Cardioprotective Effects Research Articles

Hydrogen Sulfide Attenuates Sepsis-Induced Cardiac Dysfunction in Infant Rats by Inhibiting the Expression of Cold-Inducible RNA-Binding Protein.

Sepsis-induced cardiac dysfunction is one of the most common complications of sepsis. It is also a major cause of death in pediatric intensive care units. The underlying mechanism of sepsis-induced cardiac dysfunction remains elusive. CIRP is a damage-associated molecular pattern that is upregulated during sepsis. H2S has been shown to play a protective role in sepsis-induced cardiac dysfunction in adult animals. This study aimed to determine whether H2S ameliorates the cardiac function in infant rats by inhibiting CIRP-mediated sepsis-induced cardiac dysfunction. Rat pups aged 17-18 days were subjected to CLP to induce sepsis. Six hours after CLP, hemodynamic results demonstrated that there was a significant decrease in ±dP/dtmax, LVEF and LVFS, indicating cardiac dysfunction. The plasma levels of myocardial injury markers such as CKMB, andCTnIwere significantly increased at 6 h after CLP. The inhibition of CIRP with C23 improved the cardiac function of the rats with CLP-induced sepsis, accompanied by a significant decrease in ERS activation. Moreover, treatment with4-PBA (an inhibitor of ERS) ameliorated myocardial injury and dysfunction, accompanied by a significant decrease in ERS activation. Sodium hydrosulfide, a H2S donor, ameliorated CLP-induced cardiac dysfunction and decreased CIRP levels and ERS. In contrast, the inhibition of endogenous H2S production by propargylglycine (aCSE inhibitor) aggravated CLP-induced cardiac dysfunction and increased CIRP levels. In conclusion, this study demonstrated that H2S exerted cardioprotective effects by inhibiting the CIRP/ERS pathway in infant rats with sepsis. These findings might indicate a novel target in the treatment of sepsis in infants.

Obesity and Adipose-Derived Extracellular Vesicles: Implications for Metabolic Regulation and Disease

Obesity, a global epidemic, is a major risk factor for chronic diseases such as type 2 diabetes, cardiovascular disorders, and metabolic syndrome. Adipose tissue, once viewed as a passive fat storage site, is now recognized as an active endocrine organ involved in metabolic regulation and inflammation. In obesity, adipose tissue dysfunction disrupts metabolic balance, leading to insulin resistance and increased production of adipose-derived extracellular vesicles (AdEVs). These vesicles play a key role in intercellular communication and contribute to metabolic dysregulation, affecting organs such as the heart, liver, and brain. AdEVs carry bioactive molecules, including microRNAs, which influence inflammation, insulin sensitivity, and tissue remodeling. In the cardiovascular system, AdEVs can promote atherosclerosis and vascular dysfunction, while those derived from brown adipose tissue offer cardioprotective effects. In type 2 diabetes, AdEVs exacerbate insulin resistance and contribute to complications such as diabetic cardiomyopathy and cognitive decline. Additionally, AdEVs are implicated in metabolic liver diseases, including fatty liver disease, by transferring inflammatory molecules and lipotoxic microRNAs to hepatocytes. These findings highlight the role of AdEVs in obesity-related metabolic disorders and their promise as therapeutic targets for related diseases.

Cardioprotective Effects of Green Tea and Honey on Albino Wistar Rats Exposed to Atrazine

Cardioprotective Effects of Green Tea and Honey on Albino Wistar Rats Exposed to Atrazine

Cardioprotective effects of a 'twincretin' drug tirzepatide in heart failure following myocardial infarction.

Cardioprotective effects of a 'twincretin' drug tirzepatide in heart failure following myocardial infarction.

Cellular signalling of melatonin and its role in metabolic disorders.

