title: Protective effects of ginsenoside Re on lipopolysaccharide-induced cardiac dysfunction in mice.
abstract: The impaired cardiac function caused by reduced myocardial contractility is a typical manifestation of sepsis/septic shock. Ginsenoside Re (GS-Re) is one of the most abundant ingredients of ginseng. This study was designed to investigate the protective effects of GS-Re on lipopolysaccharide (LPS)-induced septic cardiac dysfunction and inflammatory response in mice. Mice were intragastrically administered with GS-Re (15 mg kg(-1)) for 1 week before the LPS challenge (10 mg kg(-1), i.p.). Cardiac function was evaluated 6 h after LPS induction. GS-Re pretreatment significantly protected against LPS-induced cardiac dysfunction. GS-Re ameliorated the imbalance between iNOS and eNOS, and prevented NF-κB activation and subsequent myocardial inflammatory responses in endotoxemic mice. The effects of GS-Re were closely associated with estrogen receptors (ERs), phosphatidylinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, and the mitogen-activated protein kinase signaling pathway, as characterized by the GS-Re-induced preservation of ERα, ERβ, and phospho-Akt and inhibition of phospho-ERK1/2, phospho-JNK, phospho-P38. However, GS-Re had no effect on LPS-induced activation of TLR-4. All these results showed that GS-Re pretreatment significantly attenuated LPS-induced cardiac dysfunction and inflammatory response.
authors.affiliation: Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Ministry of Education, Institute of Medicinal Plant Development, Chinese Academy of Medical Science, Peking Union Medical College, No 151, North Road Malianwa, Haidian District, Beijing 100094, China. Sunguibo@126.com.cn sunxiaoboyzs@163.com.
authors.forename: Rong-Chang
authors.initials: RC
authors.lastname: Chen
authors.forename: Jian
authors.initials: J
authors.lastname: Wang
authors.forename: Longpo
authors.initials: L
authors.lastname: Yang
authors.forename: Gui-Bo
authors.initials: GB
authors.lastname: Sun
authors.forename: Xiao-Bo
authors.initials: XB
authors.lastname: Sun
mesh_terms: D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D016207:Cytokines / Q000187:drug effects / Q000378:metabolism; D019446:Endotoxemia / Q000188:drug therapy; D005786:Gene Expression Regulation / Q000187:drug effects; D036145:Ginsenosides / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006331:Heart Diseases / Q000097:blood / Q000139:chemically induced* / Q000517:prevention & control*; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000097:blood; D007962:Leukocytes / Q000187:drug effects / Q000473:pathology; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D020928:Mitogen-Activated Protein Kinases; D009206:Myocardium / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism; D020556:Neutrophil Infiltration / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011960:Receptors, Estrogen; D012772:Shock, Septic / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D015996:Survival Rate; D051197:Toll-Like Receptor 4 / Q000187:drug effects
chemical_list: D016207:Cytokines; D036145:Ginsenosides; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; D011960:Receptors, Estrogen; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4; C049864:ginsenoside Re; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D020928:Mitogen-Activated Protein Kinases; D003402:Creatine Kinase