = .04). Additionally, HPSD was more beneficial in terms of procedural time [Weighted Mean Difference, (WMD): −44.62; 95% CI, −63.00 to −26.23, P < .001], ablation time (WMD: −21.25; 95% CI: −25.36 to −17.13, P < .001), and fluoroscopy time (WMD: −4.13; 95% CI: −7.52 to −0.74, P < .001). Moreover, major complications and esophageal thermal injury (ETI) were similar between two groups (RR: 0.75; 95% CI: 0.44‐1.30, P = .31) and (RR: 0.64; 95% CI: 0.17‐2.39, P = .51). Conclusion HPSD was safe and efficient for treating AF with clear advantages of procedural features, it also showed benefits of higher first‐pass PVI and reducing recurrence of atrial arrhythmias compared with the LPLD. Moreover, major complications and ETI were similar between two groups.

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