Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Department of Basic Sciences, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Metab Brain Dis. 2023 Apr;38(4):1379-1388. doi: 10.1007/s11011-023-01169-8. Epub 2023 Jan 26.
Neuroinflammation is a key pathological event triggering neurodegenerative process, resulting in neurologic sequelae. Curcumin (cur) has recently received increasing attention due to its anti-inflammatory properties. Therefore, we investigated the protective effects of curcumin on lipopolysaccharide (LPS)-induced memory impairments, long-term potentiation (LTP) deficits, hippocampal inflammatory cytokines, and neuronal loss in male rats. Rats were randomly divided into four groups as follows: (1) Vehicle; (2) cur; (3) LPS; and (4) cur/LPS. Following curcumin pretreatment (50 mg/kg, per oral via gavage, 14 consecutive days), animals received a single dose of LPS (1 mg/kg, intraperitoneally) or saline. Twenty-four hours after LPS/or saline administration, passive avoidance test (PAT), hippocampal LTP, inflammatory cytokines (TNFα, IL-1β), and neuronal loss were assessed in hippocampal tissue of rats. Our results indicated that pretreatment with curcumin in LPS-challenged rats attenuates memory impairment in PAT, which was accompanied by significant increase in the field excitatory post-synaptic potential (fEPSP) slope and population spike (PS) amplitude. Hence, pretreatment with curcumin in LPS-treated rats decreased hippocampal concentration of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β), as well as reduced neuronal loss in the hippocampal tissue. This study provide evidence that pretreatment with curcumin attenuates LPS-induced memory impairment and LTP deficiency, which may be partly related to the amelioration of inflammatory cytokines and neuronal loss in the hippocampal tissue.
神经炎症是触发神经退行性过程的关键病理事件,导致神经系统后遗症。姜黄素(cur)由于其抗炎特性,最近受到越来越多的关注。因此,我们研究了姜黄素对脂多糖(LPS)诱导的记忆障碍、长时程增强(LTP)缺陷、海马炎性细胞因子和雄性大鼠神经元丢失的保护作用。大鼠随机分为四组:(1)载体;(2)姜黄素;(3)LPS;(4)姜黄素/LPS。姜黄素预处理(50mg/kg,灌胃,连续 14 天)后,动物接受单次 LPS(1mg/kg,腹腔内)或生理盐水注射。LPS/生理盐水给药后 24 小时,评估大鼠海马组织中的被动回避测试(PAT)、海马 LTP、炎性细胞因子(TNFα、IL-1β)和神经元丢失。我们的结果表明,LPS 应激大鼠给予姜黄素预处理可减轻 PAT 中的记忆障碍,同时显著增加场兴奋性突触后电位(fEPSP)斜率和群体锋电位(PS)幅度。因此,LPS 处理大鼠给予姜黄素预处理可降低海马肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)浓度,并减少海马组织中的神经元丢失。这项研究提供了证据表明,姜黄素预处理可减轻 LPS 诱导的记忆障碍和 LTP 缺陷,这可能部分与海马组织中炎性细胞因子和神经元丢失的改善有关。