OBJECTIVE To investigate the effects and potential mechanism of Qiangxin decoction on mitochondrion of rats with chronic heart failure （CHF）. METHODS The CHF model was established by ligating the left anterior descending branch of the coronary artery. Modeled rats were divided into model group， Qiangxin decoction low-dose and high-dose groups （12.25， 24.50 g/kg， calculated by crude drug）， and chemical medicine group （Sacubitril valsartan sodium tablets， 10.42 mg/kg）， with 10 rats in each group； control group was set up without treatment. Each group of rats was orally administered with the corresponding medication or normal saline twice a day for 28 consecutive days. After the last medication， the contents of N-terminal pro-brain natriuretic peptide （NT-proBNP） and adenosine triphosphate （ATP） in serum and phosphatidic acid （PA） and cardiolipin （CL） in myocardial tissue were all detected； the pathological damage and collagen fibrosis of rat myocardial tissue were observed； the apoptosis of myocardial cells was determined； the ultrastructure of myocardial tissue was observed； the protein expressions of mitofusin 1 （Mfn1）， Mfn2， optic atrophy protein 1 （OPA1） and dynamin-related protein 1 （Drp1） were all detected in myocardial tissue. RESULTS Compared with control group，the serum content of NT-proBNP， apoptotic rate of myocardial cells， and relative expressions of S-OPA1 and Drp1 proteins were all increased significantly； serum content of ATP，contents of PA and CL， and relative expressions of Mfn1， Mfn2 and L-OPA1 proteins were all significantly reduced （P＜0.05）. There were abnormal membrane tissue structure in various layers of myocardial tissue， degeneration and necrosis of myocardial cells， and severe fibrosis； the mitochondria were swollen， with reduced or absent cristae， and uneven matrix density. After intervention with Qiangxin decoction， the levels of the aforementioned quantitative indicators in serum and myocardial tissue of rats （excluding CL content in the Qiangxin decoction low- dose group） were significantly reversed （P＜0.05）； the pathological damage of myocardial tissue had significantly improved， fibrosis had significantly reduced， mitochondrial morphology tended to be normal， cristae had increased， and matrix density was uniform. CONCLUSIONS Qiangxin decoction can regulate myocardial mitochondrial function and structural integrity of CHF rats， thereby improving myocardial energy metabolism and antagonizing myocardial fibrosis， the mechanism of which may be associated with activating PA/Mfn/CL signaling pathway.

OBJECTIVE To investigate the effects and potential mechanism of Qiangxin decoction on mitochondrion of rats with chronic heart failure （CHF）. METHODS The CHF model was established by ligating the left anterior descending branch of the coronary artery. Modeled rats were divided into model group， Qiangxin decoction low-dose and high-dose groups （12.25， 24.50 g/kg， calculated by crude drug）， and chemical medicine group （Sacubitril valsartan sodium tablets， 10.42 mg/kg）， with 10 rats in each group； control group was set up without treatment. Each group of rats was orally administered with the corresponding medication or normal saline twice a day for 28 consecutive days. After the last medication， the contents of N-terminal pro-brain natriuretic peptide （NT-proBNP） and adenosine triphosphate （ATP） in serum and phosphatidic acid （PA） and cardiolipin （CL） in myocardial tissue were all detected； the pathological damage and collagen fibrosis of rat myocardial tissue were observed； the apoptosis of myocardial cells was determined； the ultrastructure of myocardial tissue was observed； the protein expressions of mitofusin 1 （Mfn1）， Mfn2， optic atrophy protein 1 （OPA1） and dynamin-related protein 1 （Drp1） were all detected in myocardial tissue. RESULTS Compared with control group，the serum content of NT-proBNP， apoptotic rate of myocardial cells， and relative expressions of S-OPA1 and Drp1 proteins were all increased significantly； serum content of ATP，contents of PA and CL， and relative expressions of Mfn1， Mfn2 and L-OPA1 proteins were all significantly reduced （P＜0.05）. There were abnormal membrane tissue structure in various layers of myocardial tissue， degeneration and necrosis of myocardial cells， and severe fibrosis； the mitochondria were swollen， with reduced or absent cristae， and uneven matrix density. After intervention with Qiangxin decoction， the levels of the aforementioned quantitative indicators in serum and myocardial tissue of rats （excluding CL content in the Qiangxin decoction low- dose group） were significantly reversed （P＜0.05）； the pathological damage of myocardial tissue had significantly improved， fibrosis had significantly reduced， mitochondrial morphology tended to be normal， cristae had increased， and matrix density was uniform. CONCLUSIONS Qiangxin decoction can regulate myocardial mitochondrial function and structural integrity of CHF rats， thereby improving myocardial energy metabolism and antagonizing myocardial fibrosis， the mechanism of which may be associated with activating PA/Mfn/CL signaling pathway.

