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10.1142/S0192415X19500812

http://scihub22266oqcxt.onion/10.1142/S0192415X19500812
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31645122!ä!31645122

suck abstract from ncbi


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pmid31645122      Am+J+Chin+Med 2019 ; 47 (7): 1589-1609
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  • Red Ginseng Reduces Inflammatory Response via Suppression MAPK/P38 Signaling and p65 Nuclear Proteins Translocation in Rats and Raw 264 7 Macrophage #MMPMID31645122
  • Adam GO; Kim GB; Lee SJ; Lee H; Kang HS; Kim SJ
  • Am J Chin Med 2019[]; 47 (7): 1589-1609 PMID31645122show ga
  • Lipopolysaccharides (LPS) cause systemic inflammatory responses, which are characterized by high mortality and multiple signs, including metabolic disturbances, respiratory acidosis, hypotension, and vital organs disorder. Cytokines secretion and oxidative stress are the main features of the disease. Diagnosis and treatment of systemic inflammation (SI) remain a challenge. Korean Red Ginseng (RG) is one of medicinal herbs that showed a potent anti-oxidant effect. We aimed to study the protective effects of RG on systemic inflammatory response in rats and RAW 264.7 macrophage cells induced by LPS. The rats were treated with water and alcohol extracts of RG for four weeks to prevent the inflammatory response. The result showed that LPS toxin increased morbidity and mortality, and induced liver, kidney, and lung injuries manifested by deteriorated biomarkers. Hypotension, hypomagnesemia, acidosis, and oxidative stress were observed in septic rats. However, RG extracts attenuated liver, kidney, and lung enzymes and metabolites in treated groups via its anti-inflammatory and anti-oxidant properties. Furthermore, RG improved magnesium and blood pressure in the treated groups. RAW 264.7 macrophage cells exposed to LPS disturbance in translocation of p65 and MAPK/p38. Nevertheless, RG-pretreated cells did not significantly alter. In conclusion, RG reduced the rates of mortality and morbidity of treated rats - liver, kidney, and lung injuries were protected in the treated groups through the potentiation of anti-oxidant defense. RG was able to conserve mitochondrial function, inhibiting the activation of MAPK/p38 signaling and suppressing NF-kappaB p65 cytoplasm-nucleus transport. Further studies are needed to examine the effects on chronic conditions in animal models and human.
  • |Animals[MESH]
  • |Anti-Inflammatory Agents/*administration & dosage[MESH]
  • |Humans[MESH]
  • |Inflammation/*drug therapy/genetics/immunology/metabolism[MESH]
  • |MAP Kinase Signaling System/drug effects[MESH]
  • |Macrophages/*drug effects/immunology/metabolism[MESH]
  • |Male[MESH]
  • |Mice[MESH]
  • |Panax/*chemistry[MESH]
  • |Plant Extracts/*administration & dosage[MESH]
  • |Protein Transport/drug effects[MESH]
  • |RAW 264.7 Cells[MESH]
  • |Rats[MESH]
  • |Rats, Sprague-Dawley[MESH]
  • |Transcription Factor RelA/genetics/*immunology[MESH]


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