این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Iranian Journal of Basic Medical Sciences، جلد ۲۲، شماره ۸، صفحات ۸۵۶-۸۶۵
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی Pharmacological evidence for lithium-induced neuroprotection against methamphetamine-induced neurodegeneration via Akt-1/GSK3 and CREB-BDNF signaling pathways
چکیده انگلیسی مقاله 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.
کلیدواژه‌های انگلیسی مقاله Akt, BDNF, CREB, Lithium, Methamphetamine, GSK3
نویسندگان مقاله | Shafagh Mehrafza
Department of pharmaceutical chemistry, faculty of pharmaceutical chemistry, pharmaceutical sciences branch, Islamic Azad University (IUAPS), Tehran, Iran


| Sareh Kermanshai
Department of pharmaceutical chemistry, faculty of pharmaceutical chemistry, pharmaceutical sciences branch, Islamic Azad University (IUAPS), Tehran, Iran


| Shahnaz Mostafidi
Department of pharmaceutical chemistry, faculty of pharmaceutical chemistry, pharmaceutical sciences branch, Islamic Azad University (IUAPS), Tehran, Iran


| Majid Motaghinejad
Research Center for Addiction and Risky Behaviors (ReCARB), Iran Psychiatric Center, Iran University of Medical Sciences, Tehran, Iran


| Manijeh Motevalian
Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran


| Sulail Fatima
Department of Physiology, Tehran University of Medical Sciences-International Campus (TUMS-IC), Tehran, Iran
نشانی اینترنتی http://ijbms.mums.ac.ir/article_13235.html
فایل مقاله اشکال در دسترسی به فایل - ./files/site1/rds_journals/87/article-87-1627320.pdf
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Original Article
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات