Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Division of Neurology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand.
Mol Med Rep. 2017 Oct;16(4):4710-4720. doi: 10.3892/mmr.2017.7205. Epub 2017 Aug 10.
Reperfusion is the only approved therapy for acute ischemic stroke; however, it can cause excessive inflammation responses and aggravate brain damage. Therefore, supplementary treatment against inflammation caused by reperfusion is required. In a previous study from our group, curcumin was demonstrated to decrease infarction volume, brain edema and blood‑brain barrier (BBB) disruption against cerebral ischemia/reperfusion (I/R) injury. However, the underlying mechanisms remain unclear. The present study was conducted to understand whether curcumin protects against cerebral I/R injury through anti‑inflammatory and antiapoptotic properties. Ischemia for 1 h was induced in vivo in Wistar rats by middle cerebral artery occlusion (MCAO), followed by reperfusion for 24 h, and curcumin was injected intraperitoneally at 30 min prior to reperfusion. Immunohistochemistry was performed to analyze the expression levels of nuclear factor (NF)‑κB, intercellular adhesion molecule (ICAM)‑1, matrix metalloproteinase (MMP)‑9 and caspase‑3. The findings revealed that inflammation (NF‑κB, ICAM‑1 and MMP‑9) and apoptosis (caspase‑3)‑related markers were significantly downregulated in the curcumin‑treated MCAO group compared with the vehicle‑treated MCAO group. Furthermore, brain infarction size, brain edema and neurological dysfunction were attenuated in the curcumin‑treated MCAO group compared with the vehicle‑treated MCAO group. Taken together, the present results provided evidence that the protective effect of curcumin against cerebral I/R injury might be mediated by anti‑inflammatory and anti‑apoptotic properties. Therefore, curcumin may be a promising supplementary agent against cerebral I/R injury in the future.
再灌注是治疗急性缺血性脑卒中唯一被批准的疗法；然而，它会引起过度的炎症反应，加重脑损伤。因此，需要针对再灌注引起的炎症进行补充治疗。在我们之前的研究中，姜黄素被证明可以减少脑缺血/再灌注（I/R）损伤引起的梗死体积、脑水肿和血脑屏障（BBB）破坏。然而，其潜在机制尚不清楚。本研究旨在探讨姜黄素是否通过抗炎和抗凋亡特性来保护脑 I/R 损伤。通过大脑中动脉闭塞（MCAO）在体内诱导 1 小时缺血，然后再灌注 24 小时，在再灌注前 30 分钟腹腔内注射姜黄素。通过免疫组织化学分析核因子（NF）-κB、细胞间黏附分子（ICAM）-1、基质金属蛋白酶（MMP）-9 和半胱天冬酶-3 的表达水平。结果表明，与 vehicle-MCAO 组相比，姜黄素治疗的 MCAO 组炎症（NF-κB、ICAM-1 和 MMP-9）和细胞凋亡（caspase-3）相关标志物的表达水平显著下调。此外，与 vehicle-MCAO 组相比，姜黄素治疗的 MCAO 组脑梗死面积、脑水肿和神经功能障碍减轻。综上所述，本研究结果提供了证据表明，姜黄素对脑 I/R 损伤的保护作用可能是通过抗炎和抗凋亡特性介导的。因此，姜黄素可能是未来治疗脑 I/R 损伤的有前途的辅助药物。
