سامانه مدیریت نشریات علمی دانشگاه علوم پزشکی مشهد

Mehrafza, Shafagh, Kermanshai, Sareh, Mostafidi, Shahnaz, Motaghinejad, Majid, Motevalian, Manijeh, Fatima, Sulail. (1398). Pharmacological evidence for lithium-induced neuroprotection against methamphetamine-induced neurodegeneration via Akt-1/GSK3 and CREB-BDNF signaling pathways. , 22(8), 856-865. doi: 10.22038/ijbms.2019.30855.7442
Shafagh Mehrafza; Sareh Kermanshai; Shahnaz Mostafidi; Majid Motaghinejad; Manijeh Motevalian; Sulail Fatima. "Pharmacological evidence for lithium-induced neuroprotection against methamphetamine-induced neurodegeneration via Akt-1/GSK3 and CREB-BDNF signaling pathways". , 22, 8, 1398, 856-865. doi: 10.22038/ijbms.2019.30855.7442
Mehrafza, Shafagh, Kermanshai, Sareh, Mostafidi, Shahnaz, Motaghinejad, Majid, Motevalian, Manijeh, Fatima, Sulail. (1398). 'Pharmacological evidence for lithium-induced neuroprotection against methamphetamine-induced neurodegeneration via Akt-1/GSK3 and CREB-BDNF signaling pathways', , 22(8), pp. 856-865. doi: 10.22038/ijbms.2019.30855.7442
Mehrafza, Shafagh, Kermanshai, Sareh, Mostafidi, Shahnaz, Motaghinejad, Majid, Motevalian, Manijeh, Fatima, Sulail. Pharmacological evidence for lithium-induced neuroprotection against methamphetamine-induced neurodegeneration via Akt-1/GSK3 and CREB-BDNF signaling pathways. , 1398; 22(8): 856-865. doi: 10.22038/ijbms.2019.30855.7442

Pharmacological evidence for lithium-induced neuroprotection against methamphetamine-induced neurodegeneration via Akt-1/GSK3 and CREB-BDNF signaling pathways

Iranian Journal of Basic Medical Sciences
مقاله 3، دوره 22، شماره 8، آبان 2019، صفحه 856-865    اصل مقاله (1.48 M)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2019.30855.7442
نویسندگان
Shafagh Mehrafza1؛ Sareh Kermanshai1؛ Shahnaz Mostafidi1؛ Majid Motaghinejad* 2؛ Manijeh Motevalian3؛ Sulail Fatima4
1Department of pharmaceutical chemistry, faculty of pharmaceutical chemistry, pharmaceutical sciences branch, Islamic Azad University (IUAPS), Tehran, Iran
2Research Center for Addiction and Risky Behaviors (ReCARB), Iran Psychiatric Center, Iran University of Medical Sciences, Tehran, Iran
3Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
4Department of Physiology, Tehran University of Medical Sciences-International Campus (TUMS-IC), Tehran, Iran
چکیده
Objective(s): Neurodegeneration is an outcome of Methamphetamine (METH) abuse. Studies have emphasized on the neuroprotective properties of lithium. The current study is designed towards evaluating the role of Akt-1/GSK3 and CREB-BDNF signaling pathways in mediating lithium neuroprotection against METH-induced neurodegeneration in rats.
Materials and Methods: Sixty adult male rats were randomly divided into five groups: control group (received 0.7 ml normal saline per rat for 28 days), METH group (given 10 mg/kg of METH intraperitoneally for 28 days), groups 3, 4, and 5 (given  METH (10 mg/kg) and lithium (75, 150, and 300 mg/kg intraperitoneally, individually for 28 days). Morris water maze (MWM) was used to assess mental functions. In addition to hippocampal neurodegeneration, Brain-derived neurotrophic factor (BDNF), cAMP response element binding (CREB), Glycogen synthase kinase 3 (GSK3), and Protein kinase B (Akt-1) were assessed in isolated hippocampus.
Results: METH abuse caused marked disorders in learning and memory that were dramatically improved with various doses of lithium. Furthermore, METH increased lipid peroxidation and the levels of oxidized form of interleukin 1 beta (IL-1β), glutathione (GSSG), Bax, tumor necrosis factor alpha (TNF-α), and GSK3,  while attenuating the extent of glutathione (reduced form (GSH)), P-CREB, Bcl-2, BDNF,  and Akt-1 in the hippocampus. Moreover, METH declined superoxide dismutase (SOD), glutathione reductase (GR), and glutathione peroxidase (GPx) activity in the hippocampus. Conversely, lithium attenuated METH-stimulated apoptosis, oxidative stress, and inflammation; while improving the extent of BDNF and P-CREB.
Conclusion: Probably lithium possesses neuroprotection against METH-stimulated neurodegeneration in the hippocampus via Akt-1/GSK3β and CREB/BDNF signaling pathways.
کلیدواژه‌ها
Akt؛ BDNF؛ CREB؛ Lithium؛ Methamphetamine؛ GSK3
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