Melatonin released from the pineal gland plays an important role in maintaining the light/dark cycle. Melatonin exerts its effects on various organs through receptor and nonreceptor pathways. Recently, the role of melatonin in various metabolic disorders has been investigated. This review focuses on the molecular pathways associated with melatonin and its role in metabolic disorders. In humans, melatonin acts through two G protein-coupled receptors (MT1 and MT2). Melatonin modulates insulin release, such as elevated insulin levels in the evening compared to morning hours, exerts cardioprotective effects through the cGMP pathway and nitric oxide production in endothelial cells, and controls oxidative stress and apoptosis in myocardial tissue. Melatonin through MT2 receptors increases lipolysis and thermogenesis, which have a positive effect on weight reduction in obese individuals. Currently, most drugs that target melatonin receptors are primarily used to treat neurological disorders. A detailed investigation to explore the role of melatonin and its signalling pathway in peripheral organs is essential to develop therapeutic molecules for managing metabolic disorders.

Galium verum L. extract mitigates cardiovascular events in psoriasis rats.

Psoriasis has been considered a systemic immune-mediated disease that can affect function of the heart. However, certain herbal therapy approaches may nullify side effects of psoriasis on the heart. The aim of this study was to investigate the cardioprotective effects of Galium verum extract administration of the heart of psoriatic rats. The study included 24 Wistar albino male rats, divided into 4 groups: control (CTRL), G.verum (GV), psoriasis (PSORI), and psoriasis with G.verum (PSORI + GV). Seven-day topical application of 5% imiquimod cream was used for induction of psoriasis. After induction, animals were received 125mg/kg G.verum extract for 4weeks. Isolated hearts were perfused on the Langendorff apparatus and measured: dp/dt max/min, SLVP, DLVP, HR and coronary flow. The oxidative stress biomarkers: TBARS, NO2, O2- and H2O2 were measured in coronary venous effluent. Isolated hearts were fixed and stained with H/E and Picro-sirius red staining. Psoriasis decreased cardiac contractility and relaxation and increased SLVP and DLVP at all perfusion pressure. Treatment with G.verum in psoriasis rats improved contractility and relaxation of the heart and rise SLVP and DLVP. In PSORI + GV group, the decrease of oxidative stress biomarkers were observed in comparison to PSORI group. Diameter and cross-section area of cardiomyocytes were increased in PSORI and PSORI + GV groups compared to the control. Collagen content was increased in PSORI group by 283% and in PSORI + GV group by 188% compared to control. Treatment with G.verum extract exhibited a positive effect on cardiac function, morphometry and redox state of heart of psoriatic rats.

Cardioprotective Potential of Moringa Oleifera Leaf Extract Loaded Niosomes Nanoparticles - Against Doxorubicin Toxicity In Rats.

Doxorubicin (DOX) is one of the most potent anticancer drugs that has ubiquitous usage in oncology; however, its marked adverse effects, such as cardiotoxicity, are still a major clinical issue. Plant extracts have shown cardioprotective effects and reduced the risk of cardiovascular diseases. The current study is intended to explore the cardioprotective effect of ethanolic Moringa oleifera extracts (MOE) leaves loaded into niosomes (MOE-NIO) against DOXinduced cardiotoxicity in rats. MOE niosomes nanoparticles (NIO-NPs) were prepared and characterized by TEM. Seventy male Wistar rats were randomly divided into seven groups: control, NIO, DOX, DOX+MOE, DOX+MOE-NIO, MOE+DOX, and MOE-NIO+DOX. DOX (4 mg/kg, IP) was injected once per week for 4 weeks with daily administration of MOE or MOENIO (250 mg/kg, PO) for 4 weeks; in the sixth and seventh groups, MOE or MOE-NIO (250 mg/kg, PO) was administered one week before DOX injection. Various parameters were assessed in serum and cardiac tissue. Pre and co-treatment with MOE-NIO have mitigated the cardiotoxicity induced by DOX as indicated by serum aspartate aminotransferase (AST), creatine kinase - MB(CK-MB) and lactate dehydrogenase (LDH), cardiac Troponin 1(cTn1) and lipid profile. MOE-NIO also alleviated lipid peroxidation (MDA), nitrosative status (NO), and inflammatory markers levels; myeloperoxidase (MPO) and tumor necrosis factor-alpha (TNF-α) obtained in DOX-treated animals. Additionally, ameliorated effects have been recorded in glutathione content and superoxide dismutase activity. MOE-NIO effectively neutralized the DOXupregulated nuclear factor kappa B (NF-kB) and p38 mitogen-activated protein kinases (p38 MAPK), and DOX-downregulated nuclear factor-erythroid 2-related factor 2 (Nrf2) expressions in the heart. It is concluded that pre and co-treatment with MOE-NIO could protect the heart against DOX-induced cardiotoxicity by suppressing numerous pathways including oxidative stress, inflammation, and apoptosis and by the elevation of tissue antioxidant status. Thus, it may be reasonable to suggest that pre and co-treatment with MOE-NIO can provide a potential cardioprotective effect when doxorubicin is used in the management of carcinoma.

