Chronic heart failure （CHF） is a complex clinical syndrome caused by ventricular dysfunction， with mitochondrial energy metabolism disorder being a critical factor in disease progression. Heart-Yang deficiency syndrome， as the core pathogenesis of CHF， persists throughout the disease course. Insufficiency of heart-Yang leads to weakened warming and propelling functions， resulting in the accumulation of phlegm-fluid， blood stasis， and dampness. This eventually causes Qi stagnation with phlegm obstruction and blood stasis with water retention， forming a vicious cycle that exacerbates disease progression. According to the theory of reinforcing Yang， the clinical experience of the traditional Chinese medicine （TCM） master Tang Zuxuan in treating CHF with heart-Yang deficiency syndrome， and achievements from molecular biological studies， this study innovatively proposes an integrated research framework of "TCM syndrome differentiation and staging-mitochondrial metabolism mechanisms-intervention with Yang-reinforcing prescriptions" which is characterized by the integration of traditional Chinese and Western medicine. Heart-Yang deficiency syndrome is classified into mild （Stage Ⅰ-Ⅱ）， severe （Stage Ⅲ）， and critical （Stage Ⅳ） stages. The study elucidates the precise correlations between the pathogenesis of each stage and mitochondrial metabolism disorders from theoretical， pathophysiological， and therapeutic perspectives. The mild stage is characterized by impaired biogenesis and substrate-utilization imbalance， corresponding to heart-Yang deficiency and phlegm-fluid aggregation. Linggui Zhugantang and similar prescriptions can significantly improve the expression of peroxisome proliferator-activated receptor gamma co-activator-1α（PGC-1α）/silent information regulator 2 homolog 1 （SIRT1） and ATPase activity. The severe stage centers on oxidative stress and structural damage， reflecting Yang deficiency with water overflow and phlegm-blood stasis intermingling. At this stage， Zhenwu Tang and Qiangxin Tang can effectively mitigate oxidative stress damage， increase adenosine triphosphate （ATP） content， and repair mitochondrial structure. The critical stage arises from calcium overload and mitochondrial disintegration， leading to the collapse of Yin-Yang equilibrium. At this stage， Yang-restoring and crisis-resolving prescriptions such as Fuling Sini Tang and Qili Qiangxin capsules can inhibit abnormal opening of the mitochondrial permeability transition pore （MPTP）， reduce cardiomyocyte apoptosis rate， and protect mitochondrial function. By summarizing the characteristics of mitochondrial energy metabolism disorders at different stages of CHF， this study explores the application of the theory of reinforcing Yang in treating heart-Yang deficiency syndrome and provides new insights for the clinical diagnosis and treatment of CHF.

ObjectiveTo explore the mechanism of ventricular remodeling mediated by the p38 mitogen-activated protein kinase （MAPK）/nuclear factor kappa B （NF-κB） signaling pathway in the rat model of chronic heart failure （CHF） with heart-blood stasis syndrome， as well as the intervention effect of Danhong injection. MethodsIn vivo experiment： SPF-grade male SD rats were assigned via the random number table method into 4 groups： Sham operation， model， captopril （8.8 mg·kg^-1）， and Danhong injection （6.0 mL·kg^-1）. The model of CHF with heart-blood stasis syndrome was established by abdominal aortic constriction， and the sham operation group only underwent laparotomy without constriction. All the groups were treated continuously for 15 days. The tongue color of rats was observed. Echocardiography， hemorheology， heart mass index （HMI）， and left ventricular mass index （LVMI） were measured. Hematoxylin-eosin （HE） staining and Masson staining were performed to observe the pathological and fibrotic changes of the myocardial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to quantify the levels of N-terminal pro-B-type natriuretic peptide （NT-proBNP）， interleukin-6 （IL-6）， angiotensin Ⅱ （AngⅡ）， tumor necrosis factor-α （TNF-α）， and Creactive protein （CRP） in the serum， as well as the levels of matrix metalloproteinase-2 （MMP-2） and matrix metalloproteinase-9 （MMP-9） in the myocardial tissue. Western blot was used to quantify the protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 in the myocardial tissue. In vitro experiment： H9C2 cardiomyocytes were treated with 1×10^-6 mol·L^-1 AngⅡ to establish a model of myocardial hypertrophy. H9C2 cardiomyocytes were allocated into normal， model， inhibitor + Danhong injection， Danhong injection （20 mL·L^-1）， and inhibitor （SB203580， 5 μmol·L^-1） groups. CCK-8 assay was used to detect the viability of H9C2 cardiomyocytes. Rhodamine-labeled phalloidin staining was used to reveal the area of cardiomyocytes. Real-time PCR was performed to determine the mRNA levels of atrial natriuretic peptide （ANP） and brain natriuretic peptide （BNP）. Western blot was used to assess the protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65. ResultsIn vivo experiment： Compared with the sham operation group， the model group showed