Dai Peng, Xu Lingyu, Zhang Peng, Liang Zheng, Chu Yunhang, Yu Ziqiao, Cao Lin, Sun Peng, Li Xia
College of Traditional Chinese Medicine, Chang Chun University of Chinese Medicine, Changchun, China.
The Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, China.
Front Pharmacol. 2025 Jul 10;16:1602716. doi: 10.3389/fphar.2025.1602716. eCollection 2025.
The purpose of this study is to systematically evaluate the therapeutic effect of curcumin on rodent epilepsy models through a meta-analysis of multiple animal experiments. It will also explore its potential mechanism of anti-oxidative stress and anti-inflammation to provide a theoretical basis for the application of curcumin in the clinical treatment of epilepsy.
A total of 23 eligible animal studies were identified by searching eight databases (up to March 2025), including PubMed, Embase, Web of Science, Cochrane Library, and CNKI, Wan Fang, VIP, CBM. SYRCLE's risk of bias tool was used to assess the quality of the literature, and Meta-analysis was performed using Review Manager 5.4 and Stata 18 software. Primary outcome measures included epilepsy latency, Morris water maze escape latency, oxidative stress markers (MDA, GSH, SOD), inflammatory factors (IL-1β, TNF-α), and Glial fibrillary acidic protein (GFAP).
Meta-analysis showed that the curcumin intervention group significantly extended the epilepsy latency (SMD = 1.85, 95% CI = 1.05-2.64, P < 0.00001) and shortened the water maze escape latency (SMD = -1.69, 95% CI = -2.23-1.16, P < 0.00001). In terms of antioxidant indicators, curcumin significantly decreased MDA levels (SMD = -3.50, P < 0.00001) and increased GSH (SMD = 2.87, P < 0.00001) and SOD (SMD = 2.42, P < 0.00001). The anti-inflammatory results showed that the levels of IL-1β (SMD = -1.73, P = 0.04) and TNF-α (SMD = -1.65, P < 0.00001) were significantly decreased, and the levels of GFAP-positive cells were decreased (SMD = -1.72, P = 0.05). Subgroup analysis showed that medium and high doses (100-299 mg/kg and ≥300 mg/kg) of curcumin were more stable, but the low dose group (<100 mg/kg) did not conduct in-depth analysis due to insufficient sample size of individual indicators. Sensitivity analysis and funnel plots suggest robust results, but some publication bias exists.
Curcumin can effectively improve epileptic seizures and cognitive dysfunction in epileptic rodents through the dual mechanisms of antioxidative stress (inhibiting lipid peroxidation and enhancing antioxidant enzyme activity) and anti-inflammatory (reducing the release of pro-inflammatory factors and inhibiting glial cell activation). However, species differences and potential publication bias have certain effects on the results, and high-quality clinical studies can be carried out in the future to verify their clinical application value.
本研究旨在通过对多项动物实验的荟萃分析，系统评价姜黄素对啮齿类癫痫模型的治疗效果。同时探讨其抗氧化应激和抗炎的潜在机制，为姜黄素在癫痫临床治疗中的应用提供理论依据。
通过检索8个数据库（截至2025年3月），包括PubMed、Embase、Web of Science、Cochrane Library以及CNKI、万方、维普、CBM，共识别出23项符合条件的动物研究。使用SYRCLE的偏倚风险工具评估文献质量，并使用Review Manager 5.4和Stata 18软件进行荟萃分析。主要结局指标包括癫痫潜伏期、莫里斯水迷宫逃避潜伏期、氧化应激标志物（丙二醛、谷胱甘肽、超氧化物歧化酶）、炎症因子（白细胞介素-1β、肿瘤坏死因子-α）和胶质纤维酸性蛋白（GFAP）。
荟萃分析表明，姜黄素干预组显著延长癫痫潜伏期（标准化均数差=1.85，95%可信区间=1.05 - 2.64，P<0.00001）并缩短水迷宫逃避潜伏期（标准化均数差=-1.69，95%可信区间=-2.23 - 1.16，P<0.00001）。在抗氧化指标方面，姜黄素显著降低丙二醛水平（标准化均数差=-3.50，P<0.00001），增加谷胱甘肽（标准化均数差=2.87，P<0.00001）和超氧化物歧化酶（标准化均数差=2.42，P<0.00001）。抗炎结果显示，白细胞介素-1β（标准化均数差=-1.73，P = 0.04）和肿瘤坏死因子-α（标准化均数差=-1.65，P<0.00001）水平显著降低，GFAP阳性细胞水平降低（标准化均数差=-1.72，P = 0.05）。亚组分析表明，中高剂量（100 - 299mg/kg和≥300mg/kg）的姜黄素效果更稳定，但低剂量组（<100mg/kg）因个别指标样本量不足未进行深入分析。敏感性分析和漏斗图表明结果可靠，但存在一定的发表偏倚。
姜黄素可通过抗氧化应激（抑制脂质过氧化和增强抗氧化酶活性）和抗炎（减少促炎因子释放和抑制胶质细胞活化）双重机制有效改善癫痫啮齿动物的癫痫发作和认知功能障碍。然而，物种差异和潜在的发表偏倚对结果有一定影响，未来可开展高质量的临床研究以验证其临床应用价值。