Sodium valproate reverses aortic hypercontractility in acute myocardial infarction in rabbits.

Sympathetic nervous system (SNS), endothelin 1 (ET-1) and angiotensin II (Ang II) are involved in the pathophysiology of acute myocardial infarction (AMI). Valproic acid (VPA) is under study for the treatment against AMI due to its beneficial cardiac effects. However, the vascular effects of VPA on the activation of the SNS, ET-1 and Ang II after AMI are not fully studied. In our study, we used aorta from New Zealand White rabbits without AMI, with AMI and AMI treated with VPA (500mg/kg/day). AMI was induced by occluding the left circumflex coronary artery for 1h, followed by reperfusion. After 5 weeks, we studied the ex vivo vascular reactivity in organ bath and measured protein expression by Western blot. Our findings indicated that AMI increased vasoconstriction to exogenous and endogenous NE and ET-1, which was reversed by VPA eliciting upregulation of α2-adrenergic and ETB receptors and downregulating ETA receptors. Although no changes in the vascular response to Ang II were observed in AMI or VPA-treated rabbits, an increase in Ang II type 2 receptor expression was found in VPA-treated rabbits. We conclude that VPA could be considered a vascular protector by modulating SNS, ET-1 and Ang II in the aorta, which together with its cardioprotective effect would make it a promising candidate for the treatment of AMI.

Evolution of myocardial steatosis in high cardiovascular risk T2DM patients treated by GLP1 receptor agonists: LICAS study.

We hypothesized that the reduction of intramyocardial fat content may be involved in the cardioprotective effect of glucagon-like peptide-1 receptor agonists (GLP1-RA) in patients with type 2 diabetes (T2D). Therefore, we aimed to evaluate the change in intramyocardial triglyceride content in T2D patients treated with GLP1-RA. This monocentric proof-of-concept cohort study included patients with unbalanced T2D prior to the introduction of GLP1-RA. Patients underwent cardiac magnetic resonance imaging (MRI) coupled with nuclear magnetic resonance (NMR) spectroscopy at baseline and six months after the introduction (M6) of a GLP1-RA to assess changes in intramyocardial triglyceride levels and morphological, functional, and cardiac tissue parameters. The relative delta (Δr) between baseline and M6 was calculated and analyzed by Student test or sign test. Twenty-six patients (mean age = 62.2 ± 6.7 years, median HbA1c = 9.1 %) fulfilled inclusion criteria and had both NMR measures. Compared with baseline, relative intramyocardial triglyceride levels significantly decreased after six months of treatment (mean Δr = -26 % [95 %CI:-39; -13]p = 0.003), as well as glycated hemoglobin (HbA1c) (median Δr = -26 % [IQR:25], p < 0.0001), body mass index (BMI) (mean Δr = -6% [-9; -4], p < 0.0001) and left ventricular mass (mean Δr = -6 [-12; -1] p = 0.02). The relative evolution of intramyocardial triglyceride content was not correlated with the relative evolution of HbA1c (r = 0.10) and BMI (r = -0.02). We demonstrate a significant reduction in intramyocardial triglyceride content in patients with T2D after six months of treatment with GLP1-RA. The lack of correlation with reductions in HbA1c and BMI suggests a specific effect of GLP1-RA on myocardial steatosis, which might contribute to their previously demonstrated cardiovascular benefits.