OBJECTIVE To investigate the effects of Qiangxin decoction on myocardial mitochondrial and energy metabolism in rats with chronic heart failure （CHF） based on mitophagy. METHODS Male SD rats were collected to establish CHF model by ligating the left anterior descending branch of coronary artery. The successful modeling rats were divided into model group， Qiangxin decoction group [12.25 g/（kg·d）， calculated by crude drug]， captopril group [10.38 mg/（kg·d）]， and Qiangxin decoction+captopril group （the same usage and dosage as single drug group） according to a random number table method， with 8 rats in each group. Another 8 normal rats were selected and received threading in the left anterior descending branch of the coronary artery without ligation as the sham operation group. Starting from the second day after successful modeling， the rats in administration groups were given relevant drug intragastrically， twice a day， for consecutive 28 days. After the last medication， the levels of adenosine triphosphate （ATP）， adenosine monophosphate （AMP） and free fatty acid （FFA） in infarcted myocardial tissues were detected， the pathological changes and mitochondrial morphology of the infarcted myocardial tissue were observed， as well as the protein expressions of B cell lymphoma-2 （Bcl-2）， Bcl-2 related X protein （Bax）， TANK-binding kinase 1 （TBK1）， p62 were detected in each group. RESULTS Compared with the sham operation group， the infarcted myocardial tissue fibrosis was changed evidently， with a large number of mitochondrial swelling and fusion， and internal cristae rupture； the levels of AMP and FFA， the protein expressions of Bax and p62 were all increased or up-regulated significantly in infarcted myocardial tissue， while the level of ATP， and the protein expressions of Bcl-2 and TBK1 were all decreased or down-regulated significantly （P＜0.05）. Compared with the model group， the pathological changes of infarcted myocardial tissue and mitochondrial swelling had been improved； the levels of AMP and FFA， and the protein expressions of Bax and p62 in infarcted myocardial tissue were significantly decreased or down-regulated in administration groups， while the level of ATP， and the protein expressions of Bcl-2 and TBK1 were increased or up-regulated significantly （P＜0.05）. And the effect of Qiangxin decoction+captopril group was better than that of single drug group. CONCLUSIONS Qiangxin decoction can alleviate myocardial fibrosis and mitochondrial swelling in CHF rats， and improve their myocardial energy metabolism， which may be related to regulating the expression of Bcl-2， Bax， TBK1 and p62 proteins and promoting myocardial mitophagy.

