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Volume 32 ， Issue 6 ， 2026
Perspective
- Abstract：Objective:To evaluate the clinical effect and safety of Xinfuli Granules (心复力颗粒, XFLG) in improving patients with heart failure (HF) of qi deficiency and blood stasis syndrome.Methods:In this single-center randomized controlled trial, HF patients were randomized (1:1) to either the XFLG group (178 cases) or the control group (178 cases). Patients in the control group received standard HF therapy. In addition, patients in the XFLG group were administered XFLG (10 g, 3 times daily) for 12 weeks. The primary outcomes observed were the composite of all-cause mortality and HF-related hospitalization; and secondary outcomes included changes in left ventricular ejection fraction (LVEF), N-terminal pro-brain natriuretic peptide (NT-pro BNP), New York Heart Association (NYHA) functional class, Minnesota Living with Heart Failure Questionnaire (MLHFQ) score, Chinese medicine (CM) syndrome score, Patient Health Questionnaire-9 (PHQ-9), and Generalized Anxiety Disorder-7 (GAD-7) scores.Results:After 12 weeks, the XFLG group demonstrated a significantly lower incidence of the primary endpoint compared to the control group (hazard ratio, 0.566; 95% confidence interval: 0.325–0.988; P<0.05). Besides, the XFLG group showed greater improvements in LVEF and NT-pro BNP reduction (P<0.05 or P<0.01). Compared with the control group, the total effective rate of NYHA functional class and CM syndrome was significantly higher; the MLHFQ, PHQ-9, and GAD-7 scores were significantly lower in the XFLG group (P<0.05 or P<0.01).Conclusions:XFLG combined with standard HF therapy significantly reduced the risk of all-cause mortality and HF-related hospitalization composite events, improved cardiac function, and quality of life, alleviated depressive and anxiety states in HF patients, with a favorable safety profile. These results support XFLG as a promising adjunctive treatment for HF with qi deficiency and blood stasis. (Registration No. ChiCTR2100049197)Keywords：Xinfuli Granules;Chinese medicine;heart failure;effect;safety;randomized controlled trial47|6|0Updated：2026-08-04
- Abstract：Objective:To clarify the mechanism by which Qishen Yiqi Dripping Pill (QSYQ) inhibits oxidative stress injury in myocardial infarction (MI), with a focus on verifying whether its effect is mediated through the histone deacetylase 3 (HDAC3)/nuclear factor erythroid 2-related factor 2 (Nrf2)/paired-like homeodomain transcription factor 2 (PITX2) pathway and ultimately determining its active ingredient.Methods:The mice were divided into 6 groups using simple randomization, with 10 mice in each group: the sham group, the model group, the QSYQ-L (19.5 mg/kg), QSYQ-M (39 mg/kg), and QSYQ-H (78 mg/kg) groups, and the metoprolol (19.5 mg/kg) group. A mouse model of MI was established by permanent ligation of the left anterior descending coronary artery. The experimental groups (QSYQ and metoprolol) received daily gavage of the corresponding agents for 7 days following surgery. Cardiac function was assessed longitudinally using echocardiography, electrocardiogram, and laser speckle flowmetry. Myocardial injury was evaluated through hematoxylin and eosin staining, infarct size and area-at-risk were determined using triphenyl tetrazolium chloride and evans blue dual staining, and cardiac troponin I (cTnI), creatine kinase myocardial band (CK-MB), and lipid peroxidation (LPO) were analyzed via enzyme-linked immunosorbent assay. The chemical constituents of QSYQ and their metabolites were profiled using high-performance liquid chromatography-quadrupole-time-of-flight tandem mass spectrometry, and their potential targets were predicted via network pharmacology. Key protein interactions and localizations were confirmed by co-immunoprecipitation and immunofluorescence, respectively. Target engagement was further validated by molecular docking and in vitro oxygen-glucose deprivation/reoxygenation models in H9c2 cells, using cellular thermal shift assay (CETSA) and drug affinity responsive target stability (DARTS) assays.Results:QSYQ administration demonstrated significant cardioprotective effects, markedly reducing myocardial infarct size and attenuating pathological tissue damage. Concurrently, it improved cardiac functional parameters, notably ejection fraction and fractional shortening, while enhancing myocardial perfusion efficiency (P<0.01). Network pharmacology analysis suggests that oxidative stress modulation is a primary therapeutic mechanism. At the molecular level, QSYQ effectively suppressed HDAC3 expression while activating the Nrf2/PITX2 antioxidant pathway. Protein interaction validation through co-immunoprecipitation and structural