purplish-dark tongue with decreased R， G， B values of the tongue surface （P<0.01）， increased whole blood viscosity （at low， medium， and high shear rates） （P<0.01）， decreased left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01）， increased left ventricular end-diastolic diameter （LVIDd）， left ventricular end-systolic diameter （LVIDs）， and left ventricular posterior wall thickness at end-diastole （LVPWd） （P<0.01）， raised LVMI and HMI （P<0.01）， and elevated levels of NT-proBNP， TNF-α， IL-6， and CRP in the serum and MMP-2 and MMP-9 in the myocardial tissue （P<0.01）. The HE and Masson staining of the myocardial tissue showed compensatory myocardial hypertrophy， fibrosis， and massive inflammatory cell infiltration in the model group. Additionally， the model group presented up-regulated protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 in the myocardial tissue （P<0.01）. Compared with the model group， each administration group showed increased R， G， B values of the tongue surface （P<0.05， P<0.01）， decreased whole blood viscosity （at low， medium， and high shear rates） （P<0.05， P<0.01）， increased LVEF and LVFS （P<0.01）， decreased LVIDd， LVIDs， and LVPWd （P<0.05， P<0.01）， declined LVMI and HMI （P<0.05， P<0.01）， and lowered levels of NT-proBNP， TNF-α， IL-6， and CRP in the serum and MMP-2 and MMP-9 in the myocardial tissue （P<0.01）. HE and Masson staining showed alleviated compensatory myocardial hypertrophy， reduced fibrosis， and decreased expression of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 in the myocardial tissue （P<0.01）. In vitro experiment： When the concentration of Danhong injection reached 20 mL·L^-1， the survival rate of H9C2 cardiomyocytes was the highest （P<0.01）. Compared with the normal group， the model group showed up-regulated mRNA levels of ANP and BNP （P<0.01）， increased relative cell surface area （P<0.01）， and raised protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 （P<0.01）. Compared with the model group， each administration group showed down-regulated mRNA levels of ANP and BNP （P<0.01）， reduced relative cell surface area （P<0.05， P<0.01）， and down-regulated protein levels of p-p38 MAPK/p38 MAPK and p-NF-κB p65/NF-κB p65 （P<0.05， P<0.01）. ConclusionDanhong injection can regulate ventricular remodeling through the p38 MAPK/NF-κB pathway， thereby exerting a protective effect on the rat model of CHF with heart-blood stasis syndrome.

ObjectiveTo investigate the incidence and influencing factors of posttraumatic stress disorder （PTSD） three months after a traffic accident， and to explore the role of social support and coping strategies. MethodsA total of 117 individuals exposed to trauma following road traffic accidents were recruited. General demographic and clinical information was collected within one week， and the hamilton anxiety rating scale （HAMA）， the hamilton depression rating scale-24 （HAMD-24）， the social support rating scale （SSRS）， and the simplified coping style questionnaire （SCSQ） were administered. A 3-month follow-up was subsequently conducted， during which PTSD symptoms were assessed using the post-traumatic stress disorder checklist for DSM-5 （PCL-5）. Participants were divided into a PTSD group and a non-PTSD group according to whether PTSD occurred. Between-group comparisons were performed using the Mann-Whitney U non-parametric test or the χ² test， as appropriate. Spearman correlation analysis was used to examine the associations between general characteristics and PCL-5 scores. Binary Logistic regression was applied to identify factors influencing PTSD， and receiver operating characteristic （ROC） curve analysis was conducted to evaluate the diagnostic value of the SCSQ and SSRS. ResultsDuring the 3-month follow-up of the 117 trauma-exposed individuals， 17 cases developed PTSD， with a higher proportion of females （70.59%）. Between-group comparisons showed that， compared with the PTSD group， the non-PTSD group had higher scores for positive coping， objective support， and subjective support （P<0.05）， and lower scores for negative coping， HAMA， HAMD， and PCL-5 （P<0.05）. Correlation analysis indicated that female gender， negative coping， and higher HAMA and HAMD scores were associated with greater PTSD severity. Logistic regression analysis demonstrated that educational level （OR=1.715， 95% CI： 1.020-2.883， P=0.042） and negative coping （OR=1.590， 95% CI： 1.003-2.522， P=0.048） were risk factors for PTSD， whereas objective support （OR=0.646， 95% CI： 0.451-0.925， P=0.017） was a protective factor. The ROC analysis showed that the total SCSQ score and its negative and positive coping dimensions， the total SSRS score and its subjective and objective support dimensions， as well as their combined use， all demonstrated good discriminative ability in distinguishing between the PTSD and non-PTSD groups. ConclusionThe results suggest that individuals who are female， with higher HAMA and HAMD scores after a motor vehicle accident， and those with lower social support and negative coping strategies， should be given particular attention. Early interventions for these individuals may reduce the incidence of PTSD.