Efficacy and safety of Shexiang Baoxin Pill (MUSKARDIA) in patients with stable coronary artery disease across different weight subgroups.

Shexiang Baoxin Pill (MUSKARDIA), a traditional Chinese patent medicine, plays a crucial role in both preventing and treating diverse cardiovascular diseases, including coronary heart disease, myocardial infarction (MI), and heart failure. Preclinical research has demonstrated that the cardioprotective effects of MUSKARDIA are achieved through multiple pathways, such as enhancing coronary artery dilation, fostering new blood vessel growth, reducing inflammation and oxidative stress, improving lipid metabolism, and protecting vascular endothelium. This subgroup analysis aimed to evaluate the efficacy and safety of Shexiang Baoxin Pill (MUSKARDIA) plus optimal medical therapy (OMT) across different weight categories in treating stable coronary artery disease (CAD). This investigation was a subgroup analysis of a multicenter, randomized, double-blind, placebo-controlled phase IV clinical study. Patients receiving OMT were randomly assigned to either MUSKARDIA or placebo group for a 24-month period. This analysis focused on body weight as a distinguishing factor, using 65kg as the cutoff. The primary efficacy endpoint was the composite of major adverse cardiovascular events (MACEs), including cardiovascular death, non-fatal myocardial infarction (MI), and non-fatal stroke. Secondary efficacy endpoint comprised a composite of all-cause mortality, non-fatal MI, non-fatal stroke, hospitalizations for unstable angina or heart failure, and coronary revascularization procedures. A total of 2646 patients were included in the analysis, with 916 patients weighing less than 65kg and 1730 patients weighing 65kg or more. The median ages were 68 (range: 35-90) years and 62 (range: 29-90) in these two subgroups, respectively. For patients weighing less than 65kg, the MUSKARDIA group exhibited a significantly lower incidence of the primary efficacy endpoint (0.65%) compared to the placebo group (2.64%) (P=0.018), with a reduced risk of MACEs (HR=0.241, 95%CI: 0.068-0.856; P=0.0168). Conversely, in patients weighing 65kg or more, no significant differences were observed in the incidence rates or risks of primary or secondary efficacy endpoints between the MUSKARDIA and placebo groups (All P>0.05). Adverse events were similar between two groups across both weight subgroups. MUSKARDIA plus OMT demonstrated promising efficacy and acceptable safety in CAD patients weighing less than 65kg, potentially reducing the risk of MACEs. For patients weighing 65kg or more, further investigation is needed to optimize dosing strategies.

BDNF-induced BDNF release: A virtuous loop for the cardioprotective effects of exercise in post-ischemic heart failure

BDNF-induced BDNF release: A virtuous loop for the cardioprotective effects of exercise in post-ischemic heart failure

Impact of Boldine Treatment on Hypertrophy and Lipid Peroxidation in the Right Ventricle Subjected to Experimental Adrenergic Overstimulation.

Adrenergic overstimulation is detrimental to the left ventricle. However, its effects on the right ventricle (RV) are not clear. Because adrenergic overload increases metabolic demand and oxidative stress, boldine could be a therapeutic option in the treatment of cardiovascular disease because of its antioxidant role. This study aimed to investigate the impact of adrenergic overload on RV remodeling and the cardioprotective effect of boldine. Animals were divided into 4 groups: control (C), boldine (25 mg/kg i. P .) (B), isoproterenol (ISO) (5 mg/kg subcutaneously), and boldine+isoproterenol (B+ISO). Echocardiography, Fulton index (FI), histology, oxidative stress, inflammation, and β-adrenergic receptor (ADR) were analyzed. The diastolic parasternal length [C 0.698 (0.623-0.724) versus ISO 0.77 (0.73-0.81)], FI [C 0.268 (0.231-0.275) versus ISO 0.340 (0.280-0.353)], inflammatory infiltration (∼40%), and ADR [C 0.78 (0.71-0.84) versus ISO 1.74 (1.52-2.00)] were increased in the ISO group ( P < 0.05). Boldine treatment (B+ISO) reduced the FI [0.240 (0.228-0.263)], lipid peroxidation [2.07 (2.01-2.61)], and ADR [0.71(0.62-0.80)]. Boldine increased total SH levels in B+ISO [C 2.4 (1.78-2.71); ISO 4.01 (2.95-4.66) versus B+ISO 6.77(5.15-8.60)] ( P < 0.05). There was a positive correlation between lipid peroxidation and the FI, and a negative correlation between total SH and the FI ( P < 0.05). This is the first study to explore the effects of adrenergic overstimulation on RV and the protective effect of boldine. Such data pave the way for further research involving RV remodeling, such as in pulmonary hypertension, and a new therapeutic option.