analysis confirmed the formation of an HDAC3-Nrf2-PITX2 regulatory complex. Crucially, cryptotanshinone, a core bioactive constituent of QSYQ, exhibited high-affinity binding to HDAC3 (P<0.01), which was validated by CETSA and DARTS experiments.Conclusions:QSYQ effectively ameliorates MI injury, at least in part, by inhibiting HDAC3, which consequently activates the Nrf2/PITX2 signaling pathway and suppresses oxidative stress damage. Mechanistically, cryptotanshinone is identified as the critical molecular entity directly targeting HDAC3 to mediate this cardioprotective effect.Keywords：Qishen Yiqi Dripping Pills;Chinese medicine;oxidative stress;histone deacetylase 3;nuclear factor erythroid 2-related factor 2;paired-like homeodomain transcription factor 234|1|0Updated：2026-08-04
- Abstract：Objective:To investigate the underlying mechanism of Ling-Gui-Zhu-Gan Decoction (LGZGD) in reducing hyperinflammatory responses to provide cardioprotective effects.Methods:The main chemical components of LGZGD were identified using ultra-high performance liquid chromatography. In vivo, the rats were randomly divided into 4 groups using simple randomization: the sham group, the model group, the LGZGD (4.2 g/kg) group, and captopril (4.375 mg/kg) group, 6 in each group. A rat model of ventricular remodeling (VR) after acute myocardial infarction (AMI) was established by ligation of the left anterior descending coronary artery. After 4 weeks of treatment, cardiac function was evaluated by echocardiography, and histopathological changes were examined using HE and Masson stainings. Serum levels of cardiac enzymes and oxidative stress markers were measured with microplate assays. Reactive oxygen species (ROS) were visualized by fluorescence staining, while protein and mRNA levels were analyzed by Western blot and RT-qPCR. Levels of proinflammatory cytokines and trimethylamine N-oxide (TMAO) were quantified through ELISA. In vitro, H9c2 cells were exposed to 400 μmol/L TMAO, and oxidative stress markers were measured by microplate assay. ROS levels were visualized using fluorescence staining, and gene and protein expression were analyzed by RT-PCR and Western blot. Proinflammatory cytokines and TMAO levels were further evaluated by ELISA.Results:LGZGD was found to contain liquiritin, isoliquiritin, coumarin, liquiritigenin, cinnamic acid, kaempferol, cinnamaldehyde, glycyrrhizic acid, and atractylenolide Ⅲ. In vivo, LGZGD improved cardiac function, reduced myocardial pathology, lowered serum cardiac enzymes and TMAO, decreased oxidative stress, regulated the expression of genes and proteins within the ROS/thioredoxin-interacting protein (TXNIP)/NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) pathway, and suppressed the secretion of IL-1β and IL-18 (P<0.01). In vitro analysis showed that LGZGD significantly decreased markers of myocardial injury, alleviated oxidative stress, and inhibited the secretion of IL-1β and IL-18 in TMAO-stimulated H9c2 cells (P<0.01).Conclusion:LGZGD ameliorates TMAO-induced myocardial injury by modulating the ROS/TXNIP/NLRP3 signaling pathway.Keywords：Ling-Gui-Zhu-Gan Decoction;acute myocardial infarction;ROS/TXNIP/NLRP3 signaling pathway;ventricular remodeling;Chinese medicine42|1|0Updated：2026-08-04
- Abstract：Objective:To evaluate the protective effect of Qingxin Jieyu Granule (QXJYG) on myocardial ischemia/reperfusion (I/R) injury by inhibiting cardiomyocyte pyroptosis via circulating exosomes.Methods:Seventy-five Wistar rats were randomly assigned to 5 groups using a random number table (15 rats per group): sham-operated, model, low-, medium-, and high-dose QXJYG groups (L-QXJYG, M-QXJYG, and H-QXJYG). The L-QXJYG, M-QXJYG, and H-QXJYG groups were administered QXJYG at doses of 2.87, 5.73, and 11.46 g/kg, respectively, twice daily via intragastric administration for 28 consecutive days. The model group received an equal volume of normal saline following the same schedule. Following 28 days of administration, myocardial I/R injury was induced 1 h after the final dose. Myocardial infarction size, histopathological changes, and expression of key pyroptosis-related molecules in cardiac tissue were assessed. An oxygen-glucose deprivation/reperfusion model using H9c2 cardiomyocytes was established to investigate the cardioprotective mechanism of QXJYG, emphasizing the role of circulating exosomes in modulating pyroptosis through evaluations of cell viability, pyroptotic morphology, and associated molecular expression.Results:In vivo experiments demonstrated that QXJYG significantly reduced myocardial infarction size, improved histopathological morphology, suppressed the inflammatory response, and inhibited myocardial pyroptosis (all P<0.05). In vitro, QXJYG was shown to enhance H9c2 cardiomyocyte viability, attenuate inflammation, and suppress pyroptosis by inhibiting the NLRP3/Caspase-1/GSDMD pathway via circulating exosomes (all P<0.05).Conclusion:QXJYG alleviates myocardial I/R injury by inhibiting cardiomyocyte pyroptosis through circulating exosomes, potentially via modulation of the NLRP3/ Caspase-1/GSDMD pathway.Keywords：myocardial ischemia/reperfusion injury;pyroptosis;exosome;Qingxin Jieyu Granule;NLRP3/Caspase-1/GSDMD32|2|0Updated：2026-08-04