Objective This study reports on the obligatory parasitism of water mites Arrenurus sp. on Anopheles messeae at the Manzhouli Port, Inner Mongolia, China. Methods Duing July 2024, a survey on the mosquito diversity was conducted at the Manzhouli Port. Captured mosquitoes and their ectoparasites were identified to species level. Results A total of 1840 adult mosquitoes were collected, representing species from three genera: Culex(Cx. modestus, Cx. pipiens pallens), Aedes(Ae. dorsalis, Ae. flavidorsalis, Ae. flavescens), and Anopheles (An. messeae). Among all the mosqutioes specimens,3 out of 150 captured An. messeae were found to carry ectoparasitic mites, with number of 2,4,27 mites separately. Morphological and molecular identification reached the same result as water mites(Hydrachnidiae, Hydracrina). COI gene sequence showed 94% similarity with the closest species Arrenurus truncatellus. Conlusions Literature review suggests water mites are host-specific parasitism of mosquito species and herein with the first record of Arrenurus sp. parasiting on An. Messeae in the most high-latitude region globally.

ObjectiveTo investigate the impact of a cold environment on the pathophysiological changes in dogs after abdominal gastrointestinal blast injury. MethodsEight healthy common-grade adult male Beagles were selected and randomly divided into a cold group and a normal temperature group, with 4 dogs in each group. Prior to surgery, Beagles dogs were fasted and deprived of water for 12 hours; after establishing a vein at the edge of the ear, propofol （2 mg·kg^-1·min^-1） was continuously infused using a microinfusion pump to maintain anesthesia. Tracheal intubation was performed while preserving spontaneous breathing, and the electroencephalogram bifrequency index was maintained at 40-60 to ensure stable anesthesia. A model of abdominal gastrointestinal blast injury in Beagle dogs was established using a multifunctional combat trauma modeling platform. After blast injury, the cold group was exposed to a cold chamber at -20 ℃ combined with 10% body surface area ice water immersion for 40 min, while the normal temperature group was kept in an environment at (25±2) ℃ for 40 min after blast injury. Vital signs such as heart rate, blood pressure, and blood oxygen saturation were monitored in both groups before blast injury, immediately after blast injury, and 40 min after blast injury. And arterial blood gas parameters, including pH, partial pressure of oxygen in arterial blood (PaO₂), partial pressure of carbon dioxide in arterial blood (PaCO₂), actual bicarbonate radical (HCO₃^-), lactic acid (Lac), and blood base excess (BEb), were measured. After the experiment, gastrointestinal tissues (gastric antrum and upper jejunum 5 cm distal to the suspensory ligament of the duodenum) were harvested for pathological analysis via hematoxylin-eosin (HE) staining combined with semi-quantitative scoring. ResultsPhysiological indicators showed that the body temperature of the cold group was significantly lower than that of the normal temperature group (P<0.01), and the heart rate and systolic blood pressure of the cold group were significantly higher than those of the normal temperature group (P<0.000 1). PaCO₂ was markedly elevated and BEb was markedly decreased in the cold group relative to the normal temperature group (P<0.000 1), suggesting aggravated respiratory acidosis and metabolic acidosis. Pathological analysis showed that gastro-intestinal tissue damage was more severe in the cold group: the gastric mucosal epithelial shedding rate was > 60% (vs. <25% in the normal temperature group), the necrosis rate of the epithelial cells at the tips of intestinal villi reached more than 70% (vs. < 30% in the normal temperature group), and inflammatory cell infiltration involved the submucosa (vs. limited to the superficial mucosa in the normal temperature group). The semi-quantitative scoring results were consistent with the pathological analysis results, further confirming that the cold environment exacerbated gastrointestinal tissue damage caused by abdominal gastrointestinal blast injury. ConclusionA cold environment can exacerbate circulatory dysfunction and gastrointestinal tissue damage in Beagle dogs after blast injury, providing experimental evidence for early rewarming intervention for combat trauma in cold regions.

