Association of gut microbiota with depression post-myocardial infarction: A systematic evaluation and meta-analysis protocol.

BACKGROUND: Depression post-myocardial infarction (MI) is becoming more prevalent. The gut-brain axis (GBA), influenced by the gut microbiota, is a critical component in understanding depression post-MI. Despite the well-established connection between gut microbiota and depression post-MI, this relationship remains incompletely understood. METHODS AND ANALYSIS: This protocol will follow the Preferred Reporting Items for Systematic Review and Meta-analysis Protocol (PRISMA-P) 2020 statement. Beginning from inception to October 2023, a systematic search will be conducted across eight electronic databases, including PubMed, MEDLINE, Scopus, Embase, Cochrane Clinical Trials Database, Web of Science, China National Knowledge Infrastructure, and China Biomedical Literature Database. Pre-selected studies will be independently assessed by two researchers following a standard inclusion, data extraction and quality assessment protocol. The primary outcome measures are differences in the profile of gut microbiota and rating scale scores for depression. Fixed-effects models will be used when both clinical heterogeneity and statistical heterogeneity are low, otherwise random-effects models will be used. Furthermore, subgroup analyses will be conducted on the depression severity of the participants using the same psychiatric scales employed, study type and geographic region. Random forest plot runs and research-related statistical analyses will be carried out using Rev Man V.5.3 software. EXPECTED RESULTS: This study will identify the association between the gut microbiota and the onset of depression post-MI, and provide evidence for the use of probiotics as an adjunctive treatment for depression post-MI. TRIAL REGISTRATION: Prospero registration number: CRD42023444026.

Triglyceride-glucose index as a potential predictor of major adverse cardiovascular and cerebrovascular events in patients with coronary heart disease complicated with depression.

Background: Triglyceride-glucose (TyG) index is a surrogate marker of insulin resistance and metabolic abnormalities, which is closely related to the prognosis of a variety of diseases. Patients with both CHD and depression have a higher risk of major adverse cardiovascular and cerebrovascular events (MACCE) and worse outcome. TyG index may be able to predict the adverse prognosis of this special population. Methods: The retrospective cohort study involved 596 patients with both CHD and depression between June 2013 and December 2023. The primary outcome endpoint was the occurrence of MACCE, including all-cause death, stroke, MI and emergent coronary revascularization. The receiver operating characteristic (ROC) curve, Cox regression analysis, Kaplan-Meier survival analysis, and restricted cubic spline (RCS) analysis were used to assess the correlation between TyG index and MACCE risk of in patients with CHD complicated with depression. Results: With a median follow-up of 31 (15-62) months, MACCE occurred in 281(47.15%) patients. The area under the ROC curve of TyG index predicting the risk of MACCE was 0.765(0.726-0.804) (P<0.01). Patients in the high TyG index group(69.73%) had a significantly higher risk of developing MACCE than those in the low TyG index group(23.63%) (P<0.01). The multifactorial RCS model showed a nonlinear correlation (nonlinear P<0.01, overall P<0.01), with a critical value of 8.80 for the TyG index to predict the occurrence of MACCE. The TyG index was able to further improve the predictive accuracy of MACCE. Conclusions: TyG index is a potential predictor of the risk of MACCE in patients with CHD complicated with depression.

Efficacy and safety of non-pharmacological therapy under the guidance of TCM theory in the treatment of anxiety in patients with myocardial infarction: A protocol for systematic review and meta-analysis.

