Moringin is a potent and selective TRPA1 ion channel natural agonist with an EC 50 of 3.14 μM. Moringin does not activate or activates very weakly the vanilloids somatosensory channels TRPV1, TRPV2, TRPV3 and TRPV4, and the melastatin cooling receptor TRPM8. Moringin has hypoglycemic, antimicrobial, anti-inflammatory, anticancer and neuroprotection activities. In Vitro In SH-SY5Y human neuroblastoma cells, Moringin (16.4 µM; 24-72 h) significantly reduces SH-SY5Y cell growth in a time and concentration-dependent manner. Moringin (1.64-8.2 μM; 24 h) increases the expression of p53, p21, and Bax at both the protein and transcriptional level in SH-SY5Y cells. Moringin significantly increases the gene expression of both caspase 3 and 9 and enhanced their cleavage, thereby initiating an intrinsic apoptotic cascade. Moringin inhibits nuclear translocation of NF-κB. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo In experimental autoimmune encephalomyelitis (EAE) mice, Moringin (10 mg/kg; intraperitoneally daily for 5 week) pretreatment normalizes the aberrant Wnt-β-catenin pathway, resulting in GSK3β inhibition and β-catenin upregulation, which regulates T-cell activation (CD4 and FoxP3), suppresses the main inflammatory mediators (IL-1β, IL-6, and COX2), through activation of PPARγ. Moringin increases antioxidant Nrf2 expression in EAE mice. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Form:Solid