Ginsenoside Re Improves Isoproterenol-Induced Myocardial Fibrosis and Heart Failure in Rats.

Objective. Panax ginseng is used widely for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of P. ginseng. We aimed to investigate the protective effect of ginsenoside Re on isoproterenol-induced myocardial fibrosis and heart failure in rats. Methods. A model of myocardial fibrosis and heart failure was established by once-daily subcutaneous injection of isoproterenol (5 mg/kg/day) to rats for 7 days. Simultaneously, rats were orally administrated ginsenoside Re (5 or 20 mg/kg) or vehicle daily for 4 weeks. Results. Isoproterenol enhanced the heart weight, myocardial fibrosis, and hydroxyproline content in rat hearts. Ginsenoside Re inhibited (at least in part) the isoproterenol-induced increase in heart weight, myocardial fibrosis, and hydroxyproline content. Compared with the isoproterenol group, treatment with ginsenoside Re ameliorated changes in left ventricular systolic pressure, left ventricular end diastolic pressure, and the positive and negative maximal values of the first derivative of left ventricular pressure. Ginsenoside Re administration also resulted in decreased expression of transforming growth factor (TGF)-ß1 in serum and decreased expression of Smad3 and collagen I in heart tissue. Conclusion. Ginsenoside Re can improve isoproterenol-induced myocardial fibrosis and heart failure by regulation of the TGF-ß1/Smad3 pathway.

Ginsenoside Re Attenuates Isoproterenol-Induced Myocardial Injury in Rats.

Objective. Panax ginseng is widely used for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of Panax ginseng. This study aimed to investigate the protective effect of Ginsenoside Re on isoproterenol-induced myocardial injury in rats. Methods. Male Wistar rats were orally given Ginsenoside Re (5, 20 mg/kg) daily for 7 days. Isoproterenol was subcutaneously injected into the rats for two consecutive days at a dosage of 20 mg/kg/day (on 6th and 7th day). Six hours after the last isoproterenol injection, troponin T level and creatine kinase-MB (CK-MB) activity were assayed. Histopathological examination of heart tissues was performed. The levels of malondialdehyde (MDA) and glutathione (GSH) in heart tissues were measured. The nuclear factor erythroid 2-related factor 2 (Nrf2) content in nucleus and the proteins of glutathione cysteine ligase catalytic subunit (GCLC) and glutathione cysteine ligase modulatory subunit (GCLM) in heart tissues were assayed by western blotting method. Results. Treatment with Ginsenoside Re at dose of 5, 20 mg/kg reduced troponin T level and CK-MB activity of rats subjected to isoproterenol. The cardioprotective effect of Ginsenoside Re was further confirmed by histopathological examination which showed that Ginsenoside Re attenuated the necrosis and inflammatory cells infiltration. Ginsenoside Re inhibited the increase of MDA content and the decrease of GSH in heart tissues. Moreover, the Nrf2 content in nucleus and the expressions of GCLC and GCLM were significantly increased in the animals treated with Ginsenoside Re. Conclusion. These findings suggested that Ginsenoside Re possesses the property to attenuate isoproterenol-induced myocardial ischemic injury by regulating the antioxidation function in cardiomyocytes.

Ginsenoside Rg3 Improves Cardiac Function after Myocardial Ischemia/Reperfusion via Attenuating Apoptosis and Inflammation.

Objectives. Ginsenoside Rg3 is one of the ginsenosides which are the main constituents isolated from Panax ginseng. Previous study demonstrated that ginsenoside Rg3 had a protective effect against myocardial ischemia/reperfusion- (I/R-) induced injury. Objective. This study was designed to evaluate the effect of ginsenoside Rg3 on cardiac function impairment induced by myocardial I/R in rats. Methods. Sprague-Dawley rats were subjected to myocardial I/R. Echocardiographic and hemodynamic parameters and histopathological examination were carried out. The expressions of P53, Bcl-2, Bax, and cleaved caspase-3 and the levels of TNF-α and IL-1ß in the left ventricles were measured. Results. Ginsenoside Rg3 increased a left ventricular fractional shortening and left ventricular ejection fraction. Treatment with ginsenoside Rg3 also alleviated increases of left ventricular end diastolic pressure and decreases of left ventricular systolic pressure and ±dp/dt in myocardial I/R-rats. Ginsenoside Rg3 decreased apoptosis cells through inhibiting the activation of caspase-3. Ginsenoside Rg3 also caused significant reductions of the contents of TNF-α and IL-1ß in left ventricles of myocardial I/R-rats. Conclusion. The findings suggested that ginsenoside Rg3 possessed the effect of improving myocardial I/R-induced cardiac function impairment and that the mechanism of pharmacological action of ginsenoside Rg3 was related to its properties of antiapoptosis and anti-inflammation.