Objective To explore the validity and feasibility of the left transthoracic and esophageal hiatal approach for Siewert type Ⅱ adenocarcinoma of the esophagogastric junction under a single position.Methods The clinical data of 64 patients with Siewert type Ⅱ AEG(single position transthoracic approach group)treated with the left transthoracic and esophageal hiatal approach under a single position and 56 patients with the laparoscopic transesophageal slit approach(transabdominal approach group)in the Department of Thoracic Surgery,Huaihe Hospital of Henan University,from January 2017 to December 2018 were retrospectively analyzed.The clinical and pathological data,perioperative indicators(operation time,intraoperative blood loss,postoperative first ambulation time,postoperative first peristalsis time,postoperative drainage volume at 3 d,incidence of postoperative complications,postoperative hospital stay),postoperative complications(positive surgical margin,proximal esophageal resection margin,tumor diameter,total number of dissected lymph nodes,positive lymph node dissection rate,postoperative histopathology,and TNM staging of tumor pathology),and survival indicators(tumor recurrence and metastasis rate and survival at 1 month,3 months,6 months,1 year,3 years,5 years after surgery)were compared between the two groups.Kaplan-Meier method was used to analyze the postoperative survival rate of the two groups.Univariate analysis using χ2 test was employed to analyze factors influencing 5-year postoperative survival rate in Siewert type Ⅱ AEG patients.Results No significant difference was observed in clinical and pathological data,such as gender,age,American Society of Anesthesiologists(ASA)grade,tumor differentiation,pTNM stage,and tumor diameter between the two groups(P>0.05).No significant differences were noted in intraoperative blood loss,incidence of postoperative complications,and survival rates at 1 month,3 months,6 months,1 year,and 3 years after surgery between the two groups(P>0.05).The single position transthoracic approach group exhibited a higher postoperative drainage volume at 3 d compared to the transabdominal approach group(P<0.001),a shorter surgical time(P<0.001),a longer time to first mobilization,first intestinal peristalsis,and hospital stay after surgery(P<0.01),a longer proximal esophageal margin(P<0.001),a higher total number of lymph node dissections(P<0.001),and a higher positive lymph node dissection rate(P<0.05)than the transabdominal approach group.The 5-year recurrence-free survival rate of the single position transthoracic approach group was higher than that of the transabdominal approach group,with a statistically significant difference(P=0.013).The Kaplan-Meier survival curve showed no statistically significant difference in the 5-year overall survival rate between the two groups of patients after surgery(P=0.456).The results of univariate analysis indicated that there are significant relationships between tumor differentiation degree,pTNM stage,tumor diameter,and lymph node positivity rate with the 5-year postoperative survival rate in Siewert type Ⅱ AEG patients(P<0.05).Conclusion Siewert type Ⅱ AEG patients can be treated with the left transthoracic and esophageal hiatal approach under a single position,achieving the same effect as laparoscopic transesophageal slit approach,and it can be actively promoted as a complementary choice of operation in the clinic.

Objective To investigate the effect of up-regulating tumor necrosis factor alpha induced protein 3(TNFAIP3)expression on hippocampal neurons in mice with cerebral ischemia-reperfusion.Methods The mice were randomly divided into 6 groups:sham group,sham empty vector group(sham-),sham TNFAIP3 high expression group(sham+),model group,model empty vector group(model-),model TNFAIP3 high expression group(model+).A mouse model of middle cerebral artery occlusion and cerebral ischemia-reperfusion was established using the suture method.After the successful establishment of the model,lentivirus was injected into the hippocampus 24 hours later.Two weeks later,samples were collected and Western blotting was used to detect the expressions of TNFAIP3 and ERK signaling pathway proteins.The changes in ischemic area were observed by 2,3,5-triphenyltetrazolium chloride(TTC)staining;HE staining was used to observe the morphological changes of hippocampal neurons,and ELISA was used to detect the expressions of lipoprotein-associated phospholipase A2(Lp-PLA2)and interleukin(IL)-8.Results The results of Western blotting indicated that the TNFAIP3 expression in the model group decreased significantly compared with the sham group(P＜0.05);Compared with the model group,there was no significant change in TNFAIP3 expression in the model-group(P＞0.05);The TNFAIP3 expression in the model+group increased significantly compared with the model group and model-group(P＜0.05).Compared with the sham group,the results of the sham+group showed that the ischemic area had no significant changes in TTC staining,and there were no significant changes in hippocampal neuronal morphology,and the expressions ERK signaling pathway proteins,Lp-PLA2 and IL-8(P＞0.05);Compared with the sham-and sham+groups,the model group showed an increase in ischemic area,significant damage to hippocampal neurons,a decrease in the number of Nissl bodies,and a significant increase in the expressions of ERK signaling pathway proteins,Lp-PLA2,and IL-8(P＜0.05);Compared to the model-group,the model+group showed a decrease in ischemic area,an increase in the number of neurons in the hippocampus and the number of Nissl bodies,and a significant decrease in the expressions of ERK signaling pathway proteins,Lp-PLA2,and IL-8(P＜0.05).Conclusion Up-regulation of TNFAIP3 may be one of the methods for repairing hippocampal neuronal damage caused by cerebral ischemia reperfusion.