Geniposide Protects Against Myocardial Infarction Injury via the Restoration in Gut Microbiota and Gut-Brain Axis.

Improving gut dysbiosis and impaired gut-brain axis has been a potent therapeutic strategy for treating myocardial infarction (MI). Geniposide (GEN), a traditional Chinese medicine extract, has demonstrated substantial cardioprotective properties post-MI. Nevertheless, the effect of GEN on gut microbial, gut-brain communication, and its potential mechanism remains unclear. In this study, we initially found that GEN significantly alleviated MI-induced cardiac dysfunction from echocardiographic data and decreased myocardial fibrosis, inflammation, apoptosis and hypertrophy post-MI. Additionally, we investigated the effects of GEN on gut pathology, and observed that GEN led to a remarkable change in gut microbiota as evidenced by altering β-diversity and short-chain fatty acids (SCFAs) levels, and alleviated intestinal damage indicated by reduced inflammation and barrier permeability post-MI. Finally, our investigation into brain pathology revealed that GEN induced a remarkable inhibition in PVN inflammation and sympathetic activity following MI. Collectively, these findings imply that the cardioprotective effects of GEN against MI were mediated possibly via an improvement in the impaired gut-brain axis. Mechanically, GEN-induced increase of microbiota-derived SCFAs might be the critical factor linking gut microbiota and reduced neuroinflammation with PVN, which leads to the suppression of sympathetic activation, therefore protecting the myocardium against MI-induced damage.

Modulation of α7nAchR for Cardioprotection against Isoprenaline- Induced Myocardial Injury

The α7nAchR gene is expressed in immune cells, including macrophages, and is linked to cardiovascular diseases. The cardioprotective effects of α7nAchR activation against inflammation in isoprenaline-induced myocardial injury are unclear. This study aims to assess the cardioprotective effects of α7nAChR activation on isoprenaline-induced myocardial injury rats. We hypothesized that α7nAChR activation provides cardioprotection against the myocardial injury via the cholinergic anti-inflammatory pathway. Isoprenaline hydrochloride (85 mg/kg) was injected subcutaneously in rats to induce myocardial injury and activated the a7nAchR through daily transcutaneous tragus stimulation for 14 days at 20 Hz, 0.2 ms, and 2 mA. Examination on Langendorff isolated heart perfusion technique showed improvement in cardiac functions. The electrical stimulation affected collagen deposition, circulating troponin T, and circulating inflammatory marker TNFα. The effects were abolished with pharmacological inhibition of α7nAChR. Further, the role of α7nAChR in ischemia-induced inflammation was studied in RAW264.7 macrophages. Inflammation was activated in RAW264.7 macrophages that were treated with glucose-free media, flushed with 95% N2, and 5% CO2 for 1 h, and reoxygenated in a normoxic incubator for 24 h. a7nAchR stimulation in the activated macrophages reduced pro-inflammatory markers (NO, TNFα) but did not affect anti-inflammatory (IL10, TGFb) expression levels. The reduction in pro-inflammatory factors was linked to the modulation of the transcriptional regulator NFκB, but not STAT3. Our findings suggest that activation of the cholinergic anti-inflammatory pathway may protect against isoprenaline-induced cardiac injury by improving cardiac performance and regulating inflammatory macrophage activity potentially via the NFκB/TNFα pathway.