BACKGROUND: With the increasing pressures of modern life and work, combined with a growing older population, the incidence of comorbid anxiety and myocardial infarction (MI) is increasing. Anxiety increases the risk of adverse cardiovascular events in patients with MI and significantly affects their quality of life. However, there is an ongoing controversy regarding the pharmacological treatment of anxiety in patients with MI. The concomitant use of commonly prescribed selective serotonin reuptake inhibitors (SSRIs) and antiplatelet medications such as aspirin and clopidogrel may increase the risk of bleeding. Conventional exercise-based rehabilitation therapies have shown limited success in alleviating anxiety symptoms. Fortunately, non-pharmacological therapies based on traditional Chinese medicine (TCM) theory, such as acupuncture, massage, and qigong, have demonstrated promising efficacy in treating MI and comorbid anxiety. These therapies have been widely used in community and tertiary hospital settings in China to provide new treatment options for patients with anxiety and MI. However, current studies on non-pharmacological TCM-based therapies have predominantly featured small sample sizes. This study aims to comprehensively analyze and explore the effectiveness and safety of these therapies in treating anxiety in patients with MI. METHOD: We will systematically search six English and four Chinese databases by employing a pre-defined search strategy and adhering to the unique rules and regulations of each database to identify studies that fulfilled our inclusion criteria, to qualify for inclusion, patients must be diagnosed with both MI and anxiety, and they must have undergone non-pharmacological TCM therapies, such as acupuncture, massage, or qigong, whereas the control group received standard treatments. The primary outcome measure will be alterations in anxiety scores, as assessed using anxiety scales, with secondary outcomes encompassing the evaluations of cardiopulmonary function and quality of life. We will utilize RevMan 5.3 to conduct a meta-analysis of the collected data, and subgroup analyses will be executed based on distinct types of non-pharmacological TCM therapies and outcome measures. RESULTS: A narrative summary and quantitative analysis of the existing evidence on the treatment of anxiety patients with MI using non-pharmacological therapies guided by Traditional Chinese Medicine theory. CONCLUSION: This systematic review will investigate whether non-pharmacological interventions guided by TCM theory are effective and safe for anxiety in patients with MI, and provide evidence-based support for their clinical application. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42022378391.

Chaihujialonggumulitang shows psycho-cardiology therapeutic effect on acute myocardial infarction with comorbid anxiety by the activation of Nrf2/HO-1 pathway and suppression of oxidative stress and apoptosis.

BACKGROUND: Anxiety is a common comorbidity of cardiovascular diseases, which deteriorated cardiac function. Chaihujialonggumulitang (BFG) was reported to have antioxidant properties, alleviate myocardial ischemia injury and improve anxiety-like behavior. The Nuclear factor erythroid 2-related factor 2 (Nrf2) /heme oxygenase-1 (HO-1) pathway is the main mechanism to defend against oxidative stress, and improve cardiac function. This study was to investigate the possible mechanism of BFG in the treatment of psycho-cardiology. METHODS: AMI with comorbid anxiety rat model was established by ligation of the left anterior descending coronary artery combined with uncertain empty bottle stimulation, followed by the administration of BFG (1 mL/100 g/d by gavage) or Dimethyl fumarate (DMF, 10 mg/kg/d by intraperitoneal injection) for 6 days. Echocardiography, myocardial injury markers, H&E, and Masson staining were employed to evaluate cardiac function. Behavioral tests and hippocampus neurotransmitters were applied to record anxiety-like behavior. We employed immunohistochemistry, RT-PCR, western blotting, and biochemical analysis to detect the protein and gene expression of Nrf2/HO-1 pathway-related factors, and oxidative stress and apoptosis parameters. RESULTS: Rats in the AMI and complex groups showed cardiac function deterioration, as well as anxiety-like behavior. BFG improved echocardiography indicators, reduced myocardial injury markers, and attenuated myocardial pathological changes. BFG also ameliorated anxiety-like behaviors and elevated neurotransmitters levels. BFG promoted the activation of Nrf2/HO-1 pathway, increased antioxidant enzyme activities, reduced lipid peroxidation levels, and alleviated oxidative damage and apoptosis. DMF showed therapeutic effects and molecular mechanisms similar to BFG. CONCLUSION: BFG may possess a psycho-cardiology therapeutic effect on AMI with comorbid anxiety by the activation of the Nrf2/HO-1 pathway and suppression of oxidative stress and apoptosis.

Shuangxinfang Prevents S100A9-Induced Macrophage/Microglial Inflammation to Improve Cardiac Function and Depression-Like Behavior in Rats After Acute Myocardial Infarction.