The efficacy of Xiangmei Pills on rats with ulcerative colitis(UC) was investigated by characterizing the spectrum of the active chemical components of Xiangmei Pills. Rapid identification and classification of the main chemical components were performed,and the therapeutic effects of Xiangmei Pills on the proteins and intestinal flora of UC rats were analyzed to explore the mechanism of its action in treating UC. Fifty SD rats were acclimatized to feeding for 3 d and randomly divided into blank group, model group,mesalazine group(0. 4 g·kg~(-1)), low-dose group of Xiangmei Pills(1. 89 g·kg~(-1)), and high-dose group of Xiangmei Pills(5. 67 g·kg~(-1)), with 10 rats in each group. 5% dextrose sodium sulfate(DSS) was given by gavage to induce the male SD rat model with UC,and the corresponding medicinal solution was given by gavage after 10 days, respectively. The therapeutic effect of Xiangmei Pills on rats with UC was evaluated according to body mass, disease activity index(DAI), and hematoxylin-eosin(HE) staining, and the histopathological changes in the colon were observed. Ultra-high performance liquid chromatography-quadrupole/electrostatic field orbitrap high-resolution mass spectrometry(UHPLC-Q-Orbitrap HRMS) technique was used to rapidly and accurately identify the main chemical constituents of Xiangmei Pills. Immunohistochemistry was used to detect the expression of aryl hydrocarbon receptor(AhR),interferon-γ(IFN-γ), mucin-2(MUC-2), and cytochrome P450 1A1(CYP1A1) in colon tissue. Interleukin-22(IL-22) expression in colon tissue was detected by immunofluorescence. The 16S r DNA high-throughput sequencing technique was used to study the modulatory effects of Xiangmei Pills on the intestinal flora structure of rats with UC. Pharmacodynamic results showed that compared with that of the blank group, the colon tissue of the model group was congested, and ulcers were visible in the mucosa; compared with that in the model group, the histopathology of the colon of the rats with UC in the groups of Xiangmei Pills were improved, with scattered ulcers and reduced inflammatory cell infiltration. Chemical analysis showed that a total of 45 components were identified by mass spectrometry information, including 15 phenolic acids, 8 coumarins, 15 organic acids, 3 amino acids, 2 flavonoids, and 2 other components. Compared with those in the blank group, the levels of Ah R, CYP1A1, MUC-2, and IL-22 proteins in the colon tissue of rats in the model group were significantly decreased, and the level of IFN-γ protein was significantly increased; the intestinal flora of rats in the model group was disorganized, with a decrease in the abundance of the flora; the relative abundance of Bacteroidetes,unclassified genera of Ascomycetes, Prevotella of the Prevotella family, and Prevotella decreased significantly, and that of Firmicutes decreased, but the difference was not statistically significant. The relative abundance of Bacteroidetes, Bifidobacterium, and Lactobacillus increased significantly. Compared with those of the model group, the levels of Ah R, CYP1A1, MUC-2, and IL-22proteins in the colonic tissue of the groups of Xiangmei Pills were significantly higher, and the levels of IFN-γ proteins were significantly lower. The recovery of the intestinal flora was accelerated, and the diversity of the intestinal flora was significantly increased. The relative abundance of Bacteroidetes was significantly increased, and that of unclassified genera of Ascomycetes,Lactobacillus, Prevotella of the Prevotella family, and Prevotella was significantly increased. The relative abundance of Bacteroidetes and Bifidobacterium was significantly decreased. This study demonstrated that Xiangmei Pills can effectively treat UC, mainly through the phenolic acid and organic acid components to stimulate the intestinal barrier, regulate protein expression and the relative abundance and diversity of intestinal flora, and play a role in the treatment of UC.
