This study aimed to investigate the potential mechanisms underlying the protective effects of 20(S)-ginsenoside Rg3 on diabetes-related myocardial injury. Diabetes was induced in rats by a single dose of streptozotocin (45 mg/kg). The rats were then treated with 20(S)-ginsenoside Rg3 for 12 weeks. The lipids, glucose levels, cardiac enzymes and antioxidant system parameters of the rats were recorded at 12 weeks after the treatment. Myocardial samples were analyzed using transmission electron microscopy. The expression levels of receptor for advanced glycation end products (RAGE), nuclear factor-κB (NF-κB), transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF) were also determined. Induction of the diabetic model significantly enhanced extracellular matrix deposition and increased the levels of type I and III collagen. The level of malondialdehyde (MDA) in the cardiac tissue of the diabetic rats was significantly increased, while the levels of superoxide dismutase (SOD), glutathione (GSH) and catalase (CAT) were decreased compared to the control rats. Treatment with 20(S)-ginsenoside Rg3 resulted in an obvious recovery of these indexes, decreased accumulation of collagen, improved structure of the muscular fiber bundle and restored morphology of mitochondria of the LV myocardium. Compared to the control group, the expression levels of RAGE, NF-κB, TGF-β1 and CTGF proteins were significantly increased in the DM group, while 20(S)-ginsenoside Rg3 significantly reduced their expression. This study shows that the AGE-RAGE pathway may be involved in the mechanism of myocardial injury in diabetic rats and that 20(S)-ginsenoside Rg3 protects the myocardium via the AGE-RAGE pathway.

In this study, the rapid resolution liquid chromatography. quadrupole time-of-flight mass spectrometry (RRLC-QTOF/MS) was used to profile the metabolites of urine samples from chronic heart failure (CHF) patients and healthy controls to find the differential metabolites which could provide the scientific evidence to explain the pathogenesis of the disease and supply a better therapy plan. Urine samples from 15 CHF patients (age (62. 27 +/- 3. 14) years) and 15 healthy controls (age (65. 41 +/- 4. 63) years) were analyzed by RRLC. QTOF/MS. After processing the data, the multivariate statistical analysis (principal component analysis, PCA) was performed to find the potential biomarkers. Result showed that urine samples of CHF patients were successfully distinguished from those of healthy controls. Two significantly differentially expressed metabolites, uridine and alanyltryptophan, were found and identified as potential biomarkers. The result showed that the LC-MS based metabolomics approach had good performance to identify potential biomarkers, and the disorder of uracil metabolism and Tryptophan metabolism may play an important role in the mechanism of CHF.

This study aimed to investigate the potential mechanisms underlying the protective effects of carbamylated erythropoietin (CEPO) on diabetic-related myocardial fibrosis. Wistar rats were fed a high-fat/high-carbohydrate diet and intraperitoneally injected with streptozotocin to induce diabetic cardiomyopathy (DCM). The rats were then treated with recombinant human erythropoietin (rhEPO) or CEPO. The lipid and glucose levels of the rats were recorded 4 and 8 weeks after the treatment. Myocardial samples were analyzed through Massons trichrome staining and transmission electron microscopy. The expression levels of transforming growth factor-beta 1 (TGF-beta 1) and connective tissue growth factor (CTGF) were also detected. Moreover, myocardial apoptosis and extracellular signal-regulated kinase (ERK) signaling were investigated. Induction of the diabetic model significantly promoted myocardial cell apoptosis and upregulated the protein expression levels of TGF-beta 1 and CTGF. Treatment with CEPO or rhEPO decreased the number of apoptotic cells, ameliorated the dissolution of myocardial myofilaments and damage of mitochondria, and downregulated TGF-beta 1 and CTGF expression levels in the myocardium of diabetic rats. Furthermore, CEPO increased ERK (44/42) protein expression levels in the hearts of diabetic rats. Overall, it was found that myocardial fibrosis may contribute to myocardial injury in diabetes mellitus and that CEPO might protect the myocardium of diabetic rats against fibrosis through the ERK (44/42) signaling pathway.