- Abstract：Objective:To evaluate active components of Tianma Gouteng Yin (TMGTY) and its mechanisms in treating hypertension-associated vascular cognitive impairment (VCI).Methods:Network pharmacology and molecular docking were used to identify major active ingredients and potential targets of TMGTY in treating hypertension-associated VCI. An in vivo model was established using spontaneously hypertensive rats subjected to unilateral common carotid artery occlusion and a high-salt diet. Rats were randomly divided into 7 groups by a simple randomization method: control, model, sham, low-, medium-, and high-dose TMGTY, and nimodipine groups (n=6). After 28 days of oral administration, blood pressure, behavioral studies, pathological staining, and molecular mechanisms were assessed via tail artery blood pressure monitoring, the morris water maze test, HE staining, immunofluorescence staining, ELISA, and Western blotting.Results:Network analysis identified quercetin, kaempferol, beta-sitosterol, and stigmasterol as key ingredients. Pathway enrichment analysis identified the NF-κB signaling pathway as a key pathway through which TMGTY antagonizes the development of hypertension combined with VCI. Core targets included glyceraldehyde-3-phosphate dehydrogenase (GAPDH), interleukin 6 (IL-6), insulin (INS), tumor necrosis factor (TNF), and tumor protein p53 (TP53), and molecular docking confirmed stable binding to TNF and INS. In vivo experiments demonstrated that TMGTY significantly enhanced cognitive performance and reduced blood pressure. Furthermore, it lowered the levels of pro-inflammatory factors (IL-1β, IL-6, TNF-α, Ang-Ⅱ) and malondialdehyde (MDA), while elevating superoxide dismutase (SOD) expression (P<0.05 or P<0.01). Immunofluorescence staining further revealed that TMGTY treatment reduced the number of Iba1- and CD16-labeled microglia in the hippocampal CA1 region, thereby alleviating neuroinflammation. Additionally, TMGTY inhibited the expression levels of p-NF-κB p65/NF-κB p65 proteins and attenuated neuroinflammation.Conclusion:TMGTY exerts multi-component, multi-target effects on hypertension-associated VCI, mitigating neuroinflammation and oxidative stress via modulation of NF-κB signaling pathway.Keywords：Tianma Gouteng Yin;Chinese medicine;hypertension;vascular cognitive impairment;network pharmacology;molecular docking;experimental validation;neuroinflammation26|0|0Updated：2026-08-04
- Abstract：Objective:To determine whether berberine (BBR) attenuates angiotensin Ⅱ (AngⅡ)-induced endothelial dysfunction by antagonizing AT1R and modulating the phosphodiesterase 4b (PDE4b)-related signaling pathway.Methods:Primary aortic endothelial cells were isolated and cultured from control and AngⅡ-induced hypertensive mice. Human umbilical vein endothelial cells (HUVECs), mouse aortic endothelial cells (MAECs) and ex vivo mouse aortae were treated with AngⅡ (1 μmol/L), in the presence or absence of BBR, or the PDE4b inhibitor piclamilast. Quantitative real-time PCR (qPCR), Western blot, immunofluorescence, and microplate assays were employed to assess mRNA and protein expressions of PDE4b, AngⅡ type 1 receptor (AT1R), endothelial nitric oxide synthase (eNOS) and protein kinase B (PKB, as known as Akt) phosphorylation, and intra- and extracellular nitric oxide (NO) levels. Vascular ring assays were conducted to evaluate the endothelium-dependent relaxation (EDR) of isolated mouse aortae. In addition, molecular docking and cellular thermal shift assays were performed to investigate the interaction between BBR and the AT1R, with comparison to valsartan.Results:AngⅡ reduced eNOS phosphorylation and NO levels in HUVECs and impaired EDR in isolated mouse aortae (P<0.01), which were reversed by BBR co-treatment (P<0.05). BBR showed a binding free energy of –8.6 kCal/mol with AT1R and significantly enhanced AT1R thermal stability in 60, 65, 75 ℃, exhibiting similar effects as valsartan in 60, 65, 75 ℃ (all P<0.05). AngⅡ upregulated PDE4b mRNA and protein levels in HUVECs and MAECs, while BBR reversed this effect in HUVECs (P<0.05 or P<0.01). AngⅡ also suppressed Akt phosphorylation in HUVECs, which was restored by BBR, like the effect of piclamilast (P<0.05 or P<0.01).Conclusions:BBR ameliorates AngⅡ-induced endothelial dysfunction primarily by antagonizing AT1R, suppressing PDE4b expression and restoring Akt/eNOS signaling. These findings provide mechanistic insights into BBR's endothelial-protective actions and highlight its therapeutic potential in treating hypertension-related vascular complications.Keywords：angiotensin Ⅱ type 1 receptor;berberine;endothelial dysfunction;hypertension;phosphodiesterase 4b48|1|0Updated：2026-08-04