Background: Depression is a common complication of cardiovascular disease, which deteriorates cardiac function. Shuangxinfang (psycho-cardiology formula, PCF) was reported to alleviate myocardial ischemia injury and improve depression-like behavior. Interestingly, our previous proteomics study predicted that the protein S100A9 appeared as an important target, and macrophage/microglial inflammation might be involved in the process of PCF improving depression induced by acute myocardial infarction (AMI). This study aims to validate the proteomics results. Methods: AMI rat models were established in vivo, followed by the administration of PCF or ABR-215757 (also named paquinimod, inhibiting S100A9 binding to TLR4) for 5 days. Forced swimming test (FST) and open field test (OFT) were applied to record depression-like behavior, and echocardiography was employed to evaluate cardiac function. Morphological changes of cardiomyocytes were assessed by HE staining and TUNEL staining on day 7 after cardiac surgery, as well as Masson trichrome staining on day 21. Hippocampal neurogenesis was determined by Nissl staining, while 5-hydroxytryptamine (5-HT), tryptophan/kynurenine ratio, and brain-derived neurotrophic factor (BDNF) in the hippocampus were analyzed as biochemical indicators of depression. We employed RT-qPCR, western blotting, and immunofluorescence to detect the expression of pathway-related genes and proteins. Myocardial and hippocampal expression of inflammatory factors were performed by ELISA. The activation of macrophage and microglia was assessed via immunoreaction using CD68 and Iba1, respectively. For in vitro confirmation, BV2 cells were primed with recombinant protein S100A9 and then treated with PCF serum or ferulic acid to determine alterations in microglial inflammation. Results: Rats in the AMI group showed heart function deterioration and depression-like behavior. Coronary ligation not only brought about myocardial inflammation, cell apoptosis, and fibrosis but also reduced the neurogenesis, elevated the tryptophan/kynurenine ratio, and decreased the content of 5-HT. PCF could ameliorate the pathological and phenotypic changes in the heart and brain and inhibit the expression of the S100A9 protein, the activation of the microglial cell, and the secretion of IL-1ß and TNF-α raised by AMI. ABR-215757 showed therapeutic effect and molecular biological mechanisms similar to PCF. Treatment with PCF serum or ferulic acid in vitro was proved to efficiently block the hyperactivation of BV2 cells and increment of cytokine contents induced by recombinant protein S100A9. Conclusion: We identify S100A9 as a novel and potent regulator of inflammation in both the heart and brain. Macrophage/microglia inflammation mediated by S100A9 is considered a pivotal pathogenic in depression after AMI and a major pathway for the treatment of PCF, suggesting that PCF is a promising therapeutic candidate for psycho-cardiology disease.

Efficacy of Atorvastatin Plus Conventional Disease-Modifying Antirheumatic Drugs on Disease Activity in Rheumatoid Arthritis: A Systematic Review and Meta-analysis of Randomized Controlled Trials.

METHODS: We queried the PubMed, Embase, Web of Science, and the CENTRAL (Cochrane Central Register of Controlled Trials) databases for this study. The pooled efficacy was evaluated using standardized mean differences. The inverse of the variance model was used for data pooling. RESULTS: Based on the search, we identified 9 randomized controlled trials. The trials included 258 patients in the atorvastatin plus DMARD groups and 246 patients in the DMARD alone groups. The primary outcome was the change from baseline in the 2018 (209:228 Disease Activity Score in 28 Joints). Based on the Disease Activity Score in 28 Joints, disease activity in RA patients decreased significantly in patients given atorvastatin plus DMARD compared with patients given DMARD alone (standardized mean difference, -2.46; 95% confidence interval, -3.98 to -0.95; p = 0.0015; I2 = 97%; p < 0.01). Subgroup analysis did not identify any confounding factors, and no publication bias was detected in the meta-analysis. CONCLUSIONS: The result supports that atorvastatin could be added to DMARDs to treat patients with RA.

The cardioprotective and anxiolytic effects of Chaihujialonggumuli granule on rats with anxiety after acute myocardial infarction is partly mediated by suppression of CXCR4/NF-κB/GSDMD pathway.