Dioscin pretreatment ameliorates ferroptosis in cardiomyocytes after myocardial infarction via inhibiting endoplasmic reticulum stress

BackgroundMyocardial infarction (MI) remains a leading cause of mortality globally, often resulting in irreversible damage to cardiomyocytes. Ferroptosis, a recently identified form of regulated cell death driven by iron-dependent lipid peroxidation, has emerged as a significant contributor to post-MI cardiac injury. The endoplasmic reticulum (ER) stress response has been implicated in exacerbating ferroptosis.MethodsHere, we investigated the potential of Dioscin, a natural compound known for its diverse pharmacological properties, in mitigating ferroptosis in cardiomyocytes following MI by targeting ER stress.ResultsIn animal models subjected to MI, administration of Dioscin notably improved cardiac function, reduced infarct size by approximately 24%, and prevented adverse remodeling, highlighting its therapeutic potential. Through in vitro and in vivo models of MI, we demonstrated that Dioscin treatment significantly attenuates ferroptosis in cardiomyocytes, as evidenced by a decrease in lipid peroxidation by about 19% and preserved mitochondrial integrity. Moreover, Dioscin exerted its protective effects by inhibiting ER stress markers, such as the phosphorylation levels of PERK and eIF2α proteins, and the expression levels of BIP and ATF4 proteins, thus disrupting the ER stress-mediated signaling cascade associated with ferroptosis.ConclusionOverall, our findings suggested that Dioscin holds promise as a therapeutic agent against post-MI cardiac injury by mitigating ferroptosis via the suppression of ER stress. Further investigations into the precise molecular mechanisms and clinical translation of Dioscin’s cardioprotective effects are warranted, offering a potential avenue for novel therapeutic interventions in MI-related cardiac complications.Graphical

Effects of SGLT2i on right ventricule function in HFpEF: an echocardiographic study

Abstract Background several studies have demonstrated the cardioprotective effects of Sodium-glucose co-transporter 2 inhibitors (SGLT-2i) in patients with heart failure (HF), irrespective of the presence of diabetes. These findings have culminated in new recommendations for SGLT2i in the treatment of HF, either with reduced or preserved ejection fraction (EF). Purpose the purpose of this study was to analyze the effect of Gliflozin on right ventricular function, in patients with HFpEF, using speckle tracking echocardiography and new echocardiographic surrogates of right ventricular-pulmonary artery (RV-PA) coupling. Methods we enrolled 105 symptomatic HF patients (aged 71,143 ± 9,913 years) with EF &amp;gt; 40% (47,9 ± 7,26) into a multicentric prospective observational study; main anamnestic information, NT-proBNP values and complete echocardiographic data were collected in an ambulatory setting, at time of enrolment and after 6 months of therapy with SGLT-2i. The echocardiographic analysis included conventional, tissue-derived imaging, and myocardial deformation speckle tracking echocardiography of left and right sections. TAPSE/PASP (tricuspid annular plane systolic excursion/pulmonary artery systolic pressure) and RVFWLS/PASP (Right ventricle free wall longitudinal strain) were also collected as surrogates of RV-PA coupling such as Results after 6 months of SGLT-2i therapy echocardiographic evaluation revealed improvement of LVEF (47,909 ± 7,260; 49,562 ± 8,784; p value 0.003) LVGLS (-13,312 ± 3,555; -14,894 ± 3,970; p value &amp;lt; 0.001), RVFWLS (-18,324 ± 6,430; -20,705 ± 6,469; p value 0.002). Echocardiographic parameters of diastolic function such as E/E’m (11,270 ± 6,282; 9,782 ± 6,622; p value 0.003) and PASP (36,580 ± 14,879; 31,757 ± 10,740; p value 0.036) were also ameliorated. Both TAPSE/PASP (0,567 ± 0,267; 0,762±0,536; p value 0.036) and RV FWLS/PASP (-0,588 ± 0,299; -0,785 ± 0,663 p value 0.003) showed higher values. Conclusions our study has demonstrated a significant impact of SGLT-2i on echocardiographic parameters of LV diastolic function and on both left and right ventricle systolic function in patients with HFpEF in a 6 months follow up. Moreover, our findings of RV-PA coupling echocardiographic surrogates improvement, after SGLT-2I use, could underscore the potential of SGLT-2i in managing RV dysfunction in HFpEF.