In the present study, we investigated the effect and possible mechanism of action of trimetazidine in pirarubicin-induced myocardial damage. Thirty-six Wistar rats were randomly divided into control, model, and treatment groups. The rats in the model and treatment groups were injected through the vena caudalis with pirarubicin (2.5 mg/kg once a week) for six weeks. The control group rats were injected in the same manner with 0.9% NaCl for 6 weeks. The rats in the treatment group received an intragastric infusion of trimetazidine at 5.4 mg/kg/d for 8 weeks, while those in the control and model groups received infusions of 0.9% NaCl. At the end of the experiment, we measured the levels of superoxide dismutase, cardiac enzymes, and free radical mediators. Myocardial tissue was examined using light and electron microscopy. The levels of myoglobin, troponin, and alanine aminotransferase (ALT) were lower in the treatment group than in the model group (P < 0.05). Malondialdehyde (MDA) and nitric oxide (NO) levels were lower after treatment than in the model group (P < 0.05), and nonprotein sulfhydryl (NPSH) and superoxide dismutase (SOD) levels were higher in the treated animals than in the model group (P < 0.05). In the model group, the structure of myocardial cells was severely damaged, they were arranged in a disorderly manner, and myocardial myofilament dissolution and fracturing were observed. In the treatment group, the structure of myocardial cells was orderly, and the structure of the myocardium was essentially preserved. Treatment with trimetazidine reduced mitochondrial damage and relieved myocardial injury, indicating that trimetazidine exerted a protective effect on cardiomyocytes that were exposed to pirarubicin. The mechanism underlying this effect may be related to its antioxidative activities.

Objective The aim of the present study was to investigate the cardiac protective effects of erythropoietin derivative on diabetic rat. Methods Healthy male Wistar rats were fed a high-fat, high-carbohydrate diet for four weeks, and then were injected with STZ twice (50 mg/kg, intraperitoneally). Once DM was confirmed, the rats were divided randomly into the following groups:Control (group A); DCM (group B); CEPO 500 IU/kg (group C); CEPO 1 000 IU/kg (group D);CEPO 2 000 IU/kg (group E) and rhEPO 1 000 IU/kg (group F). The morphological changes of myocardium were observed by HE staining and Masson staining. The expression levels of transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF) were also detected. Results All data were analyzed by one-way ANOVA and SNK-test using SPSS software. In rats with diabetic rats, collagen tissues significantly increased. The protein expression levels of TGF-β1 and CTGF significantly increased compared with those of control rats (TGF-β1: 9.84±1.33 vs. 4.91±1.16, CTGF: 9.67±1.52 vs. 3.44±1.34;P<0.05). CEPO decreased the amount of myocardial collagen and dose-dependently decreased TGF-β1 and CTGF protein expression levels in myocardial cells (TGF-β1: 6.38±1.26, CTGF: 6.09±1.66; P<0.05). Conclusion CEPO protects the myocardium of diabetic rats against fibrosis, with a dose-response&nbsp;relationship.

Ginsenoside Rg1 has been demonstrated to have cardiovascular protective effects. However, whether the cardioprotective effects of ginsenoside Rg1 are mediated by endoplasmic reticulum (ER) stress-induced apoptosis remain unclear. In this study, among 80 male Wistar rats, 15 rats were randomly selected as controls; the remaining 65 rats received a diet rich in fat and sugar content for 4weeks, followed by intraperitoneal injection of streptozotocin (STZ, 40mg/kg) to establish a diabetes model. Seven days after STZ injection, 10 rats were randomly selected as diabetic model (DM) controls, 45 eligible diabetic rats were randomized to three treatment groups and administered ginsenoside Rg1 in a dosage of 10, 15 or 20mg/kg/day, respectively. After 12weeks of treatment, rats were killed and serum samples obtained to determine cardiac troponin (cTn)-I. Myocardial tissues were harvested for morphological analysis to detect myocardial cell apoptosis, and to analyse protein expression of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and Caspase-12. Treatment with ginsenoside Rg1 (10-20mg/kg) significantly reduced serum cTnI levels compared with DM control group (all P<0.01). Ginsenoside Rg1 (15 and 20mg/kg) significantly reduced the percentage of apoptotic myocardial cells and improved the parameters of cardiac function. Haematoxylin and eosin and Masson staining indicated that ginsenoside Rg1 could attenuate myocardial lesions and myocardial collagen volume fraction. Additionally, ginsenoside Rg1 significantly reduced GRP78, CHOP, and cleaved Caspase-12 protein expression in a dose-dependent manner. These findings suggest that ginsenoside Rg1 appeared to ameliorate diabetic cardiomyopathy by inhibiting ER stress-induced apoptosis in diabetic rats.