Original Article
- Abstract：Objective:To evaluate the clinical efficacy of Taoren Honghua Jian Granule (THJ) in stable coronary artery disease (SCAD) patients with syndrome of qi stagnation and blood stasis, and to investigate its effect on the expression of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in peripheral blood mononuclear cells (PBMCs).Methods:In this multicenter, double-blind, randomized controlled trial, 80 eligible SCAD patients from 3 Shanghai hospitals were randomly assigned to receive either the THJ (18.3 g, twice daily, orally) or a matched placebo for 4 weeks 40 in each group, followed by a 4-week follow-up. Chinese medicine (CM) Syndrome Scores and Seattle Angina Questionnaire (SAQ) assessments were conducted pre- and post-intervention. Quantitative PCR was used to analyze mRNA levels of NLRP3 inflammasome components [NLRP3, apoptosis-associated speck-like protein (ASC), caspase-1, interleukin (IL)-1β, and IL-18] in PBMCs, while ELISA was used to detect plasma inflammatory cytokines [IL-10, IL-1β, IL-2, IL-6, IL-8, IL-18, tumor necrosis factor (TNF-α), and high-sensitive C-reactive protein (hs-CRP)].Results:After 4 weeks of treatment, the overall treatment efficacy was higher in the treatment group than in the placebo group; the CM syndrome scores of the two groups were significantly lower after treatment, and the THJ group was considerably lower than the placebo group (P<0.05, P<0.01). The THJ group had significantly higher scores for 5 SAQ dimensions than the placebo group (P<0.01). Both mRNA expression of NLRP3 inflammasome components (NLRP3, ASC, caspase-1, IL-1β, IL-18) decreased in PBMCs (P<0.01). In addition, plasma levels of IL-2, IL-8, IL-18, and TNF-α significantly decreased in THJ group compared with the placebo group after treatment (P<0.05, P<0.01).Conclusions:THJ alleviates angina symptoms and improves quality of life in SCAD patients, potentially through NLRP3 inflammasome inhibition and subsequent attenuation of pro-inflammatory cytokine release. These findings position THJ as a promising adjunct therapy for inflammation-driven coronary atherosclerosis. (Registration No. ChiCTR1900021772)Keywords：Taoren Honghua Jian;stable coronary artery disease;qi stagnation and blood stasis;peripheral blood mononuclear cells;NOD-like receptor family pyrin domain containing 3;randomized controlled trial20|0|0Updated：2026-08-04
Clinical Experience
- Abstract：Objective:To determine risk factors associated with the severity of Xuebijing Injection (XBJ)-related adverse events (AEs).Methods:Totally 16,031 cases reported XBJ-related AEs were retrospectively analyzed from China national spontaneous reporting system (SRS) from its inception to 2022. Factors including age, gender, weight, ethnicity, family history, and allergic history were examined. Univariate and multivariate logistic regression analyses were performed, followed by propensity score matching (PSM) to control for confounding factors.Results:A total of 11,131 XBJ-related AE cases were identified after excluding duplicates and incomplete reports, including 9,771 general and 1,360 serious AEs. Serious AEs were mainly distributed among respiratory, thoracic and mediastinal disorders (27.00%). Univariate analysis identified gender, age, history of allergies, and previous AE history, XBJ-other β-lactam antimicrobials combination and XBJ-aminoglycoside antimicrobials combination were potential risk factors of serious AEs (P<0.05 or P<0.01). Multivariate analysis identified age, gender, history of allergies, and XBJ-other β-lactam antimicrobials combination as significant risk factors of AE severity (P<0.05 or P<0.01). PSM further confirmed that patients receiving XBJ combined with β-lactam antibiotics had a significantly higher risk of severe AEs (odds ratio=1.913, P=0.019).Conclusions:The risk factors influencing the severity of XBJ include age, gender, history of allergies, and its combination with other β-lactam antimicrobials. Among them, PSM further proved that the XBJ-other β-lactam antimicrobials combination needs to be given attention in clinical practice.Keywords：Xuebijing Injection;risk factor;adverse event;safety;other β-lactam antimicrobials;propensity score-matched analysis16|0|0Updated：2026-08-04
Herb-Drug Interaction
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