The Preventive And Curative Effect Of Acer Truncatum Oil On Ms And Its Mechanism

Multiple Sclerosis(MS)is an autoimmune demyelinating disease with complex pathogenesis,which involve the central nervous system(CNS).MS has multiple lesions and repeated pathogenesis,which makes the patients disabled with a high probability and seriously affecting the patients’ lives.The pathogenesis of MS is still unclear,and it may be caused by various factors including immunity,environment,genetics,etc.The currently recognized pathogenesis is: abnormal immunity leads to damage to the blood-brain barrier,a variety of inflammatory factors and immune cells enter the CNS,act on microglia and immune cells,lead an inflammation,then cause demyelination,neuronal death,and axonal damage.At present,the treatment of MS mainly focuses on anti-inflammatory,but this is only effective in the relapse and remission stages of the disease.Therefore,the development of new therapeutic methods for MS has become an urgent problem to be solved.Acer truncatum(A.T)is a unique tree species in China.Its seeds are rich in oil,which has a balanced proportion and rich in long chain unsaturated fatty acids(LCUFA).As a worldrecognized healthy fatty acid,it has been proven to have good therapeutic effects on many diseases.Both omega ω-3 LCUFA and ω-6 LCUFA are essential fatty acids and cannot be synthesized by the body.Among them,α-linolenic acid(α-ALA)of ω-3 LCUFA is converted into docosahexaenoic acid(DHA)and eicosapentaenoic acid(EPA)which can resist platelet aggregation,relax blood vessels,improve brain function,reduce inflammation,and avoid cell damage.ω-6 LCUFA is not only the main energy source of the body,but it plays a vital role in brain function and is recommended as a supplementary diet for the treatment of MS clinically.ω-9 LCUFA is a kind of fatty acid with great development potential,which has been found to have the potential to treat white matter disease,especially nervonic acid(NA)of ω-9 LCUFA.In addition,A.T oil is rich in diacylglycerol,which is a key lipid mediator connecting antagonism between overnutrition and insulin pheromone signal,and it is easy to accumulate in lipids.The product of its decomposition by diacylglycerol kinase is an important component of the phospholipid bilayer.In order to verify the effect of lipids of A.T oil on the regeneration of MS demyelination,this experiment used primary cell culture,multiple immunofluorescence,laser confocal,Western blot,ethology,chemical staining,and other techniques to test by the primary suckling mouse cells,cuprizone(CUP)and experimental autoimmune encephalomyelitis(EAE).The results of the study are as follows:(1)By adding A.T oil to the culture medium,it was found that A.T oil can not only promote the maturation of primary oligodendrocytes(OLs)of suckling mice but also promote the production of myelin-related mature proteins and promote myelination.(2)CUP-induced acute demyelination and chronic demyelination models showed significant demyelination in both white and gray matter,and both activated endoplasmic reticulum stress through the IRE1-XBP and PERK-e IF2α pathways to promote OLs apoptosis.In turn,endoplasmic reticulum stress affects myelination and leads to demyelination.(3)A.T oil can effectively improve disturbance of spatial consciousness and limb coordination caused by CUP.It effectively promotes the maturation of OLs by inhibiting the activation of astrocytes,then promotes the recovery of myelin.(4)N-acetyl-D-(+)-glucosamine(Glc NAc)is used as a clinical agent for the treatment of arthritis and can effectively inhibit Th17 and Th1 cells.A.T oil and Glc NAc act together on Th17 or Th1 cells,inhibit inflammatory factors,and the production of related glial cells.This synergism protects myelin while promoting the production of new myelin by promoting the maturation of OLs(Oligodendrocytes),which in turn improved clinical scores,gait,and limb coordination in EAE model mice.In addition,through the correlation analysis between genus of gut microorganisms and demyelination,it was found that A.T oil and Glc NAc may have a common target genus PAC002172＿g in inhibiting Th17 or Th1 cells.