Mohd Sairazi Nur Shafika, Sirajudeen Kuttulebbai N S, Muzaimi Mustapha, Mummedy Swamy, Asari Mohd Asnizam, Sulaiman Siti Amrah
Department of Chemical Pathology, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, 16150 Kubang Kerian, Kota Bharu, Kelantan, Malaysia.
Department of Neurosciences, School of Medical Sciences, Health Campus, Universiti Sains Malaysia, 16150 Kubang Kerian, Kota Bharu, Kelantan, Malaysia.
Evid Based Complement Alternat Med. 2018 Jul 15;2018:7287820. doi: 10.1155/2018/7287820. eCollection 2018.
The protective effect of tualang honey (TH) on neuroinflammation and caspase-3 activity in rat cerebral cortex, cerebellum, and brainstem after kainic acid- (KA-) induced status epilepticus was investigated. Male Sprague-Dawley rats were pretreated orally with TH (1.0 g/kg body weight) five times at 12 h intervals. KA (15 mg/kg body weight) was injected subcutaneously 30 min after last oral treatment. Rats were sacrificed at 2 h, 24 h, and 48 h after KA administration. Neuroinflammation markers and caspase-3 activity were analyzed in different brain regions 2 h, 24 h, and 48 h after KA administration. Administration of KA induced epileptic seizures. KA caused significant () increase in the level of tumor necrosis factor alpha (TNF-), interleukin 1 beta (IL-1), glial fibrillary acidic protein (GFAP), allograft inflammatory factor 1 (AIF-1), and cyclooxygenase-2 (COX-2) and increase in the caspase-3 activity in the rat cerebral cortex, cerebellum, and brainstem at multiple time points. Pretreatment with TH significantly () reduced the elevation of TNF-, IL-1, GFAP, AIF-1, and COX-2 level in those brain regions at multiple time points and attenuated the increased caspase-3 activity in the cerebral cortex. In conclusion, TH reduced neuroinflammation and caspase-3 activity after kainic acid- (KA-) induced status epilepticus.
研究了特琅蜂蜜(TH)对海藻酸(KA)诱导的癫痫持续状态后大鼠大脑皮层、小脑和脑干神经炎症及半胱天冬酶 - 3活性的保护作用。雄性Sprague-Dawley大鼠每隔12小时口服TH(1.0 g/kg体重),共5次。在最后一次口服给药后30分钟皮下注射KA(15 mg/kg体重)。在给予KA后2小时、24小时和48小时处死大鼠。在给予KA后2小时、24小时和48小时分析不同脑区的神经炎症标志物和半胱天冬酶 - 3活性。给予KA诱发癫痫发作。KA导致大鼠大脑皮层、小脑和脑干在多个时间点肿瘤坏死因子α(TNF - )、白细胞介素1β(IL - 1)、胶质纤维酸性蛋白(GFAP)、同种异体移植炎症因子1(AIF - 1)和环氧化酶 - 2(COX - 2)水平显著()升高以及半胱天冬酶 - 3活性增加。用TH预处理可显著()降低这些脑区在多个时间点TNF - 、IL - 1、GFAP、AIF - 1和COX - 2水平的升高,并减弱大脑皮层中增加的半胱天冬酶 - 3活性。总之,TH可减轻海藻酸(KA)诱导的癫痫持续状态后的神经炎症和半胱天冬酶 - 3活性。