[Comparison on clinical features between dilated cardiomyopathy patients with or without pulmonary hypertension].

OBJECTIVE: The clinical data of dilated cardiomyopathy (DCM) patients with or without pulmonary hypertension (PH) diagnosed by echocardiography were compared. METHODS: During January 2007 to December 2009, 61 cases of DCM with PH and 51 cases of DCM without PH were admitted in our department. The demographic and clinical data, heart function, echocardiography and serum total bilirubin and creatinine levels of all patients were analyzed. RESULTS: Sex, age, vital signs, combined diseases and arrhythmias as well as the serum creatinine level [(103.5 ± 49.7) µmol/L vs. (90.3 ± 37.3) µmol/L, P > 0.05] were similar between the two groups, while the incidence of NYHA III and IV (95% vs. 65%), the left ventricle end-systolic dimension[(71.0 ± 9.6) mm vs. (65.5 ± 7.2) mm], dimension of the left atrium [(52.8 ± 8.93) mm vs. (43.9 ± 6.3) mm], right ventricular outflow tract [(29.1 ± 5.3) mm vs. (22.1 ± 3.3) mm] incidence of pericardial effusion (29/61 vs. 7/51) and the serum total bilirubin level [(45.3 ± 31.8) µmol/L vs. (19.5 ± 9.08) µmol/L] were significantly higher while ejective fraction was significantly lower in DCM with PH than those in DCM without PH (0.28 ± 0.10 vs. 0.36 ± 0.10, all P < 0.05). CONCLUSION: DCM patients with PH is linked with worse clinical features than DCM patients without PH.

Hypolipidemic effects of kaempferide-7-O-(4''-O-acetylrhamnosyl)-3-O-rutinoside in hyperlipidemic rats induced by a high-fat diet.

Kaempferide-7-O-(4''-O-acetylrhamnosyl)-3-O-rutinoside (A-F-B) is a novel flavonoid which is extracted from the leaves of Actinidia kolomikta. The aim of this study was to investigate the hypolipidemic effects of A-F-B in hyperlipidemic rats induced by a high-fat diet. Male Wistar rats were randomly divided into six groups: normal diet group, high-fat diet group, lovastatin (2.5 mg/kg) group and A-F-B (12.5, 25 or 50 mg/kg) groups. To evaluate the lipid-lowering effects of A-F-B, total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), atherogenic index (AI) and coronary risk index (CRI) were investigated. The activities of phosphatidate phosphohydrolase (PAP) and hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase in hepatic tissue were evaluated. Treatment with A-F-B to hyperlipidemic rats resulted in a significant decline in TC, TG, LDL-C, AI and CRI, with an increase in HDL-C level. The results also showed that A-F-B significantly decreased the activities of PAP and HMG-CoA reductase in hepatic tissue. These findings suggest that A-F-B improves lipid profiles. The mechanisms of A-F-B were associated with regulating the activities of PAP and HMG-CoA reductase in hepatic tissue.

[Risk factors of pulmonary embolism among 303 patients in the First Clinical Hospital of Jilin University].

OBJECTIVE: To study the trend and changes regarding risk factors of pulmonary embolism among inpatients in the last 10 years from the First Clinical Hospital of Jilin University. METHODS: 303 cases of pulmonary embolism inpatients in our hospital from 2001 - 2010 were included and analyzed on related incidence, mortality and risk factors. RESULTS: Data showed that: (1) the incidence of pulmonary embolism increased from 0.09‰ to 1.12‰ while the mortality dropped from 73.3% to 12.0%; (2) major risk factors would include thrombosis of deep veins, surgical operations, heart diseases, varicosity or phlebitis of lower extremities, trauma and fracture etc., according to the order of incidence rates. Surgical operations had become the second major risk factor in the last 10 years. CONCLUSION: The incidence of pulmonary embolism in our hospital showed a gradual drop while the mortality had a remarkable drop. Surgical operations had become one of the major risk factors of pulmonary embolism.