AIMS: Over-expression of CXCR4 activates nuclear translocation of NF-κB, induces high expression of NLRP3, GSDMD, IL-1ß and IL-18, which promotes severe inflammatory response following myocardial infarction. Previous studies revealed inflammation induces anxiety after myocardial infarction. The Chaihujialonggumuli granule has anti-inflammatory properties and could tranquillize mind. But the mechanism of its efficacy remains unknown. This study was to investigate the possible mechanism of BFG on cardioprotective and anxiolytic. METHODS: The expression of CXCR4, NF-κB, NLRP3and GSDMD was measured with western-blot, QRT-PCR. The expression location of CXCR4, NLRP3, GSDMD were determined by immunohistochemistry. IL-1ß、IL-18 in the peripheral blood were measured by ELISA. HE staining, Masson staining and transmission electron microscopy were used to observe morphological changes of cardiomyocytes. Echocardiography was used to assess cardiac function after cardiac surgery. Elevated cross maze test and open field test were used to evaluate behaviours. Western blot was used to detect the protein expressions of 5-HT, DA, IL-1ß, IL-18 and neuron damage was investigated by Nissl staining in the hippocampus. RESULTS: The up-regulation of CXCR4, NF-κB, NLRP3 and GSDMD were found in the infarcted area after left coronary artery ligation. Pathological staining and analysis showed that more severe inflammatory cytokines infiltration, myocardial fibrosis, were found in myocardial tissue of the complex group rats. And when compared to the sham group, the levels of IL-1ß, IL-18 was increased of the complex group in both peripheral blood and brain. Behavioural test and echocardiography indicated that the rats in complex group exploration behaviours was significantly reduced, and with poor cardiac functional recovery. The AMD3100 had an inhibitory impact of CXCR4 on the activition of its downstream effectors, alleviating inflammatory reaction. Furthermore, the BFG decreased the expression level of CXCR4, NF-κB, GSDMD, NLRP3 in the infarcted area after myocardial infarction, when compared to the complex group. The assays in the brain indicated the BFG suppressed expression and activity of IL-1ß, IL-18, and improved 5-HT and DA synthesis. CONCLUSIONS: In sum, our study indicated that BFG may reduce inflammation, treat co-existing anxiety after myocardial infarction through inhibition of CXCR4/NF-κB/GSDMD signalling.

[Effect of chronic emotional stress induced by empty bottle stimulation on inflammatory factors in rats with acute myocardial infarction: analysis of the CXCL12/CXCR4 axis].

OBJECTIVE: To investigate the effect of chronic emotional stimulation induced by empty bottle stimulation on CXCL12/CXCR4-mediated inflammatory response in rats with acute myocardial infarction (AMI). METHODS: Rat models of anxiety were established by a 21-day stimulation with uncertain empty bottle drinking water, and myocardial infarction was induced by ligating the left anterior descending branch of the coronary artery; compound models were established by performing myocardial infarction operation on the 15th day of anxiety modeling. The rats were randomly divided into 4 groups: shamoperated group (n=6), myocardial infarction group (n=6), compound model group (with myocardial infarcted and anxiety; n= 6), and inhibitor group (compound models treated daily with 1 mg/kg AMD3100 for 6 days; n=7). Echocardiography was used to examine the LVEF and LVFS to evaluate the cardiac function of the rats. Elevated maze test and open field test were used to evaluate the behaviors of the rats. The expressions of CXCL12, CXCR4, IL-1ß, IL-18 and neutrophil active protease (NE) in the myocardial tissues and blood samples were detected with ELISA and immunohistochemistry. RESULTS: The LVEF and LVFS were lower in the compound model group than in the sham group and myocardial infarction group (P < 0.05), and were higher in inhibitor group than in the compound model group (P < 0.05). LVID; d and LVID; s were lower in the inhibitor group than in the compound model group (P < 0.05). Compared to those in the sham group and myocardial infarction group, the rats in the compound model group more obviously preferred to stay in the closed arm (P < 0.05) in EPM; the rats in the inhibitor group had more times of entering and staying in the open arm than the compound model rats (P < 0.05); the horizontal and vertical movements were less in the compound model rats than in those in the sham group and the myocardial infarction group (P < 0.05) in OFT, and the vertical movement of the rats in inhibitor group was higher than those in the compound model group (P < 0.05). The expression of CXCR4 in the marginal zone of myocardial infarction was significantly higher in the compound model group than in the sham-operated group, myocardial infarction group and inhibitor group (P < 0.05). The expressions of IL-1ß, IL-18 and NE in the inhibitor group were significantly lower than those in the compound model group (P < 0.05). Compared with at in the sham-operated group, the number of Nissl bodies in the compound model group decreased significantly (P < 0.01). CONCLUSIONS: Chronic emotional stress induced by empty bottle stimulation can lead to dysfunction of the CXCL12/CXCR4 axis, which causes inflammatory cascade after myocardial infarction to worsen myocardial cell necrosis, cardiac function and hippocampal neuronal damage after the infarction.

