Cardiovascular diseases (CVD) are the leading cause of death in the world. However, due to the limited effectiveness and potential adverse effects of current treatments, the long-term prognosis of CVD patients is still discouraging. In recent years, several studies have found that berberine (BBR) has broad application prospects in the prevention and treatment of CVD. Due to its effectiveness and safety for gastroenteritis and diarrhea caused by bacterial infections, BBR has been widely used in China and other Asian countries since the middle of the last century. The development of pharmacology also provides evidence for the multi-targets of BBR in treating CVD. Researches on CVD, such as arrhythmia, atherosclerosis, dyslipidemia, hypertension, ischemic heart disease, myocarditis and cardiomyopathy, heart failure, etc., revealed the cardiovascular protective mechanisms of BBR. This review systematically summarizes the pharmacological research progress of BBR in the treatment of CVD in recent years, confirming that BBR is a promising therapeutic option for CVD.

Percutaneous coronary intervention (PCI) is one of the most effective reperfusion strategies for acute myocardial infarction (AMI) despite myocardial ischemia/reperfusion (I/R) injury, causing one of the causes of most cardiomyocyte injuries and deaths. The pathological processes of myocardial I/R injury include apoptosis, autophagy, and irreversible cell death caused by calcium overload, oxidative stress, and inflammation. Eventually, myocardial I/R injury causes a spike of further cardiomyocyte injury that contributes to final infarct size (IS) and bound with hospitalization of heart failure as well as all-cause mortality within the following 12 months. Therefore, the addition of adjuvant intervention to improve myocardial salvage and cardiac function calls for further investigation. Phytochemicals are non-nutritive bioactive secondary compounds abundantly found in Chinese herbal medicine. Great effort has been put into phytochemicals because they are often in line with the expectations to improve myocardial I/R injury without compromising the clinical efficacy or to even produce synergy. We summarized the previous efforts, briefly outlined the mechanism of myocardial I/R injury, and focused on exploring the cardioprotective effects and potential mechanisms of all phytochemical types that have been investigated under myocardial I/R injury. Phytochemicals deserve to be utilized as promising therapeutic candidates for further development and research on combating myocardial I/R injury. Nevertheless, more studies are needed to provide a better understanding of the mechanism of myocardial I/R injury treatment using phytochemicals and possible side effects associated with this approach.

Acute myocardial infarction (AMI) remains a major cause of cardiovascular mortality worldwide. The inflammatory immune response after AMI plays a dual role: it facilitates the clearance of necrotic tissue but can also exacerbate injury, significantly affecting patient outcomes. Conventional anti-inflammatory therapies are often limited by systemic toxicity and insufficient targeting, highlighting the need for more refined approaches. This review systematically examines the interplay between AMI's key inflammatory immune mechanisms—including neutrophil N1/N2 phenotypic switching, macrophage M1/M2 polarization, and Treg/Th17 lymphocyte balance—and advancements in nanoparticle-based drug delivery systems (NP-NDDSs) designed to target these mechanisms. NP-NDDSs utilize properties such as size-dependent accumulation, surface functionalization, and stimuli-responsive release (e.g., to pH, ROS, or enzymes) to improve spatiotemporal control over drug delivery. Various nanocarriers, including organic (e.g., liposomes, polymers), inorganic (e.g., gold, silica), and biomimetic (e.g., cell membrane- or exosome-based) systems, have shown potential in influencing neutrophil extracellular trap formation, macrophage phenotype, and lymphocyte activity. These developments suggest that NP-NDDSs could help control excessive inflammation, support tissue repair, and limit adverse remodeling. Nevertheless, challenges in targeting precision, manufacturing scalability, and long-term biosafety remain to be addressed. By summarizing current advances and identifying future needs, this review aims to provide a basis for developing targeted therapies against immune-mediated injury in AMI.

Background: Hydroxysafflor yellow A (HSYA) possesses a variety of pharmacological activities which has been demonstrated to be effective against ischemic heart disease (IHD). This study aimed to comprehensively examine the efficacy and summarize the potential mechanisms of HSYA against IHD in animal models.Methods: We conducted electronic searches for preclinical studies on PubMed, Embase, Web of Science, Cochrane Library, CNKI, SinoMed, Wanfang, and Chinese VIP databases from inception to 31 January 2024. The CAMARADES checklist was chosen to assess the quality of evidence. STATA 14.0 software was utilized to analyze the data. The underlying mechanisms were categorized and summarized.Results: Twenty-eight studies involving 686 rodents were included and the mean score of methodology quality was 5.04 (range from 4 to 7). Meta-analysis observed that HSYA could decrease myocardial infarction size (SMD: −2.82, 95%CI: −3.56 to −2.08, p < 0.001) and reduce the levels of biomarkers of myocardial injury including cTnI (SMD: −3.82, 95%CI: −5.20 to −2.44, p < 0.001) and CK-MB (SMD: −2.74, 95%CI: −3.58 to −1.91, p < 0.001). HSYA displayed an improvement in cardiac function indicators including LVEF, LVSP, +dp/dt max and -dp/dt max. Furthermore, HSYA was able to reduce the levels of MDA, TNF-α and IL-6, while increasing SOD and NO levels. Mechanistically, the protective effect of HSYA in alleviating myocardial injury after ischemia may be associated with NLRP3 inflammasome, Bcl-2, Bax, caspase-3, eNOS proteins, and TLR/NF-κB, Nrf2/HO-1, JAK/STAT, PI3K/Akt, AMPK/mTOR, VEGFA pathways.Conclusion: This study demonstrates that HSYA exerts cardioprotective effects in decreasing infarct size, reducing myocardial enzymes and improving cardiac function, which may be mediated by anti-inflammatory, antioxidant, anti-apoptotic, regulation of autophagy, improvement of microcirculation and promotion of angiogenesis. However, the absence of safety assessment, lack of animal models of co-morbidities, and inconsistency between timing of administration and clinical practice are limitations of preclinical studies.Systematic Review Registration: clinicaltrials.gov, Identifier, CRD42023460790.

