P 34: Evidence of Panax Ginseng in Multiple Sclerosis
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چکیده مقاله:
Introduction: MS disease destroys the myelin of the central nervous system. MS causing damage to the myelin sheath of the brain and the spinal cord. The mechanism is hurt by the immune system .and disruption of myelin producing cells or disconnect interconnected processes by disconnect inner white. MS is an autoimmune disease when leukocyte antigen system varies autoimmune disease like MS spread. Ginseng, the root of the panax ginseng, has been popular traditional herbal medicine in korea , japan , china for thousands of years. The major component of ginseng is ginsenoside. Divided into two spheres: American origin and Korean origin. Materials and Methods: The literature search was performed in Mar 2017, using three electronic databases (PubMed, Web of Science and Scopus). The reference sections of the included articles were also reviewed and a search based on the first author of the articles was carried out. The search was limited to English language articles. Results: MS disorders fatigue, pain, depression, sexual problems, sleep disorders. The difference between two Ginseng models are in severity index of insulin and glucose in post prandial medicinal properties include advanced functions of the brain, pain, anti-tumor effect, enhance immune function ,anti-fatigue , anti-stress , anti-diabetes , ,enhance liver function , adjustment blood pressure , anti-inflammation effective in macrophages function , effective in neuroprotective mechanism, effective in the treatment of neurodegenerative disease. And neurological disorder like MS and Parkinson ginseng regulates immune cell models like macrophages, NK cells, T cell, dendritic cells. Conclusion: Treatment with ginseng inhibits the secretion of inflammatory mediators like TNFa and interleukin 1B .Acidic polysaccharide of panax ginseng (APG) stimulates the reduction of the brain response during experimental autoimmune encephalomyelitis (EAE).
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عنوان ژورنال
دوره 5 شماره 2
صفحات 65- 65
تاریخ انتشار 2017-04
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