Objective: To elucidate the effects of chlorogenic acid (CGA), a bioactive polyphenol compound prevalent in traditional Chinese medicine and various foods, including Lonicera japonica Thunb. (Jin Yin Hua), Eucommia ulmoides Oliv. (Du Zhong Ye), tea, and coffee, on cardiomyocyte ferroptosis and heart failure. Methods: We assessed the effect of CGA on cardiac function using a mouse model of heart failure induced by transverse aortic constriction (TAC). These indicators included the left ventricular ejection fraction (LVEF), fractional shortening (LVFS), end-systolic volume (LVESV), end-diastolic volume (LVEDV), end-systolic diameter (LVESD), and end-diastolic diameter (LVEDD). An isoprenaline hydrochloride (ISO)-induced H9c2 cardiomyocyte cell model was also established, and the cells were treated with various concentrations of CGA. To assess the effect of CGA on ferroptosis in cardiomyocytes, we measured cell viability and evaluated the levels of intracellular reactive oxygen species (ROS), ferrous ions (Fe2+), and lipid peroxidation using fluorescent staining. To clarify the ferroptosis signaling pathway regulated by CGA, western blotting was used to examine the expression of ferroptosis biomarkers, specifically solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), in H9c2 cardiomyocytes and mouse myocardial tissues. Results: CGA significantly enhanced cardiac performance indices such as LVEF, LVFS, LVESV, LVEDV, LVESD, and LVEDD. H9c2 cardiomyocytes exposed to ISO showed decreased cell viability and increased ROS levels, Fe2+ content, and lipid peroxidation levels. However, CGA treatment significantly ameliorated these changes. Additionally, in both H9c2 cardiomyocytes and myocardial tissue obtained from mice with TAC, CGA increased the expression of ferroptosis-related proteins, including SLC7A11 and GPX4. Conclusion CGA has the potential to enhance cardiac function and diminish lipid peroxidation and ROS levels in cardiomyocytes via the SLC7A11/GPX4 signaling pathway. This process alleviates ferroptosis in cardiomyocytes. These results provide new insights into the clinical use of CGA and the management of heart failure.

Objective To explore the protective effects of Yiqi Huoxue Fang(Qi-boosting Blood-activa-ting Formula,YQHXF)on rat myocardium with myocardial infarction and its possible mechanism by ob-serving the effects of YQHXF on necrosis and apoptosis of myocardial cell necrosis.Methods Male SD rats were randomly divided into the sham-surgery group,model group,YQHXF group,and perindopril group.Animal model of myocardial infarction was built by ligating coronary artery on the left anterior de-scending branch.Subsequently,YQHXF group received intragastric administration of Yiqi Huoxue Fang (compound medicine,21 g/kg)once per day,and perindopril group was given perindopril (0.4 mg/kg)once a day;Sham-surgery group and model group received sterile distilled water without drug inter-vention.The blood in abdominal aorta was drawn,and the tissue on the peripheral area of the myocardial infarction was taken at two fixed time points (on the 7 th and 28 th day)after administration.Ultrasonic ech-ocardiography was used to detect changes on cardiac morphology and function in rats:left ventricular e-jection fraction (LVEF),left ventricular short axis ratio (LVFS),left ventricular end systolic diameter (LVIDs),left ventricular end-diastolic diameter (LVIDd);serum superoxide dismutase (SOD),gluta-thione peroxidase (gsh-px),creatine kinase (CK),lactate dehydrogenase (LDH),aspertate amin-otransferase (AST),and troponin (cTnT)were measured with ELISA method.Protein imprinting meth-od (Western Blot)was used to measure cytochrome C (CytC)and protein expression of cysteine aspartic acid and protease-3 (caspase-3)in the border zone of infarcted area.Results On the 7 th day,com-pared with the model group,LVEF and LVFS in YQHXF group and perindopril group decreased without statistical significance(P >0.05).On the 28 th day,compared with the model group,LVEF and LVFS in YQHXF group and perindopril group increased significantly(P >0.05 ).LVIDs and LVIDd decreased markedly(P <0.05);LVIDd in perindopril group decreased sharply (P <0.05),and decrease presen-ted on LVIDs without statistical significace (P >0.05).On the 7 th and 28 th day,compared with the mod-el group,CK-MB,LDH,AST,cTnT in YQHXF group and perindopril group decreased significantly (P<0.05),and SOD,GSH-PX increased significantly.On the 7 th day,protein expression of cytC,caspase-3 decreased significantly in YQHXF group and perindopril group(P <0.05).Conclusion Administra-tion of YQHXF at early stage can effectively improve myocardial infarction on cardiac structure and func-tion in rats with myocardial infarction,improve oxidation resistance of myocardial cell,and inhibit myo-cardial apoptosis and necrosis.

Objective To explore the effect of 14-3-3 β gene on biological behavior ofglioma cell line and its mechanism.Methods Conventional cultured SVGp12,U251,U87 and SHG-44 cell lines and U251 cells silenced by 14-3-3[β-small interfering RNA (siRNA) were collected; real time-PCR and Western blotting were used to detect the 14-3-3β gene and protein expressions in these cells.Conventional cultured U251 cells at logarithmic phase were divided into three groups:experimental group (14-3-3β-siRNA transfection),negative control group (siRNA transfection) and blank control group; 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay was used to assess the proliferation of U251 cells,flow cytometry was used to test the cell apoptosis,and cell migration was analyzed by Transwell chamber assay.Results As compared with those in the normal glial cells,14-3-3β gene and protein expression levels in the glioma cells were significantly higher (P＜0.05); as compared with negative control and blank control groups,U251 cells in the experimental group had significantly decreased gene and protein expressions of 14-3-3β,decreased proliferation and migration abilities,significantly increased apoptosis rate and p53 mRNA level (P＜0.05).Conclusion Silence of 14-3-3 β gene decreases U251 cells proliferation and migration through p53 mediated pathway; consequently,a new explanation about how 14-3-3 β regulates glioma cells proliferation and migration can be clarified,and a potential target for glioma treatment can be provided.