Effects of Dietary Fat Profile on Gut Microbiota in Valproate Animal Model of Autism.

Autism spectrum disorder (ASD) is a developmental disability which may cause significant social, communication, and behavioral challenges. Besides certain essential symptoms, a lot of ASD individuals also suffer the comorbidity of gut microbiota dysbiosis, which possibly causes a variety of gastrointestinal (GI) difficulties. Interestingly, evidence has indicated that behavioral output may be modulated through the communication between the central nervous system and gut microbiota via the gut-brain axis. Polyunsaturated fatty acids (PUFAs) and n-3 fatty acids (n-3 PUFA) are structurally and functionally crucial components for the brain, and the state of n-3 PUFAs also affects the gut microbiota. However, how varying intake ratios of n-3/n6 PUFAs affect the gut microbiota composition in ASDs is not well-understood. Pregnant female Wistar rats with intraperitoneal administration of valproate acid (VPA) at embryonic day (E) 12.5 and their male offspring were grouped and fed three diets: a control chow (VPA group), omega-3 deficient (A group), and n-3/n6 (1:5) diet (B group). The diet of pregnant female Wistar rats with intraperitoneal administration of saline and their male offspring was a control chow (normal group). Microbial composition and species abundance were investigated accordingly by the 16S rRNA gene-based metagenomics analysis on the fecal samples. Results showed that fecal microbial abundance was decreased because of VPA administration in the period of pregnancy, and the changing pattern of gut microbiota was similar to that reported in ASD patients. Furthermore, the n-3/n6 (1:5) diet increased the fecal microbial abundance and decreased the elevated Firmicutes. In conclusion, n-3/n6 PUFAs (1:5) diet supplementation may alter gut microbiota composition in VPA-exposed rats. This study put forward a new strategy for the intervention and treatment of autism by n-3/n-6 PUFAs ratio supplementation intakes.

Chinese herbal medicine therapy for coronary heart disease complicated with anxiety: a systematic review of randomized controlled trials.

OBJECTIVE: To evaluated the effectiveness and safety of Chinese herbal medicines (CHMs) for coronary heart disease (CHD) complicated with anxiety. METHODS: Randomized controlled clinical trials (RCTs) with parallel-groups were included after searching through electric-databases from inception to May, 2017. Meta-analysis was undertaken with RevMan 5.3 software. RESULTS: Twenty-three RCTs enrolling 1654 patients were included in this systematic review. The combination therapy (CHMs combined with anxiolytic) appeared to be superior to anxiolytic in terms of reducing the score of Zung Self-rating Anxiety scale (SAS) (mean Difference (MD), －12.25; 95% confidence interval (CI), －14.01 to －10.48, eliminating method; MD, －3.92; 95% CI, －5.48 to －2.35, tranquilizing method), improving the total effect rate (relative risk (RR), 1.26; 95% CI, 1.08 to 1.46, eliminating method) and reducing the TCM symptoms scores (MD, －2.24; 95% CI, －4.25 to －0.23, tranquilizing method) with a lower incidence of adverse events (RR, 0.46; 95% CI, 0.25 to 0.85, tonifying method). CHMs demonstrated benefits in lowering the score of Hamilton Anxiety Rating scale (MD, －6.77; 95% CI, －8.16 to －5.37, tonifying method),lowering the score of SAS (MD, －10.1; 95% CI, －13.73 to －6.30, tonifying method) and reducing the TCM symptoms scores (MD, －2.18; 95% CI, －3.12 to －1.24, tranquilizing method). CONCLUSION: We got a low evidence that CHMs,which had less side effects, showed potentially benefits to patients with CHD complicated with anxiety. While the results should be interpreted with caution. Trails with higher quality are required to verify the effectiveness and safety of CHMs for CHD complicated with anxiety.

