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Tranylcypromine hemisulfate

CAS No. : 13492-01-8

MCE 站：Tranylcypromine hemisulfate

产品活性：Tranylcypromine hemisulfate (dl-Tranylcypromine hemisulfate) 是一种不可逆的非选择性单胺氧化酶 (MAO) 抑制剂，可用于研究抑郁症。Tranylcypromine hemisulfate 还是一种赖氨酸特异性脱甲基酶 1 (LSD1) 抑制剂，可抑制病变的生长并改善患有子宫内膜异位症的小鼠的全身痛觉过敏。

研究领域：Neuronal Signaling  |  Epigenetics

作用靶点：Monoamine Oxidase  |  Histone Demethylase

In Vitro: Tranylcypromine (10 nM to 10 ?M) exerts neuroprotective effects against toxicity induced by human Aβ(1-42) oligomers independently from the presence of glial cells. Tranylcypromine (100 μM) significantly protects RGCs from glutamate neurotoxicity-induced apoptosis as well as apoptosis induced by oxidative stress. Tranylcypromine promotes mitogen-activated protein kinase 12 (p38 MAPKγ) expression under conditions of glutamate (Glu)-induced stress. Besides, tranylcypromine contributes to RGC survival via alterations of p38 MAPKγ activity.

In Vivo: Tranylcypromine treatment significantly and substantially reduces the lesion size and improves generalized hyperalgesia in a dose-dependent fashion in mice with induced endometriosis. In addition, tranylcypromine treatment results in reduced immunoreactivity to biomarkers of proliferation, angiogenesis, and H3K4 methylation, leading to arrested EMT and lesion growth. Tranylcypromine (500 mM) injection exerts neuroprotective effects within intracellular apoptotic signaling pathways and suppresses morphologic changes in the retina of the rat, suppresses caspase 3 activity and recovers p38 MAPKγ expression in the retina after NMDA-induced injury, and enhances RGC survival after retinal injury via the attenuation of NMDA neurotoxicity. Tranylcypromine (10 ?g/g) causes an approximate and significant doubling of labeled cells in the combined brain regions examined, as detected by BrdU immunohistochemistry. Tranylcypromine causes the greatest increase in cell proliferation in the cerebellum.

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