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Minocycline may be useful to prevent or treat methamphetamine-induced neural cell death: Hypothetic role of autophagia and apoptosis signaling pathway
Afrah Sepehr1, Majid Motaghinejad1, Soomaayeh Heysieattalab2, Sepideh Safari1
1 Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Tabriz, Iran
2 Division of Cognitive Neuroscience, University of Tabriz, Tabriz, Iran
| Date of Submission | 12-Oct-2019 |
| Date of Acceptance | 16-Dec-2019 |
| Date of Web Publication | 25-Feb-2020 |
Correspondence Address:
Dr. Majid Motaghinejad
Tehran, Hemmat Highway Beside the Milad Tower, Iran University of Medical Sciences, P.O. Box: 1449614535. Tehran
Iran
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/abr.abr_258_19
How to cite this article:
Sepehr A, Motaghinejad M, Heysieattalab S, Safari S. Minocycline may be useful to prevent or treat methamphetamine-induced neural cell death: Hypothetic role of autophagia and apoptosis signaling pathway. Adv Biomed Res 2020;9:7 |
How to cite this URL:
Sepehr A, Motaghinejad M, Heysieattalab S, Safari S. Minocycline may be useful to prevent or treat methamphetamine-induced neural cell death: Hypothetic role of autophagia and apoptosis signaling pathway. Adv Biomed Res [serial online] 2020 [cited 2021 Jan 19];9:7. Available from: https://www.advbiores.net/text.asp?2020/9/1/7/279165 |
Methamphetamine (METH) is a psychostimulant agent, and its neurotoxic and neurobehavioral consequences are serious.[1] Studies indicated that chronic abuse of METH can cause neural cell death in human and animal subjects.[1],[2] Previous studies also showed that chronic abuse of METH can cause neurodegeneration, clear mechanism to these types of neurodegeneration remains unclear, but it seems that neuroinflammatory signaling pathways involved in this manner.[1] By induction of Bcl-2 phosphorylation after beginning an autophagy or apoptosis signal on the cell surface, in particular by activating tumor necrosis factor-alpha (TNF-α) receptor, c-Jun N-terminal kinase (JNK) causes phosphorylation of Bcl-2 which this phenomenon causes inactivation and dissociation of Bcl-2 from Beclin1 or Bax which cause initiation of autophagy or apoptosis respectively and therefore cell death was occurred[3],[4] On the other way, during recent years, using new neuroprotective compounds with therapeutic probability for the treatment of drug abuses induced sequels has been amazingly increased.[5],[6] Minocycline is a broad-spectrum and long-acting antibiotic and possesses anti-inflammatory, neuroprotective, and neural survival properties.[7],[8] Pervious data suggested that minocycline has anti-inflammatory properties and can inhibit TNF-α receptor downstream signaling cascade in the neural cells.[9],[10] Thus, according to the above evidence, we can suggest and have the theory that by inhibition of TNF-receptor activation and downstream JNK/Bcl-2-Beclin1 or Bcl-2/Bax signaling pathways, minocycline will likely inhibit METH-induced apoptosis and autophagia and probably by this mechanism can inhibit METH-induced neurodegeneration and neural cell loss [Figure 1]. | Figure 1: Minocycline can inhibit METH-induced TNFR activation and c-Jun N-terminal kinase/Bcl-2-Beclin1 or c-Jun N-terminal kinase/Bcl-2/Bax signaling pathway which may reduce METH-induced autophagia and apoptosis and consequences neurodegeneration. Further, minocycline directly activates mitochondrial biogenesis which leads to inhibition of METH-induced oxidative stress and inflammation. TNFR: TNF-α receptor, METJ: Methamphetamine
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| References | |  |
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