Melatonin promotes blood-brain barrier integrity in methamphetamine-induced inflammation in primary rat brain microvascular endothelial cells.

摘要: Melatonin is a neurohormone and has high potent of antioxidant that widely reported to be active against methamphetamine (METH)-induced toxicity neuron, glial cells, brain endothelial cells. However, the role melatonin on inflammatory responses which are mostly caused by blood-brain barrier (BBB) impairment METH administration not been investigated. This study used primary rat microvascular cells (BMVECs) determine protective mechanism METH-induced in BBB via nuclear factor-ĸB (NF-κB) factor erythroid 2-related factor-2 (Nrf2) signaling. Herein, we demonstrated reduced level mediators, including intercellular adhesion molecules (ICAM)-1, vascular cell (VCAM)-1, matrix metallopeptidase (MMP)-9, inducible nitric oxide synthase (iNOS), (NO) METH. These were related decrease expression translocation NF-κB p65 subunit activity NADPH oxidase (NOX)-2. In addition, promoted processes, modulated Nrf2, also increased heme oxygenase (HO)-1, NAD (P) H: quinone oxidoreductase (NQO)-1, γ-glutamylcysteine (γ-GCLC), superoxide dismutase (SOD) through NOX2 mechanism. found was mediated receptors (MT1/2). We concluded interaction with its receptor prevented suppressing signaling promoting Nrf2 before impairment.