Silencing of LINC00461 enhances radiosensitivity of lung adenocarcinoma cells by down-regulating HOXA10 via microRNA-195.

Lung adenocarcinoma is recognized as one of the most recurrent tumours in adults. Long non-coding RNAs (lncRNAs) are non-protein-coding transcripts and have been demonstrated to regulate biological functions during tumorigenesis. Our study aims to investigate the underlying molecular mechanisms of LINC00461/microRNA-195 (miR-195)/HOXA10 responsible for its involvement in lung adenocarcinoma. We firstly selected differentially expressed lncRNAs and genes by the Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO). The functional role of LINC00461 in lung adenocarcinoma was then determined using ectopic expression, knockdown and reporter assay experiments. Besides, we detected the expression profiles of LINC00461, miR-195, HOXA10 and apoptosis- and invasion-related genes. Cell proliferation, migration and invasion were evaluated. In vivo tumour formation ability was analysed. Overexpressed LINC00461 and HOXA10 but down-regulated miR-195 were observed in primary and metastatic lung adenocarcinoma. LINC00461 negatively regulated miR-195, while miR-195 negatively regulated HOXA10. Forced LINC00461 expression decreased expression of miR-195 and Bax, increased expression of HOXA10, MMP-2, MMP-9 and Bcl-2, promoted cell proliferation, migration and invasion as well as tumour formation, and enhanced radiosensitivity of lung adenocarcinoma cells. However, these effects were reversed by lentivirus-mediated miR-195-forced expression, thereby suggesting that miR-195 could antagonize the harmful effect of LINC00461 on lung adenocarcinoma cells. Collectively, the present study provides evidence supporting the inhibitory effect of LINC00461 silencing on lung adenocarcinoma, which suppresses lung adenocarcinoma cell migration, invasion and radiosensitivity via HOXA10 by binding to miR-195, which provides a promising basis for the targeted intervention treatment for human lung adenocarcinoma.

Sjogren-Larsson syndrome associated hypermelanosis.

BACKGROUND/OBJECTIVES: Sjogren - Larsson syndrome (SLS) is a rare autosomal recessive disease of the mutation ALDH3A2 that identifies a part of fatty acids for fatty aldehyde dehydrogenase: NAD-oxidoreductase enzyme complex. This study aimed to access variant ALDH3A2 gene coded for FALDH and products regulating pathogenic melanogenesis owing to increased oxidative stress and reactive oxygen species resulting in DNA harm in SLS. By turning them into fatty acids, FALDH avoids the accumulation of toxic fatty aldehydes. The mutation results in the accumulation of aldehyde-modified lipids or fatty alcohols that may interfere with skin and brain function. METHODS: In Nov 2018, we performed a literature search in PubMed for clinical studies, clinical trials, case reports, controlled trials, randomized controlled trials, and systemic reviews. The search terms we used were "SJOGREN-LARSSON SYNDROME" AND "HYPERMELANNOSIS" OR "FALDH" (from 1985). The search resulted in 1,289 articles, out of these 95 articles met our inclusion exclusion criteria. Our inclusion criteria included relevant original articles relevant, critical systemic reviews, and crucial referenced articles, ex-clusion criteria included duplicates and articles not published in English language. RESULTS: Toxicity of long-chain aldehydes to FALDH-deficient cells owing to accumulation under the profound epidermis layer improves oxidative stress in the cell resulting in keratinocyte hyperproliferation. CONCLUSION: While it continues to be determined whether accumulated fatty alcohol and fatty aldehydes obtained from ether glycerolipids and sphingolipids improve the susceptibility of melanocytes and their element accountable for skin hyperpigmentation to biological colour.

