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

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Mehrafza Shafagh; Kermanshahi Sareh; Mostafidi Shahnaz; MOTAGHINEJAD MAJID; MOTEVALIAN MANIJEH; Fatima Sulail

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Journal: Iranian Journal of Basic Medical Sciences Year:2019 | Volume:22 | Issue:8 Page(s): 856-865

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Title

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

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Keywords

Akt

BDNF

CREB

Lithium

Methamphetamine

GSK3

Abstract

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.

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APA: Copy

Mehrafza, Shafagh, Kermanshahi, Sareh, Mostafidi, Shahnaz, MOTAGHINEJAD, MAJID, MOTEVALIAN, MANIJEH, & Fatima, Sulail. (2019). 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, 22(8), 856-865. SID. https://sid.ir/paper/725220/en

Vancouver: Copy

Mehrafza Shafagh, Kermanshahi 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. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES[Internet]. 2019;22(8):856-865. Available from: https://sid.ir/paper/725220/en

IEEE: Copy

Shafagh Mehrafza, Sareh Kermanshahi, Shahnaz Mostafidi, MAJID MOTAGHINEJAD, MANIJEH MOTEVALIAN, and Sulail Fatima, “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, vol. 22, no. 8, pp. 856–865, 2019, [Online]. Available: https://sid.ir/paper/725220/en

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