Fermented Houttuynia Cordata Juice Exerts Cardioprotective Effects by Alleviating Cardiac Inflammation and Apoptosis in Rats with Lipopolysaccharide-Induced Sepsis

Background/Objectives: Sepsis-induced cardiac dysfunction is a major problem that often leads to severe complications and a poor prognosis. Despite the growing awareness of its impact, effective treatment options for sepsis-induced cardiac dysfunction remain limited. To date, fermented products of Houttuynia cordata (HC), known for its rich bioactive properties, have shown potential in modulating inflammatory and oxidative stress pathways. However, treatment with fermented HC juice (FHJ) in lipopolysaccharide (LPS)-induced sepsis in rats has not been investigated. Methods: Rats were pretreated with FHJ at doses of 200 mg/kg and 400 mg/kg for 2 weeks. After that, the rats were injected with a single dose of LPS (10 mg/kg), and 12 h after injection, they developed sepsis-induced cardiac dysfunction. Then, cardiac function, oxidative stress, inflammation, apoptosis, and cardiac injury markers were determined. Results: Pretreatment with FHJ at doses of 200 mg/kg and 400 mg/kg prevented LPS-induced cardiac dysfunction in rats by attenuating cardiac inflammation (IL-1β, TLR-4, and NF-κB levels), oxidative stress (MDA levels), and apoptosis (cleaved-caspase 3 and Bax/Bcl-2 expression) and reducing markers of cardiac injury (LDH and CK-MB levels). Conclusions: These results suggest that FHJ could be a potential therapeutic agent for sepsis-induced heart disease.

Cardioprotective effect of crocin in patients with breast cancer receiving anthracycline-based chemotherapy: A randomized, double-blind, placebo-controlled study.

Anthracycline chemotherapy leads to cardiotoxicity in patients with breast cancer. We performed a double-blind randomized controlled trial to assess the efficacy of crocin (crocin tablets) in reducing anthracycline-induced cardiotoxicity in breast cancer patients. Eligible patients were randomly assigned to receive either treatment with crocin tablets or placebo for 6 months. Primary efficacy outcome was the proportion of patients with a drop in left ventricular ejection fraction (LVEF) of at least 10% from baseline until 6 months. We randomized 200 patients; 7 of them had no valid randomization as the change in chemotherapy scheme. A total of 193 eligible participants (mean [SD] age, 50.9 [9.6] years; all women) were randomly assigned to receive crocin tablets or placebo. The incidence of the primary efficacy outcome was 7.2% (7/97) in the crocin group and 17.7% (17/96) in the placebo group (P = 0.027). At 6 months, there were significant differences in the mean change of N-terminal pro-brain natriuretic peptide (NT-pro BNP) between the groups (3.06 [-25.18 to 6.95] vs. 3.06 [-4.85 to 24.98] pg/ml; P = 0.017). The changes in heart rate from baseline to 6 months showed a significant difference as the mean difference of -4.00 (95%CI, -6.95 to -1.05) bpm (P = 0.008). Conclusively, among patients with breast cancer treated with anthracycline-based chemotherapy, crocin tablets reduced the incidence of LVEF reduction. This finding indicated that crocin tablets might be a safe and effective therapy to prevent the cardiotoxicity in this population. (Chictr.org.cn, ID Number: ChiCTR2000041134).

Feasibility and Tolerability of Daily Microgreen Consumption in Healthy Middle-Aged/Older Adults: A Randomized, Open-Label, Controlled Crossover Trial

