Shin Hyun Joo, Lee Ji Yeong, Son Eunyung, Lee Dong Hun, Kim Hyun Joon, Kang Sang Soo, Cho Gyeong Jae, Choi Wan Sung, Roh Gu Seob
Department of Anatomy and Neurobiology, School of Medicine, Medical Research Center for Neural Dysfunction, Institute of Health Sciences, Gyeongsang National University, Jinju, Gyeongnam, South Korea.
Neurosci Lett. 2007 Apr 6;416(1):49-54. doi: 10.1016/j.neulet.2007.01.060. Epub 2007 Jan 31.
Kainic acid (KA) induced oxidative stress is associated with hippocampal cell death. Recent studies suggest that curcumin, a potent antioxidant, may provide protection for KA-induced oxidative stress. We investigated the effects of curcumin treatment on hippocampal reactive astrocytes in mice with KA-induced seizures. Eighteen hours after curcumin treatment, mice were treated with KA (30 mg/kg, i.p.), and then sacrificed after a further 48 h. Using cresyl violet staining and TUNEL analysis, histological evaluation revealed cell death in the KA-treated hippocampus. However, marked cell death was not observed in mice treated with curcumin. In addition, curcumin treatment reduced the KA-induced immunoreactivity of caspase-3. Similarly, immunoreactivity analyses indicated that KA causes upregulation of hippocampal GFAP, eNOS, and HO-1 levels, all of which were reduced in animals those received the curcumin treatment. Our findings indicate that curcumin is a potent inhibitor of reactive astrocyte expression and thus, prevents hippocampal cell death. These results also support its potential for use in the treatment of neurodegenerative diseases.
kainic 酸(KA)诱导的氧化应激与海马体细胞死亡有关。最近的研究表明,姜黄素作为一种强效抗氧化剂,可能对 KA 诱导的氧化应激起到保护作用。我们研究了姜黄素治疗对 KA 诱导癫痫发作小鼠海马反应性星形胶质细胞的影响。姜黄素治疗 18 小时后,给小鼠腹腔注射 KA(30mg/kg),再过 48 小时后处死小鼠。通过甲酚紫染色和 TUNEL 分析,组织学评估显示 KA 处理的海马体中有细胞死亡。然而,在接受姜黄素治疗的小鼠中未观察到明显的细胞死亡。此外,姜黄素治疗降低了 KA 诱导的 caspase-3 免疫反应性。同样,免疫反应性分析表明,KA 导致海马体 GFAP、eNOS 和 HO-1 水平上调,而在接受姜黄素治疗的动物中这些水平均降低。我们的研究结果表明,姜黄素是反应性星形胶质细胞表达的强效抑制剂,因此可预防海马体细胞死亡。这些结果也支持了其在治疗神经退行性疾病方面的潜在应用价值。