PNAS: Cogin acid reverses neuronal damage in multiple sclerosis

At present, the drug for the treatment of multiple sclerosis (MS) mainly plays an immunomodulatory role, which has little or no effect on the neuroregeneration of damaged central nervous system (CNS) tissueAs a result, these drugs work mainly in the acute stage of the disease, but are much less effective in the chronic phasetherefore, an MS therapy with both immunomodulation and neuroregeneration will be very beneficialIn a recent study, Chinese researchers used a variety of in vivo and in vitro strategies to prove that the anti-inflammatory natural trichomonium substance, bear fruit acid (UA), can also directly promote the maturation of less protrusive glial cells and the myelin repair of the central nervous systemin an animal model of experimental autoimmune encephalomyelitis (EAE) (an animal model of MS), oral treatment of UA significantly reduced the severity of the disease and inflammation and myelin of the central nervous systemimportant lying is important that remylastification and nerve repair of the central nervous system can be observed in EAE mice with full demyelination and axon damage, even after the 60th day of immunityIn both in vivo and in vitro brain organ-type slicing cultures, UA treatment also enhances the remyulation of cup-like cell-induced demyelination models, and promotes the maturation of less protrusive glial cells in vitro, indicating that they have direct myelinization abilitymechanism, UA activates receptor gamma (PPAR)/CREB signal transduction through peroxide proliferation, induces the primary myelin neurotrophic factor CNTF in astrological glial cells, and the expression of myelin-related genes in the process of maturation of less protrusive glial cells through PPAR activationin short, the results show that UA, as an oral anti-inflammatory and neuroremediation agent, has significant potential for MS, especially in the chronic ongoing stage