A rapid resolution liquid chromatography quadrupole time-of-flight mass spectrometric (RRLC-QTOF/MS) method was used to profile the metabolites of urine samples from atherosclerosis (AS) patients and healthy controls and find the differential metabolites which could provide the scientific evidence to explain the pathogenesis and early disease diagnose. In the study, 15 AS patients (age46. 84 +/- 2. 41 years) and 15 healthy controls (age45. 72 +/- 1. 93 years) was screened out by VaSera VS-1000. The urine samples were analyzed by RRLC-QTOF/MS and the resulting data matrices were analyzed by multivariate statistical analysis (Principal Component Analysis, PCA) to find the potential biomarkers. The results showed that the urine samples of AS patients were successfully distinguished from those of healthy controls. Besides, a total of two significantly changed metabolites, uric acid and Guanidineacetic acid, had been found and identified as potential biomarkers, which suggested that the disorder of purine metabolism and amino acid metabolism played an important role in the mechanism of AS.

Objective: To investigate the potential mechanisms underlying the protective effects of recombinant human erythropoietin (rhEPO) and carbamylated EPO (CEPO) against myocardial cell apoptosis in epilepsy. Methods: Rats were given an intra-amygdala injection of kainic acid to induce epilepsy. Groups of rats were treated with rhEPO or CEPO before induction of epilepsy, whereas additional rats were given a caudal vein injection of AG490, a selective inhibitor of Janus kinase 2 (JAK2). At different time points after seizure onset, electroencephalogram changes were recorded, and myocardium samples were taken for the detection of myocardial cell apoptosis and expression of JAK2, signal transducer and activator of transcription 5 (STAT5), caspase-3, and bcl-xl mRNAs and proteins. Results: Induction of epilepsy significantly enhanced myocardial cell apoptosis and upregulated the expression of caspase-3 and bcl-xl proteins and JAK2 and STAT5a at both the mRNA and protein levels. Pretreatment with either rhEPO or CEPO reduced the number of apoptotic cells, upregulated bcl-xl expression, and downregulated caspase-3 expression in the myocardium of epileptic rats. Both myocardial JAK2 and STAT5a mRNAs, as well as phosphorylated species of JAK2 and STAT5a, were upregulated in epileptic rats in response to rhEPO—but not to CEPO—pretreatment. AG490 treatment increased apoptosis, upregulated caspase-3 protein expression, and downregulated bcl-xl protein expression in the myocardium of epileptic rats. Conclusions: These results indicate that myocardial cell apoptosis may contribute to myocardial injury in epilepsy. EPO protects myocardial cells from apoptosis via the JAK2/STAT5 pathway in rats with experimental epilepsy, whereas CEPO exerts antiapoptotic activity perhaps via a pathway independent of JAK2/STAT5 signaling.

We evaluated the cardioprotective effects of ginsenoside Rg1 in a diabetic rat model induced with high-fat diet and intraperitoneal injection of streptozotocin. Ginsenoside Rg1 was injected intraperitoneally for 12 weeks. Myocardial injury indices and oxidative stress markers were determined. Changes in cardiac ultrastructure were evaluated with transmission electron microscopy. Myocardial apoptosis was assessed via terminal deoxynucleotidyl transferase (TDT)-mediated DNA nick-end labeling (TUNEL) and immunohistochemistry. Ginsenoside Rg1 was associated with a significant dose-dependent reduction in serum levels of creatinine kinase MB and cardiac troponin I, and lessened ultrastructural disorders in diabetic myocardium, relative to the untreated diabetic model rats. Also, compared with the untreated diabetic rats, significant reductions in serum and myocardial levels of malondialdehyde were noted in the ginsenoside Rg1-treated groups, and increased levels of the antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) were detected. TUNEL staining indicated reduced myocardial apoptosis in ginsenoside Rg1-treated rats, which may be associated with reduced levels of caspase-3 (CASP3) and increased levels of B-cell lymphoma-extra-large (Bcl-xL) in the diabetic myocardium. Ginsenoside Rg1 treatment of diabetic rats was associated with reduced oxidative stress and attenuated myocardial apoptosis, suggesting that ginsenoside Rg1 may be of potential preventative and therapeutic value for cardiovascular injury in diabetic patients.