Objective To explore the clinical significance of long non-coding RNA(lncRNA)VIM-AS5 expres-sion in human breast cancer tissues and its regulatory mechanism involved in cancer cell proliferation and mi-gration.Methods The Lnc2Cancer 3.0 database was used to analyze the expression of VIM-AS5 in breast cancer tissues and its correlation with the clinical stage and survival time of breast cancer patients.RT-qPCR was used to detect the expression of VIM-AS5 in breast cancer cell lines BT-549,MDA-MB-435,MDA-MB-231 and CAL-51.Plasmid with VIM-AS5 overexpression and negative control were all transfected into CAL-51 cells through liposome recorded as VIM-AS5 group and NC group,respectively.The proliferation and migration of CAL-51 cells were detected by colony formation assay and scratch healing method,respectively.Dual-lucif-erase reporter gene experiment verified the targeting relationship between VIM-AS5 and miR-500a.RT-qPCR was used to detect the expression of miR-500a in CAL-51 cells.Western blot was used to detect the expression of JAK/STAT3 pathway in CAL-51 cells.Results The expression of VIM-AS5 in breast cancer tissues was significantly lower than that in adjacent tissues(P＜0.01).VIM-AS5 expression was negatively correlated with the clinical stage of breast cancer patients(P＜0.01).The survival time of breast cancer patients with low VIM-AS5 expression was significantly shorter than that of breast cancer patients with high VIM-AS5 ex-pression(P＜0.01).Compared with mammary epithelial cell line MCF-10 A cells,VIM-AS5 expression was significantly reduced in breast cancer cells(P＜0.01).The counting number of colony formed in the VIM-AS5 group was significantly lower than that in the NC group(P＜0.01).The cell migration rate in the VIM-AS5 group was significantly lower than that in the NC group(P＜0.01).Dual-luciferase reporter gene experiment confirmed that miR-500a was the target gene of VIM-AS5(P＜0.01).VIM-AS5 can negatively regulate the expression of miR-500a(P＜0.01).Compared with the NC group,the expression of JAK/STAT3 pathway proteins JAK,p-STAT3,c-Myc,Bcl-2,and CDK3 in CAL-51 cells of the VIM-AS5 group were significantly decreased.Conclusions VIM-AS5 is low-expressed in breast cancer cells,and up-regulation of VIM-AS5 may inhibit the proliferation and migration of breast cancer cells CAL-51 by targeting at miR-500a/JAK/STAT3 pathway.

Hypertension is a common cardiovascular disease. At present， the prevalence and mortality of hypertension in China continue to rise， the morbidity and mortality of complications remain high. The continuous increase of blood pressure can cause damage to multiple target organs such as heart， brain， kidney and blood vessels. This article reviews the research progress of signal pathways related to the prevention and treatment of hypertension target organ damage by traditional Chinese medicine， and summarizes six signal pathways related to RhoA/ROCK， renin-angiotensin-aldosterone system， endothelin-1/nitric oxide， transforming growth factor-β1/Smads， phosphatidylinositide 3-kinases/protein kinase B， and Toll-like receptor 4/nuclear transcription factor-κB， in order to provide theoretical evidence for further research on clinical diagnosis and treatment of hypertension and its target organ damage.

Third-degree atrioventricular block is a severe bradyarrhythmia， for which there is no proven effective drugs currently. Permanent pacemaker implantation recommended by the guideline， however， is not suitable for most patients. This paper reported on a case of third-degree atrioventricular block after cardiac radiofrequency ablation who has been treated with the method of boosting qi， warming yang and unblocking collaterals. The TCM syndrome of this case was diagnosed as yang qi depletion and phlegm-stasis blocking the collaterals， for which Baoyuan Decoction and Mahuang Fuzi Xixin Decoction （保元汤合麻黄附子细辛汤） in modification has been used to boost qi， warm yang and raise the sunken， dissolve phlegm， invigorate blood and unblock collaterals. After nearly 7-month treatment， the symptoms such as palpitations， shortness of breath and fatigue were basically cured， and the electrocardiogram returned to the normal.

