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1- Department of Medicinal Chemistry, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
2- Department of pharmaceutical chemistry, Faculty of Pharmaceutical Chemistry, Pharmaceutical Sciences Branch, Islamic Azad university (IUAPS), Tehran, Iran.
3- Research Center for Addiction and Risky Behaviors (ReCARB), Iran Psychiatric Center, Iran University of Medical Sciences, Tehran, Iran.
4- Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.
5- Research and Development Department, Parsian-Exir-Aria Pharmaceutical Company, Tehran, Iran.
The neuroprotective impact of curcumin and the role of CREB-BDNF signaling in this way was evaluated in methamphetamine (METH)-induced neurodegeneration in rats. Sixty adult male rats were randomly split into 6 groups. While normal saline and 10 mg / kg METH were administered intraperitoneally in Groups 1 and 2, Groups 3, 4, 5 and 6 received METH (10 mg/kg) and Curcumin (10, 20, 40 and 80 mg/kg respectively) simultaneously. Morris Water Maze (MWM), oxidative hippocampal, antioxidant, inflammatory, apoptotic, and CREB and BDNF were assessed. Wechr('39')ve found that METH disturbs learning and memory. Concurrent curcumin therapy (40 and 80 mg / kg) decreased cognitive disturbance caused by METH. Multiple parameters, such as lipid peroxidation, oxidized form of glutathione (GSSG), interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α) and Bax, increased by METH therapy, although the reduced type of glutathione (GSH), Bcl-2, P-CREB and BDNF concentrations in the hippocampus decreased. Different doses of curcumin adversely attenuated METH-induced apoptosis, oxidative stress and inflammation, but enhanced concentrations of P-CREB and BDNF. Curcumin-caused neuroprotection against METH-induced neurodegeneration is conducted by P-CREB / BDNF signaling pathway activation.
Type of Study: Original |
Received: 2018/12/15 | Accepted: 2020/04/20 | Published: 2018/03/15

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