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Li C.,Yantai University | Gao Y.,Yantai University | Xing Y.,Shandong Luye Research and Development for Natural Drugs Co. | Zhu H.,Shandong Luye Research and Development for Natural Drugs Co. | And 2 more authors.
Food and Chemical Toxicology | Year: 2011

The aim of the study was to determine the effects of fucoidan on rat myocardial ischemia-reperfusion (I/R) model and elucidate the potential mechanisms. Myocardial I/R injury was induced by the occlusion of left anterior descending coronary artery for 30. min followed by reperfusion for 2. h. After 2. h reperfusion, hemodynamics parameters were detected. Blood samples were collected to determine serum levels of tumor necrosis factor-α (TNF-α) and interleukin 6, 10 (IL-6, 10). Hearts were harvested to assess histopathological changes, infarct size (IS), and the content of myeloperoxidase (MPO). The expression of high-mobility group box 1 (HMGB1), phosphor-IκB-α and phosphor-nuclear factor kappa B (NF-κB) were assayed by western blot. Compared with control group, treatment with fucoidan improved left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and the contractility index (P< 0.05, P< 0.01). Fucoidan reduced the myocardial IS, the levels of TNF-α and IL-6, and the activity of MPO (P< 0.05, P< 0.01). Fucoidan down-regulated the expression of HMGB1, phosphor-IκB-α and NF-κB, but increased the content of IL-10 when compared with control (P< 0.05, P< 0.01). Besides, the infiltration of polymorph nuclear leukocytes (PMNs) and histopathological damages in myocardium were decreased in fucoidan treated groups (PMNs, P< 0.05, P< 0.01). These findings revealed that the administration of fucoidan could regulate the inflammation response via HMGB1 and NF-κB inactivation in I/R-induced myocardial damage. © 2011 Elsevier Ltd. Source


Li C.,Yantai University | Gao Y.,Yantai University | Tian J.,Yantai University | Xing Y.,Shandong Luye Research and Development for Natural Drugs Co. | And 2 more authors.
Food and Chemical Toxicology | Year: 2012

The aim of the study was to determine the effects of Asperosaponin VI (ASA VI), a triterpene saponin isolated from Dipsacus asper Wall, on chronic myocardial infarction (MI) and possible mechanisms in rats. MI was induced by permanent ligation of the left coronary artery. Twenty-four hours after MI, the rats were administered the extract by gavage (once a day). Six weeks after MI/sham surgery, cardiac dysfunction, infarct size (IS), cardiac fibrosis, hydroxyproline concentration, the oxidative stress parameter and inflammation mediators were examined. The results indicated that ASA VI improved left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), ±dP/dt, heart weight/body weight, right ventricular weight/body weight and lung weight/body weight (P< 0.01, P< 0.05). These were accompanied by the attenuation of cardiac fibrosis, IS and hydroxyproline concentration (P< 0.01, P< 0.05). ASA VI could decrease the levels of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6), but increase IL-10 content (P< 0.01, P< 0.05). Furthermore, it also could raise the activities of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), but reduce malonyldialdehyde (MDA) level (P< 0.01, P< 0.05). The results indicated that ASA VI improved cardiac function and myocardial fibrosis from myocardial ischemia injury, and this cardioprotection might be attributed to reduce oxidative stress and regulate inflammation mediators. © 2012 Elsevier Ltd. Source


Li C.,Yantai University | He J.,Shandong Luye Research and Development for Natural Drugs Co. | Gao Y.,Yantai University | Xing Y.,Shandong Luye Research and Development for Natural Drugs Co. | And 2 more authors.
Cardiovascular Toxicology | Year: 2014

Choerospondias axillaris (Guangzao) is a medicinal plant used in Mongolia, and its fruit is commonly used for the treatment of cardiovascular diseases in clinic. The constituents responsible for this effect are always conceded to be the total flavonoids of C. axillaries (TFC). The present study was to evaluate the preventive effect of TFC on acute myocardial infarction induced by ischemia/reperfusion (I/R) in rats and the possible signaling pathway involved. The model of myocardial I/R was caused by occlusion of the left anterior descending coronary artery for 30 min followed by reperfusion for 2 h. Cardiac dysfunction, infarct size, pathologic histology and apoptosis were examined. Heart tissues were homogenized for biochemistry assays and Western blots analysis. The results indicated that pretreatment with TFC strongly improved cardiac function, obviously reduced heart pathologic lesion in I/R rat hearts. TFC also could protect the heart from I/R injury by increasing the levels of catalase, glutathione peroxidase and superoxide dismutase in heart homogenate, and decreasing that of malondialdehyde level. These beneficial effects were associated with the decrease in TUNEL-positive nuclear staining, Bax and caspase-3 levels, and the increase in Bcl-2 expression. Moreover, TFC counteracted the I/R-induced decreased activation of p38 mitogen-activated protein kinase (MAPK) and Jun N-terminal kinase. These data suggested that TFC improved I/R-induced myocardium impairment via anti-oxidative and anti-apoptotic activities, and this beneficial effects were intervened by MAPK signaling pathway. © 2013 Springer Science+Business Media. Source


Gao Y.L.,Yantai University | Liu Z.F.,Yantai University | Liu Z.F.,Shandong Luye Research and Development for Natural Drugs Co. | Li C.M.,Yantai University | And 5 more authors.
Food and Chemical Toxicology | Year: 2011

Compound K, i.e., 20-O-β-d-glucopyranosyl-20(S)-protopanaxadiol, is the main metabolite of the protopanaxadiol type of ginseng saponin produced by intestinal bacteria after oral administration of ginseng extract. In the present study, the toxicity of compound K was evaluated in male and female dogs after 90. days continuous intravenous infusion. Beagle dogs were treated with compound K at doses of 6.7, 20 and 60. mg/kg/day, and observed for 90. days followed by recovery periods. Measurements included clinical observations, body weight, food consumption, temperature, electrocardiogram (ECG), hematology, blood chemistry, urinalysis, gross necropsy, organ weight and histopathology. Under the conditions, the clinical condition of the animals, body weights, body weight gains and food consumption were unaffected by compound K administration relative to the control group. Hematology, ECG data and urinalysis parameters were also unaffected. However, the hepatotoxicity was evident from the observation of multiple parameters, including histopathological evaluation of liver tissue upon necropsy as well as large increases in plasma levels of liver enzymes (alanine aminotransferase, ALT, Gamma-glutamyltranspeptidase, γ-GT, alkaline phosphatase,ALP) in groups receiving compound K (20 or 60. mg/kg/day), and this hepatoxicity might be reversible. In addition, the NOAEL of compound K is 6.7. mg/kg/day in this 90. days toxicity study. © 2011 Elsevier Ltd. Source

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