We evaluated the cardioprotective effects of ginsenoside Rg1 in a diabetic rat model induced with high-fat diet and intraperitoneal injection of streptozotocin. Ginsenoside Rg1 was injected intraperitoneally for 12 weeks. Myocardial injury indices and oxidative stress markers were determined. Changes in cardiac ultrastructure were evaluated with transmission electron microscopy. Myocardial apoptosis was assessed via terminal deoxynucleotidyl transferase (TDT)-mediated DNA nick-end labeling (TUNEL) and immunohistochemistry. Ginsenoside Rg1 was associated with a significant dose-dependent reduction in serum levels of creatinine kinase MB and cardiac troponin I, and lessened ultrastructural disorders in diabetic myocardium, relative to the untreated diabetic model rats. Also, compared with the untreated diabetic rats, significant reductions in serum and myocardial levels of malondialdehyde were noted in the ginsenoside Rg1-treated groups, and increased levels of the antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) were detected. TUNEL staining indicated reduced myocardial apoptosis in ginsenoside Rg1-treated rats, which may be associated with reduced levels of caspase-3 (CASP3) and increased levels of B-cell lymphoma-extra-large (Bcl-xL) in the diabetic myocardium. Ginsenoside Rg1 treatment of diabetic rats was associated with reduced oxidative stress and attenuated myocardial apoptosis, suggesting that ginsenoside Rg1 may be of potential preventative and therapeutic value for cardiovascular injury in diabetic patients.

Objective To investigate the protection and the possible mechanism of CEPO against cardiomyopathy in experimental diabetes mellitus (DM) rat. Methods DM rat model was established by high fat and sugar feed and intraperitoneal injection streptozotocin. After confirmed DM, the rats were divided into three parts. Immunohistochemical staining was used to analyze the expression levels of TIPE2 and TUNEL was used to detect the cardiac myocyte apoptosis. Results Diabetic myocardial apoptosis increased (19.43±2.08) cells/mm2, was significantly higher (P<0.05). CEPO myocardial apoptosis increased by less than DM group (P<0.05), was (12.1±2.31) cells /mm2, but still higher than the control group (P<0.05). Diabetic rat myocardium TIPE2 protein expression increased. Compared with DM group, CEPO can reduce elevated protein TIPE2 (P<0.05). Conclusion CEPO has anti-apoptosis in experimental DM rat, which mechanisms involved in TIPE2 cell signaling pathway.

Objective * These authors contributed equally to this work. A meta-analysis to investigate the association between preoperative statin use and the risk of postoperative infectious complications in patients undergoing surgery. Methods PubMed® and Embase® databases were searched for relevant studies. Data were extracted using a standardized data collection form. The primary effect measure was the odds ratio (OR) of postoperative infectious complications. Summary OR were calculated. Results The analysis included 10 cohort studies with a total of 147 263 participants. Statin use was associated with a lower incidence of postoperative infectious complications in all studies (summary OR 0.917, 95% confidence intervals [CI] 0.862, 0.975, fixed-effects model; summary OR 0.731, 95% CI 0.584, 0.870, random-effects model); cardiac surgery (summary OR 0.673; 95% CI 0.535, 0.847); treatment in the USA (summary OR 0.678; 95% CI 0.597, 0.770); retrospective cohort studies (summary OR 0.664; 95% CI 0.521, 0.846). Conclusion Preoperative statin use is associated with a reduced risk of postoperative infectious complications.