Recognition of the toxicity of aristolochic acid.

WHAT IS KNOWN AND OBJECTIVE: Aristolochic acid (AA) is an abundant compound in Aristolochia plants and various natural herbs. In the 1990s, a slimming formula used in Belgium that contains Aristolochia fangchi was reported to cause kidney damage and bladder cancer, and aristolochic acid nephropathy (AAN) is now well recognized worldwide. In October 2017, researchers reported an AA signature that is closely associated with hepatocellular carcinoma (HCC) worldwide. COMMENT: There are differing opinions on the toxicity of AA, and different countries have taken different measures to address the issue. There is a lack of clarity on the causal role of AA in hepatocarcinogenesis and on the potential underlying mechanisms for the reported nephrotoxicity and carcinogenicity. The toxicity of AA differs depending on gender and age, and other risk factors that could explain the variability in the toxicity of AA remain to be identified. WHAT IS NEW AND CONCLUSION: Whether preparations containing AA, such as many Chinese medicines, should be used remains controversial, and this issue warrants further investigation before definite conclusions can be drawn.

Anti-depressive effect of Shuangxinfang on rats with acute myocardial infarction: Promoting bone marrow mesenchymal stem cells mobilization and alleviating inflammatory response.

Bone marrow mesenchymal stem cells (BM-MSCs) are recruited to injured site for cardiac self-repairing in acute myocardial infarction (AMI), but the spontaneous mobilization of BM-MSCs is insufficient for self-repairing. Inflammation initiated by necrosis cardiomyocytes induced cardiac remodeling and depression. Given the anti-inflammatory effects of BM-MSCs and the inextricably relationship among inflammation, ventricular remodeling and depression following AMI, methods focused on enhancing BM-MSCs mobilization are promising. Shuangxinfang (Psycho-cardiology Formula, PCF) is a classical traditional Chinese medicine prescription. In this study, we explored its psycho-cardiology effects in rats with AMI and explore its potential mechanism. Our results showed PCF inhibited inflammation caused by injured myocardium, improved heart function and depression developed from myocardial infarction, and these might partly attribute to the higher BM-MSCs mobilization efficiency promoted by PCF.

Chaihulonggumulitang Shows Psycho-cardiology Therapeutic Effects on Acute Myocardial Infarction by Enhancing Bone Marrow Mesenchymal Stem Cells Mobilization.

Ischemic myocardium initiates the mobilization and homing of bone marrow mesenchymal stem cells (BM-MSCs) to promote myocardial regeneration after acute myocardial infarction (AMI). Inflammation caused by necrotic cardiomyocytes induce major pathological changes (cardiac remodeling and myocardial apoptosis) as well as anxiety disorder. This process may be inhibited by the differentiation and paracrine effects of BM-MSCs. However, the spontaneous mobilization of BMSCs is insufficient to prevent this effect. Given the anti-inflammatory effects of BM-MSCs, ventricular remodeling and anxiety following AMI, methods focused on enhancing BMSCs mobilization are promising. BFG is a classical traditional Chinese prescription medicine and has been proved effective in treating AMI and reducing anxiety, but the potential mechanism of its function remains unknown. In the present study, we explored the effects of Chaihulonggumulitang (BFG) on AMI and anxiety in vivo and in vitro. We also tested its effects in promoting BMSCs mobilization and alleviating inflammation. Our data showed that the classical Chinese prescription BFG promoted BM-MSCs mobilization, inhibited inflammatory response, and improved heart damage and anxiety developed from AMI. Thus, we provided an underlying mechanism of BFG function in psycho-cardiology conditions such as AMI.