Background: The herbal pairing of Dangshen (DS) [Codonopsis pilosula (Franch.) Nannf.] and Huangqi (HQ) [Astragalus membranaceus (Fisch.) Bge.] (DHP) is a traditional Chinese herbal medicine that is frequently used to treat chronic heart failure (CHF) in China. However, the pharmacological mechanism of DHP has not been fully elucidated. This is the first study aimed to reveal the active mechanism of DHP in the treatment of CHF by using network pharmacology methods. Methods: The active ingredients of DHP were obtained from the TCMSP database, and the potential targets of DHP were predicted using the SwissTargetPrediction database. CHF-related targets were searched by the DisGeNET and GeneCards databases. The common targets between the disease and herbs were obtained using a Venn diagram. The STRING database was utilized to obtain the protein-protein interaction data. Next, we used Cytoscape 3.7.2 software to construct and analyze the herb-ingredient-potential targets-disease network. Topology analysis was used to identify the key ingredients and hub genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the Metascape database to reveal the mechanism. Furthermore, molecular docking simulation was performed using AutoDock Vina software to assess the affinity of the key ingredients and hub genes. Results: Five key ingredients and six hub genes were screened. The six hub genes were closely related to PI3K /AKT or ERK1/2 pathways. The KEGG pathways mainly involved the TNF signaling pathway, calcium signaling pathway, and cancer-related pathways. The GO enrichment analysis results showed that DHP might act on biological processes including positive regulation of kinase activity and cellular response to nitrogen compound via the three above-mentioned pathways in the treatment of CHF. Finally, the molecular docking results showed that the five key ingredients exhibited strong affinities to the six hub genes. Conclusions: This study revealed the molecular mechanism that the flavonoids in DHP may alleviate endothelial dysfunction and cardiac hypertrophy via regulation of the TNF pathway and its downstream PI3K/Akt or ERK1/2 signaling pathways, or improve excitation-contraction coupling by regulating calcium signaling pathway, thereby improving CHF. These results provide insights for further experimentation on its pharmacological effects.

Backgroud: Xuezhitong (XZT) is an extract of Allium macrostemon Bunge that has lipid-lowering properties. Objective: To evaluate the effects of XZT on lipids in subjects with hypertriglyceridemia (HTG) without severe dyslipidaemia. Methods: A total of 358 subjects with HTG were enrolled and randomly assigned to receive XZT (2700 mg daily), xuezhikang (XZK) (1200 mg daily) or placebo. The primary endpoint was the reduction or percent reduction in the TG level over 12 weeks of treatment. Results: At the 12-week follow-up, a reduction in the TG level from baseline was observed in both groups, but the XZT and XZK groups demonstrated a significantly greater reduction than the placebo group (30.77%, 24.02% vs 11.59%, P < 0.0167); 70.54% of subjects in the XZT group and 62.30% of subjects in the XZK group demonstrated reductions in TG levels of at least 20%, compared with 41.67% of the subjects in the placebo group (P < 0.0167). Treatment with XZT capsules also demonstrated superior performance compared with the placebo with respect to the control of lipids (17.97% vs 5.00%), total cholesterol (TC) (14.18% vs 3.89%), low-density lipoprotein cholesterol (LDL-C) (17.98% vs 2.95%), and high-density lipoprotein cholesterol (HDL-C) (21.47% vs 2.16%). Daily use of XZT for 12 weeks resulted in statistically significant (65.22% vs 38.30%, 25.00%; P < 0.0167) and clinically meaningful increases in HDL-C levels by ≥4 mg/dl compared with XZK and placebo. XZT was safe and well tolerated; the safety and tolerability profiles were similar across treatment groups. No subject experienced myopathy or markedly elevated liver transaminases or creatine kinase. Conclusions: XZT significantly reduced TG levels and was well tolerated. Longer-term studies in more diverse patient populations are needed to corroborate these findings. Clinical Trial Registration: www.chictr.org.cn Identifier: ChiCTR1900025854.