Objective To study the effect of endoplasmic reticulum stress in diabetic cardiomyopathy and the Thera-peutic effects and its mechanism of ginseng fruit saponins.Methods 50 Wistar rats were randomly divided into control group (group C,n=10);Another 40 were fed with high fat and sugar for 4 weeks,then intraperitoneally injected with strept-ozotocin (STZ)[40 mg/kg×4 weeks]to induce diabetes,25 diabetic rats were randomly d-ivided into diabetic model group (group D,n=10)and ginseng fruit saponin group (group G,n=15,40 mg/kg/D for 12 weeks),All rats were sacrificed and blood samples were coll-ected for measuring fasting blood glucose,total cholesterol (TC),triglycer-ide (TG),and myocardial enzymes (CK,CKMB,LDH)level.Tissue samples were dyed with Hemato-xylin-eosin(HE) for histopathological examination,Myocardial cell apoptosis detected by tunel method,the expressions of caspase1 2 pro-tein were detected by Immunohistoch-emical detection.Results The levels of FBG,TC,TG in group D were signifi-cantly higher than those in group C (all P<0.01).The above indexes were significantly reduced with the treatment of ginseng fruit saponins compared with group D (P<0.05).The levels of CK,CK-MB and LDH in group D is signifi-cantly higher than group C (P<0.01),ginseng fruit saponins can significantly decrease the above indexes,the differ-ence was statistically significant(P<0.01).In group C:Myocardial cell neatly and closely arranged,rich cytopl-asm is rich and red,nucleus is located in the central of cells;No dissolution of muscle fiber,vacuoles degeneration and mononu-clear cell infiltration.In group D:Disordered arrange ment of myocardial cell,the cytoplasm is distributed and relatively weak dyed.fiber breakage and irregular nucleus size were obivious.Myocardial cell abnormal conditions in group G were improved.Apoptotic cells were occasionally showed in group C,the myo cardial apoptosis index was(3.23±1.32)%, Apoptotic cells increased significantly in group D,the apoptosis index was (62.5±7.59)%,The apoptosis index of group G was (40.25±6.58)%,which decreas ed significantly compared with group D.Caspase-l2 protein expression in Group C is lower,group D rat myocardial the expression of caspase-1 2 protein present strong positive,Caspase-l2 pro-tein expression in Group G is medium.Conclusion The endoplasmic reticulum stress may be involve in pathological processes of diabetic cardiomyopathy.Ginseng fruit saponins can protect myocardium,which may be associatedwith re-duce myocardial cell apoptosis mediated by endoplasmic reticulum..

目的 探讨人参皂苷Re对糖尿病大鼠的心肌保护作用及机制.方法 取40只Wistar大鼠高脂高糖饲料喂养,腹腔注射链脲佐菌素(STZ) 35 mg/kg制作糖尿病模型,将34只造模成功大鼠随机分为模型组12只,人参皂苷11只,吡格列酮组11只,分别予以相应量纯净水、人参皂苷Re 25 mg/(kg·d)、吡格列酮10 mg/(kg·d)灌胃,连续给药4周;另取10只正常大鼠予标准饲料喂养4周作为对照组.干预4周后处死各组大鼠,分别检测血糖、血脂,血清和心肌组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平,并行心肌组织病理学观察.结果人参皂苷组和吡格列酮组空腹血糖和血清总胆固醇水平高于对照组,(P＜0.01),低于模型组(P＜0.01),两组间无统计学差异;人参皂苷组和吡格列酮组SOD活性低于对照组,MDA水平高于对照组(P均＜0.05);血清和心肌组织中SOD活性均高于模型组(P＜0.01)、MDA水平均低于模型组(P＜0.05),但两组间无统计学差异.人参皂苷组和吡格列酮组心肌组织结构损伤明显轻于模型组,心肌细胞排列较模型组整齐.结论人参皂苷Re对糖尿病大鼠具有心肌保护作用;抗脂质过氧化作用是其作用机制之一.

OBJECTIVE:To investigate vascular endothelial impairment as a result of reperfusion therapy in patients with acute myocardial infarction (AMI).METHODS:Patients with AMI underwent reperfusion therapy (percutaneous cardiac intervention [PCI] or thrombolytic therapy) or conservative drug therapy. Healthy control subjects were recruited. Endothelial impairment was assessed via endothelial nitric oxide (NO) synthase (eNOS), NO and endothelin-1 (ET-1) levels, 24 h after reperfusion or on enrolment, as appropriate.RESULTS:Patients who underwent PCI (n = 47) or thrombolytic therapy (n = 45) had significantly lower eNOS and NO levels, and higher ET-1 levels than those who received conservative drug therapy (n = 46). All patient groups had significantly lower eNOS and NO levels, and higher ET-1 levels, than controls (n = 45). There was a significant positive correlation between eNOS and NO, as well as significant negative correlations between eNOS/ET-1 and NO/ET-1 in all four groups.CONCLUSIONS:Patients with AMI who underwent reperfusion therapy displayed low eNOS activity. This may result in impairment of endothelial function via downregulation of NO and upregulation of ET-1.