ObjectiveTo reveal the targets and molecular mechanisms of the action of Qiangxin Decoction （强心汤） for the treatment of chronic heart failure based on the combination of network pharmacology and molecular docking. MethodsThe active ingredients of Qiangxin Decoction were retrieved from TCMSP database， and the targets of chronic heart failure were screened by searching GeneCards， OMIM， TTD， PharmGkb， and DrugBank databases， and the intersections were taken to obtain the intersecting targets of Qiangxin Decoction for the treatment of chronic heart failure. STRING platform was used to construct the protein-protein interaction network （PPI）， Cytoscape 3.8.0 software was used to calculate the network topology to screen the core targets， and R 4.2.3 was used to construct the “active ingredient-target” network by analyzing the GO enrichment analysis and KEGG pathway enrichment analysis. AutoDock 1.5.7 was used for molecular docking to predict the binding performance of active ingredients and core targets. ResultsSeventy-five intersecting targets were identified for the treatment of chronic heart failure with Qiangxin Decoction， among which the core targets were estrogen receptor 1 （ESR1， degree value=7）， nuclear receptor coactivator 1 （NCOA1， degree value=8）， glucocorticoid receptor （NR3C1， degree value=7）， and nuclear receptor coactivator 2 （NCOA2， degree value=7）. GO enrichment analysis showed that the top 3 items with the smallest P value in molecular function were G protein-coupled amine receptor activity， postsynaptic neurotransmitter receptor activity， and neurotransmitter receptor activity （P＜0.01）； the top 3 items with the smallest P value in biological process were adenylyl cyclase-activated adrenergic receptor signaling pathway， adrenergic receptor signaling pathway， and adenylyl cyclase-regulated G protein-coupled receptor signaling pathway （P＜0.01）； the top 3 items with the smallest P values in cellular composition were components of the postsynaptic membrane， synaptic membrane， and presynaptic membrane （P＜0.01）. KEGG enrichment analysis showed that the top 5 key signaling pathways were neuroactive ligand-receptor interactions， calcium signaling pathway， dopaminergic synapses， cocaine addiction， and cyclic guanosine monophosphate-protein kinase G （cGMP-PKG） signaling pathway. The molecular docking results showed that lignans and isoflavones had lower binding energies and more structural stability with the four core targets （ESR1， NCOA1， NR3C1， NCOA2）. ConclusionThe treatment of chronic heart failure by Qiangxin Decoction was associated with neuroactive ligand-receptor interactions， calcium signaling pathway， dopaminergic synapses， chemoattractant-receptor activation， cGMP-PKG signaling pathway， lipids and atherosclerosis， and cAMP signaling pathway， and lignans and isoflavones may be the core active compounds in its treatment of chronic heart failure.

Objective To verify the molecular mechanism of Qiangxin Decoction in treating CHF,which was created by Professor Lu Jianqi,a famous old Chinese medicine and Qihuang scholar in Guangxi,based on network pharmacological methods,molecular docking technology and animal experiments.Methods Firstly,TCMSP database and related literatures were searched to find the important compounds of Qiangxin decoction;Through TCMSP database and STITCH database,find the target of Qiangxin Tang;Get the main target points of CHF with the help of GeneCards,DisGeNET,OMIM and other databases;The Venny platform was selected to obtain the intersection target of the two;Using STRING platform and Cytoscape 3.6.1,build a"component target"network and a PPI network of Qiangxin Tang target CHF target;The DAVID 6.8 database was used for GO enrichment analysis and KEGG pathway enrichment analysis;Use AutoDock Vina software for molecular docking.Finally,the model of CHF after AMI was established by ligating the anterior descending branch of left coronary artery in rats,and the expression of core target protein was detected by Western blot.Results 185 important active components including quercetin,kaempferol,luteolin,tanshinone iia and naringenin were obtained from the analysis of network pharmacological results.The core targets were signal transduction and transcription activation factor 3(STAT3),mycobacterium tuberculosis regulatory protein(RELA),phosphorylated protein kinase 1(AKT1)100 therapeutic targets,such as mitogen activated protein kinase 1(MAPK1)and interleukin-6(IL-6),preliminarily indicate that Qiangxin decoction may regulate cytokine mediated signal pathway,positive regulation of gene expression,response to hypoxia The reaction to lipopolysaccharide,drug and other biological processes play a role in the treatment of CHF.The results of molecular docking showed that the important compounds of Qiangxin Tang had strong binding ability to the core target;The results of animal experiments showed that the components of Qiangxin decoction could significantly reduce the phosphorylation expression level of STAT3 protein and MAPK1 protein and the expression level of IL6 protein(P<0.05).The high dose group of Qiangxin Decoction was slightly better than the low dose group.Conclusion This study preliminarily clarified that Qiangxin decoction can play a role in treating CHF by reducing the phosphorylation of STAT3 protein and MAPK1 protein and the expression level of IL6 protein,and also verified that Qiangxin decoction has the characteristics of multiple components,multiple targets,and multiple ways of synergistic effect in treating CHF.Animal experiments provide experimental theoretical basis for clinical doctors to treat CHF and further research.