Objective To investigate the myocardial expressions of protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) signaling pathway and effective mechanism of Yiqi Huoxue Fang depending on model of myocardial ischemia.Methods The model of acute myocardial infarction (AMI) was established through ligation of left coronary anterior descending branch in SD rats, and randomly divided into model group, perindopril group, Qishen Yiqi Gutta Pills group, Yiqi Huoxue Fang group and sham-operation group, and all groups were given orally corresponding medications respectively 2 d after operation.The observation time points were set on the 7th d and 28th d.The changes of heart function and structure were detected by using ultrasonic testing, changes of myocardial pathomorphology were observed after HE staining, and expressions of Akt, mTOR, p-Akt and p-mTOR in infarction marginal zone were detected by using Western blot test, real-time fluorescence quantitative polymerase chain reaction (RT-PCR) and immunohistochemistry technique in all groups.Results The level of left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) decreased significantly in model group compared with sham-operation group on the 7th d and 28th d (P<0.01).The level of left ventricular end-systolic volume (LVESV) increased significantly on the 7th d (P<0.01), and levels of LVESV and left ventricular end-diastolic volume (LVEDV) increased significantly (P<0.01) on the 28th d in model group.The levels of LVEF and LVFS increased and levels of LVEDV and LVESV decreased significantly in all medicated groups compared with model group (P<0.01).The thinner ventricular wall, less cardiomyocytes, disorder myocardial cells arrangement and inflammatory cell infiltration were observed in infarction marginal zone in model group, and disorder myocardial cells arrangement and less cardiomyocytes were observed in all medicated groups.The ratio of p-Akt/Akt and p-mTOR/mTOR increased (P<0.05), expressions of Akt m-RNA and mTOR m-RNA increased significantly (P<0.01), and levels of p-Akt and p-mTOR positive cell rates increased significantly (P<0.01) in model group.The ratio of p-Akt/Akt and p-mTOR/mTOR increased (P<0.05), expressions of Akt m-RNA and mTOR m-RNA increased (P<0.05 or P<0.01), and levels of p-Akt and p-mTOR positive cell rates increased significantly (P<0.05) in all medicated groups.Conclusion Yiqi Huoxue Fang can improve heart function and protect myocardial cells through activating cardiac self-protective mechanism-Akt/mTOR signaling pathway in rats with myocardial infarction.

ObjectiveTo establish and evaluate a mouse model of heart failure with Qi deficiency syndrome. MethodForty-four KM mice were randomly divided into sham operation group， model group， and modified Si Junzitang group （12.89 g·kg^-1）. The model group and the modified Si Junzitang group underwent thoracic aortic constriction （TAC）， while the sham operation group only underwent suture without constriction. Echocardiography and pathological examination were used to assess the heart failure model and evaluate the pharmacological effects. Macroscopic characterization， microscopic biology， and formula identification were conducted to collect general signs， body weight， open-field behavior， grip strength， mitochondrial ultrastructure， and other macroscopic and microscopic characteristics of mice. Mitochondrial fission and fusion protein expression were measured to determine the syndrome type. ResultEight weeks after TAC， compared with the sham operation group， the model group showed a significant decrease in left ventricular ejection fraction （LVEF） （P<0.01）， and modified Si Junzitang improved LVEF in mice （P<0.05）. Hematoxylin-eosin （HE） staining of the heart showed inflammatory cell infiltration and thickening of blood vessel walls in the model group， which was significantly improved by modified Si Junzitang. After 6-8 weeks， compared with the sham operation group and the modified Si Junzitang group， the model group exhibited significant hair loss， hair yellowing， decreased activity， and depression. Moreover， compared with the sham operation group， the model group had a significantly lower increase in body weight （P<0.05）， while the modified Si Junzitang group showed a significant increase in body weight （P<0.05） compared with the model group. After 6-8 weeks， compared with the sham operation group， the model group showed a significant decrease in open-field distance and speed （P<0.05）， while the modified Si Junzitang group exhibited significantly improved open-field distance and speed in the 8^th week （P<0.05）. After 6-8 weeks， compared with the sham operation group， the model group exhibited a significant decrease in maximum grip strength （P<0.05）， while the modified Si Junzitang group showed a significant increase in maximum grip strength 8 weeks after TAC （P<0.05）. Transmission electron microscopy of the gastrocnemius muscle showed uneven muscle tissue matrix， mitochondrial swelling， increased volume， matrix dissolution， ridge loss， and vacuolization in the model group， while modified Si Junzitang improved mitochondrial swelling， ridge fracture， and matrix vacuolization. Western blot analysis showed that the expression of the kinetic associated protein 1 （DRP1） in the gastrocnemius muscle of the model group significantly increased （P<0.01）， and the expression of mitochondrial fusion hormone 1 （MFN1） significantly decreased （P<0.05） as compared with those in the sham operation group. Furthermore， compared with the model group， the modified Si Junzitang group exhibited a significant decrease in the expression of DRP1 （P<0.05） and a significant increase in MFN1 expression （P<0.01）. ConclusionMice exhibited significant manifestations of qi deficiency syndrome 6-8 weeks after TAC， accompanied by abnormal mitochondrial morphology and function in the gastrocnemius muscle， which were significantly improved by modified Si Junzitang.