A urinary metabonomics method based on rapid resolution liquid chromatography/mass spectrometry (RRLC/MS) was developed to study the effect mechanism of Total Ginsenoside (TG) on streptozotocin(STZ) induced Diabetic Cardiomyopathy (DCM) rats. Twenty-four STZ-induced diabetic rats were randomly divided into DCM group and TG group. DCM group was administrated with TG 30 mg/kg body weight once a day by gastric irrigation. TG group was administrated with water by gastric irrigation in parallel. Ten healthy rats were defined as control group and were also administrated with water by gastric irrigation in parallel. After twelve-week continuous irrigation, 24 h urine samples of rats in the three group were collected and analyzed by RRLC/MS. Principal component analysis (PCA) was carried out for pattern recognition and a clear separation between DCM rats and those treated with TG was achieved. Three potential biomarkers were found and identified. The significant changes of these biomarkers indicated the pharmacological effects of TG on the metabolism of rats. TG can regulate the metabolism of body include citrate cycle, fatty acid metabolism and oxidative stress. The results shows the metabonomics is a useful tool in effect mechanism research of natural product and this work is helpful in the effect mechanism study of Panax ginseng.

The aim of the present study was to investigate the protective effect of carbamylated erythropoietin (CEPO) against cardiomyopathy in high-fat, high-carbohydrate diet-fed rats with streptozotocin (STZ)-induced diabetic cardiomyopathy (DCM). Healthy male Wistar rats were fed a high-fat, high-carbohydrate diet for four weeks, and then were injected with STZ twice (50 mg/kg, intraperitoneally). Once DCM was confirmed, the rats were divided randomly into the following groups: DCM without treatment, CEPO treatment at different dosages (500, 1,000 or 2,000 IU/kg) or recombinant human erythropoietin (rhEPO) treatment (1,000 IU/kg), for a four-week short intervention or an eight-week long intervention protocol. Healthy rats were used as normal controls. Venous blood samples were drawn for routine hematological examinations, and heart tissues were collected for histological analysis, as well as the determination of myocardial apoptosis and phosphatidylinositol-3-kinase (PI3K)/Akt signaling. CEPO treatment had no significant effect on the erythrocyte or hemoglobin levels in the rats with DCM; however, it reduced myocardial cell apoptosis in the rats and protected the cellular ultrastructure. In addition, CEPO treatment inhibited caspase-3 and increased Bcl-xl protein expression (P<0.05). It also increased PI3K (p85) and Akt1 expression at the mRNA and protein levels in the hearts of the rats with DCM, with a dose-response relationship. An eight-week treatment using CEPO, in comparison with a four-week protocol, marginally increased PI3K (p85) and Akt1 expression, and did not demonstrate significant benefit. The study indicated that CEPO protects against DCM, without markedly affecting erythropoiesis, and that the activation of PI3K/Akt may be a key mechanism in the protection conferred by CEPO.

目的探讨血清骨桥蛋白水平与舒张性心力衰竭的关系。方法入选患者67例,其中对照组22例,单纯高血压组22例,高血压合并舒张性心力衰竭组23例。入院时测量血压,同时应用心脏彩超检测患者E峰、A峰、E/A比值、左室射血分数(LVEF)、室间隔侧二尖瓣瓣环E'(舒张早期二尖瓣环运动速度)。采用ELISA法检测血清OPN水平。比较三组间血清OPN浓度的变化。结果高血压合并舒张性心力衰竭组血清OPN浓度(〔143.82±43.67)μg/L〕高于对照组〔(117.10±34.64)μg/L〕及单纯高血压组(〔114.53±26.55)μg/L〕,差异具有统计学意义(P<0.05)。对照组与单纯高血压组血清OPN浓度差异无统计学意义(P>0.05)。高血压合并舒张性心力衰竭患者血清OPN浓度与E/E'值呈正相关。血清OPN浓度均值心功能Ⅱ级组(〔107.76±36.51)μg/L〕<心功能Ⅲ级组(〔143.67±16.76)μg/L〕<心功能Ⅳ级组(〔180.02±37.90)μg/L〕,差异具有统计学意义(P<0.05)。结论高血压合并舒张性心力衰竭患者的血清OPN浓度增高,与E/E'值呈正相关,并随心功能分级升高而增加。