Study the Affection of Methamphetamine on Neuroinflammation: Systematic Review

Publish Year: 1398
نوع سند: مقاله کنفرانسی
زبان: English
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NIMED03_309

تاریخ نمایه سازی: 7 آبان 1398

Abstract:

Methamphetamine(METH) is one of the most dangerous drugs worldwide. It can cause neurotoxicity, high irritability and other disorders suchas depression, hypertension and schizophrenia. The aim of this systematic review is to investigate about METH effects on neuroinflammation in neurological disease. We searched on Pubmed, Iranmedex, SID and Google Scholar database from 2000 to A pril 2019 and found219 articles that 190 of which were excluded from the research by investigating the titles and 16 others by checking abstract; finally13 articles are included in our study. Based on the studies, the effect of METH on neuroinflammation, which was dose-dependent, was through the effect on gene expression (e.g. NF-KB) and immune factors such as cytokines (e.g., interleukin1 )β, 6,(10 and tumor necrosis factor α (TNF‐α)), chemokines and the receptors (e.g. Dopaminergic Receptor, Toll- Like Receptor and Caspase-11). In people with HIV infection METH increased HIV co-receptors. METH had a direct effect on Blood Brian Barrier (BBB), causing it to open and disrupt its function .Rashomolog enriched in striatum (Rhes) protein had an important role in METH-induced neuroinflammation. The effect of METH on dopaminergic neurons, that causes Parkinson’s disease, was indirect – with Damaged neurons release danger-associated molecularpatterns (DAMPs) such as high mobility group box-1 (HMGB1) – in central nervous system (CNS). METH derivatives, such as Methylenedioxymethamphetamine (MDMA) and Methiopropamine, also had inflammatory effects. MDMA causes neuroinflammation through the effect on microglial (CD11b), astroglial (GFAP) and dopamine neuron. Chemicals such as H2S and asiatic acid had an anti-inflammatory effect on inflammation caused by METH. Conclusions: METH, bypassing BBB and affecting different cells in CNS leads to theinflammatory cytokinins secretions and finally causes neuroinflammation. Inhibiting the effect of METH on neural cells can prevent the prevalence of its hazardous effects.

Authors

Mahtab Aghaee Jaghargh

Student Research Committee, Mashhad Branch, Islamic Azad University, Mashhad, Iran

Mohammadreza Khojaste

Mashhad Branch, Islamic Azad University, Mashhad, Iran