title: Ginsenoside Rg1 improves survival in a murine model of polymicrobial sepsis by suppressing the inflammatory response and apoptosis of lymphocytes.
abstract: BACKGROUND
  Unbalanced inflammatory response and lymphocyte apoptosis are the main reasons for high mortality in patients with sepsis. Ginsenoside Rg1 (Rg1), the most important component isolated from Panax ginseng, has long been used to treat inflammatory and immune-related diseases. We designed this study to investigate the therapeutic effect of this agent on cecal ligation and puncture (CLP)-induced sepsis in mice.
  
  
  METHODS
  We randomly divided C57BL/6 mice into four experimental groups: sham, sham plus Rg1, CLP, and CLP plus Rg1. We intravenously injected Rg1 (20 mg/kg) 1 h after CLP and evaluated survival, bacterial clearance, cytokine production, histology, neutrophil emigration, and lymphocyte apoptosis.
  
  
  RESULTS
  Our study showed that treatment with Rg1 significantly improved survival in septic mice (P < 0.01). Rg1 administration suppressed the inflammatory response and enhanced bacterial clearance. Histologic examination of lung and liver showed only minor abnormalities in mice that received Rg1. In addition, Rg1 increased neutrophil counts in peritoneal cavity and inhibited lymphocyte apoptosis in thymus and spleen.
  
  
  CONCLUSIONS
  Ginsenoside Rg1 has a protective role against CLP-induced polymicrobial sepsis by attenuating the proinflammatory response, enhancing innate immunity and preserving adaptive immunity. Rg1 could be a promising new agent for treatment of sepsis.
authors.affiliation: Department of Anesthesiology and Intensive Care, Changhai Hospital, Second Military Medical University, Shanghai, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Zou
authors.forename: Tianzhu
authors.initials: T
authors.lastname: Tao
authors.forename: Ye
authors.initials: Y
authors.lastname: Tian
authors.forename: Jiali
authors.initials: J
authors.lastname: Zhu
authors.forename: Lijun
authors.initials: L
authors.lastname: Cao
authors.forename: Xiaoming
authors.initials: X
authors.lastname: Deng
authors.forename: Jinbao
authors.initials: J
authors.lastname: Li
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects*; D002432:Cecum / Q000293:injuries; D060085:Coinfection / Q000188:drug therapy / Q000382:microbiology / Q000401:mortality*; D004195:Disease Models, Animal; D036145:Ginsenosides / Q000494:pharmacology* / Q000627:therapeutic use*; D007249:Inflammation / Q000473:pathology / Q000517:prevention & control*; D008026:Ligation / Q000009:adverse effects; D008214:Lymphocytes / Q000187:drug effects / Q000473:pathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000187:drug effects / Q000473:pathology; D011677:Punctures / Q000009:adverse effects; D018805:Sepsis / Q000188:drug therapy / Q000382:microbiology / Q000401:mortality*; D013154:Spleen / Q000187:drug effects / Q000473:pathology; D015996:Survival Rate
chemical_list: D000893:Anti-Inflammatory Agents; D036145:Ginsenosides; C035054:ginsenoside Rg1
keywords: Anti-inflammation; Ginsenoside Rg1; Immune modulation; Sepsis