Animals ; Colitis, Ulcerative/metabolism* ; Drugs, Chinese Herbal/chemistry* ; Rats, Sprague-Dawley ; Male ; Rats ; Gastrointestinal Microbiome/genetics* ; Chromatography, High Pressure Liquid ; Humans ; Mass Spectrometry ; RNA, Ribosomal, 16S/genetics* ; Bacteria/drug effects*

ObjectiveTo investigate the effects of Danhong injection on mitochondrial dynamics， morphology， and function in the rat model of chronic heart failure by mediating the adenosine 5'-monophosphate （AMP）-activated protein kinase （AMPK）/dynamin-related protein 1 （Drp1） pathway. MethodsFrom 75 SD rats， 15 rats were randomly selected as the sham group， and the remaining 60 rats were used to prepare a rat model of chronic heart failure by abdominal aortic constriction （AAC）. The modeled rats were randomly allocated into model， Danhong Injection （6 mL·kg^-1）， and captopril （8.8 mg·kg^-1） groups and administrated with corresponding agents for 15 consecutive days. The levels of N-terminal pro-brain natriuretic peptide （NT-pro BNP）， adenosine diphosphate （ADP）， adenosine triphosphate （ATP）， interleukin （IL）-6， IL-1β， and tumor necrosis factor （TNF）-α and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ were determined by enzyme-linked immunosorbent assay. The changes in cardiac function were detected by echocardiography. The ultrastructural changes of myocardial mitochondria were observed by transmission electron microscopy. Western blot was employed to assess the protein levels of AMPK， p-AMPK， Drp1， p-Drp1， optic atrophy 1 （Opa1）， mitofusin （Mfn2）， and fission l （Fis1） in the myocardial tissue. Real-time PCR was performed to determine the mRNA levels of Opa1， Mfn2， and Fis1， and immunohistochemistry to detect the expression of p-AMPK. ResultsCompared with the sham group， the model group showed elevated levels of NT-pro BNP， ADP， TNF-α， IL-6， and IL-1β （P<0.01）， declined ATP level （P<0.01）， weakened activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ （P<0.01）， decreased left ventricular ejection fraction （LVEF） and left ventricular fraction shortening （LVFS） （P<0.01）， and increased left ventricular internal diameter at end-diastole （LVDd） and leaf ventricular internal diameter at end-systole （LVIDs） （P<0.01）. Electron microscopy results showed that the model group presented heavily abnormal myocardial structure， with large areas of myofilament structure destroyed and dissolved， significantly enlarged residual structural gaps， and fragmented mitochondria. Western blot results showed that the model group demonstrated down-regulated protein levels of p-AMPK， Mfn2， and Opa1 （P<0.01） and up-regulated protein levels of p-Drp1 and Fis1 （P<0.01） in the myocardial tissue. Real-time PCR results showed that the model group presented up-regulated mRNA level of Fis1 （P<0.01） and down-regulated mRNA levels of Mfn2 and Opa1 （P<0.01）. Immunohistochemistry results showed reduced expression of p-AMPK in the model group compared with sham group （P<0.01）. Compared with the model group， Danhong injection lowered the levels of NT-pro BNP， ADP， TNF-α， IL-6， and IL-1β （P<0.01）， raised the level of ATP （P<0.01）， increased the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ （P<0.05， P<0.01）， increased the LVEF and LVFS （P<0.01）， decreased the LVDd and LVIDs （P<0.05， P<0.01）， alleviated mitochondrial damage， up-regulated the protein levels of p-AMPK， Mfn2， and Opa1 （P<0.05， P<0.01）， down-regulated the protein levels of p-Drp1 and Fis1 （P<0.01）， reduced the mRNA level of Fis1 （P<0.01）， elevated the mRNA levels of Mfn2 and Opa1 （P<0.05， P<0.01）， and promoted the expression of p-AMPK （P<0.05）. ConclusionDanhong injection repairs the imbalance of mitochondrial dynamics， restores the mitochondrial function， improves the myocardial energy metabolism， and reduces the inflammatory response by regulating the AMPK/Drp1 pathway， thus improving the cardiac function.