Background/Objectives: Microgreens are rich in nutrients and phytochemicals that can support healthy aging, including attenuation of cardiovascular disease risk. The nutrient and phytochemical contents of red beet (i.e., bull’s blood’ beet, Beta vulgaris) and red cabbage (Brassica oleracea var capitate) microgreens, as well as existing preclinical evidence suggest their cardioprotective effects, but the feasibility, gastrointestinal tolerability, and human health effects of daily microgreen consumption are unknown. This study aimed to evaluate the feasibility and gastrointestinal tolerability of 2 weeks of daily microgreen consumption in healthy middle-aged/older (MA/O) adults. A secondary aim was to characterize potential health effects. Methods: Healthy MA/O adults (initial n = 26) were randomized to consume either 2 cups of ‘bull’s blood’ beet or red cabbage microgreens daily for 2 weeks in a crossover design, with each treatment period separated by 2 weeks. Feasibility was determined through participant retention and intervention compliance (i.e., total doses consumed divided by 14 days), while gastrointestinal tolerability was determined by a gastrointestinal health questionnaire and bowel movement log. Impacts of microgreen consumption on brachial and aortic hemodynamic parameters, and gut microbiota composition were evaluated. Results: Daily consumption for 2 weeks of ‘bull’s blood’ beet and red cabbage microgreens was found to be feasible as indicated by high participant retention (final n = 24) and overall treatment compliance of 95.6%. Gastrointestinal symptom severity was not impacted overall, though an improvement in gastrointestinal inflammation-associated symptom severity scores following the red cabbage microgreen intervention (p = 0.047) was observed. There were no changes in bowel movement quality, hemodynamic parameters, or on alpha or beta diversity of the gut microbiota. Conclusions: Daily consumption of ‘bull’s blood’ beet and red cabbage microgreens is feasible and tolerable in healthy MA/O adults. Future studies designed to evaluate their health impacts are needed.

Compound identification of Shuangxinfang and its potential mechanisms in the treatment of myocardial infarction with depression: insights from LC-MS/MS and bioinformatic prediction

BackgroundPatients with myocardial infarction (MI) have a high incidence of depression, which deteriorates the cardiac function and increases the risk of cardiovascular events. Shuangxinfang (Psycho-cardiology Formula, PCF) was proved to possess antidepressant and cardioprotective effects post MI. However, the compounds of PCF remain unidentified, and the pertinent mechanism is still not systematic. The purpose of this study is to determine the ingredients of PCF, further to probe the underlying mechanism for MI with depression.MethodsThe compounds of PCF were qualitatively identified by LC-MS/MS. The optimal dosage for lavage with the PCF solution in rats was determined to be 1 mL/100 g/day for a duration of 5 days. We also detected the PCF components migrating to blood in the control and model rats. Then the targets of PCF compounds were searched on Swiss target database, and the targets of depression and MI were predicted on TTD, OMIM, GeneCards, DrugBank and PharmGkb database. All the targets were intersected to construct the Protein-Protein Interaction (PPI) network on Metascape platform and the herb-compound-target (HCT) network on Cytoscape, to identify the hub targets. GO and KEGG pathway enrichment analysis were conducted on DAVID platform. Molecular docking was modeled on AutoDock Vina software.ResultsThere were 142 bioactive compounds from PCF acting on 270 targets in a synergistic way. And a total of seven components migrating to blood were identified, including Miltionone I, Neocryptotanshinone, Danshenxinkun A, Ferulic acid, Valerophenone, Vanillic acid and Senkyunolide D. Then SRC and MAPK3 were obtained as the hub proteins by degree value in PPI network, and P2RY12 was picked out as seed proteins ranked by scores from MCODES. Further analysis of biological process and signaling pathways also revealed the significance of ERK/MAPK. Statistical analyses (e.g., GO and KEGG pathway enrichment, PPI network analysis) demonstrated the significance of the identified targets and pathways (p &amp;lt; 0.05). Molecular docking results showed that the binding energies were all less than −5 kcal/mol. The stability of Neocryptotanshinone possessed the lowest binding energy to MAPK3.ConclusionWe identified PCF’s bioactive compounds and predicted its therapeutic mechanism for MI with depression using LC-MS/MS and bioinformatics. Key targets SRC, MAPK3, and seed protein P2RY12 were crucial for PCF’s cardio-neuroprotective effects. Neocryptotanshinone showed the strongest binding to MAPK3, suggesting it as a pivotal active ingredient. These findings offer new insights and targets for future research on PCF.