ObjectiveChronic heart failure （CHF） is the terminal stage of cardiovascular disease. The adverse cardiovascular events of CHF patients with weakness have increased significantly. Traditional Chinese medicine （TCM） has a good effect on CHF. However，there are few reports on the clinical observation of the treatment of CHF with weakness in elderly patients by TCM combined with conventional health-preserving exercises. This study aimed to explore the clinical efficacy of Qiangxin decoction combined with Baduanjin in the treatment of elderly patients with CHF and weakness. MethodSixty CHF patients with Qi deficiency，blood stasis，and water retention syndrome admitted to the Cardiovascular Department of the First Affiliated Hospital of Guangxi University of Chinese Medicine from January 2020 to December 2021 were enrolled. The patients in the control group were treated with conventional western medicine according to the guidelines，while those in the treatment group received additional Qiangxin decoction and Baduanjin exercise based on the therapeutic protocol of the control group. The levels of serum N-terminal B-type brain natriuretic peptide precursor （NT-proBNP），creatine kinase （CK），lactate dehydrogenase （LDH），free fatty acid （FFA），left ventricular ejection fraction （LVEF），left ventricular end-diastolic dimension （LEVDD），6-minute walk distance （6MWD），Minnesota Living with Heart Failure Questionnaire （MLHFQ）， and Tilburg Frailty Indicator （TFI） scores of the two groups were observed before and one month after treatment. At the same time，the re-admission within three months was compared between the two groups. ResultThere was no significant difference between the two groups in terms of the general data and the therapeutic indexes before treatment. After treatment，the NT-proBNP，CK，LDH，FFA，LVEDD，MLHFQ， and TFI scores of the two groups were lower than those before treatment（P<0.05，P<0.01）， and the LVEF and 6MWD were higher（P<0.05，P<0.01）. The efficacy of the treatment group was superior to that of the control group after treatment （P<0.05，P<0.01）. The re-admission rate within three months in the treatment group was 7.1% （2/28）， lower than 30.8% （8/26） in the control group （χ²=4.897，P<0.05）. ConclusionQiangxin decoction combined with Baduanjin is helpful to improve the body energy metabolism，heart function，quality of life，and weakness level of elderly CHF patients with weakness， and reduce the rate of re-admission.

Artemisinin is a sesquiterpene lactone containing a peroxide group isolated from the plant Artemisia annua. It has antimalarial activity and is effective for the treatment of malaria. With the deepening of research on artemisinin， the pharmacological effects of artemisinin and its derivatives in other systems have gradually become a research hotspot. This article reviews the research progress of artemisinin and its derivatives in the prevention and treatment of cardiovascular diseases. Artemisinin and its derivatives in the prevention and treatment of cardiovascular disease have shown anti-atherosclerosis， lipid- lowering， inhibition of vascular remodeling， reducing vascular pressure， improving ventricular remodeling， anti-arrhythmia， protection of vascular endothelium， prevention and treatment of diabetic cardiovascular complications and protection of myocardial cells and other pharmacological effects. It provides a new treatment strategy for common cardiovascular diseases such as hypertension， arrhythmia， coronary heart disease complications after stent implantation， hyperlipidemia， etc. However， there are few studies on the antiplatelet aggregation and antithrombotic effects of artemisinin and its derivatives， the molecular mechanisms behind many pharmacological effects have not yet been clarified， and there is little clinical application. A large number of basic studies and clinical trials are still needed to answer these questions.