Wei Guan, Chen Bingji, Lin Qingjiang, Li Yasong, Luo Liangqin, He Hefan, Fu Huangde
Emergency Department, the Second Affiliated Hospital, Fujian Medical University, Quanzhou, China.
Department of Neurosurgery, the Second Affiliated Hospital, Fujian Medical University, Quanzhou, China.
Neuroimmunomodulation. 2017;24(6):348-355. doi: 10.1159/000487998. Epub 2018 Apr 18.
The protective effect of tetrahydrocurcumin (THC) after experimental traumatic brain injury (TBI) has been demonstrated, as demonstrated by the inhibition of oxidative stress, mitochondrial dysfunction, and apoptosis. However, the mechanisms underlying this effect are still not well understood. This study was to investigate the neuroprotective effects of THC, and its potential mechanisms, in a rat model of TBI. To this end, rats were divided into 4 groups: the sham group, the TBI group, the TBI + vehicle (V) group, and the TBI + THC group. THC or V was administered via intraperitoneal injection to rats in the TBI + V and TBI + THC groups 30 min after TBI. After euthanasia (24 h after TBI), neurological scores, brain water content, and neuronal cell death in the cerebral cortex were recorded. Brain samples were collected after neurological scoring for further analysis. THC treatment alleviated brain edema, attenuated TBI-induced neuronal cell apoptosis, and improved neurobehavioral function. In addition, NFE2-related factor 2 (Nrf2) expression was upregulated following TBI. These results suggest that THC improves neurological outcome after TBI, possibly by activating the Nrf2 signaling pathway.
实验性创伤性脑损伤（TBI）后，四氢姜黄素（THC）的保护作用已得到证实，表现为对氧化应激、线粒体功能障碍和细胞凋亡的抑制。然而，这种作用的潜在机制仍未完全明确。本研究旨在探讨THC在TBI大鼠模型中的神经保护作用及其潜在机制。为此，将大鼠分为4组：假手术组、TBI组、TBI + 载体（V）组和TBI + THC组。在TBI后30分钟，通过腹腔注射将THC或V给予TBI + V组和TBI + THC组的大鼠。在安乐死（TBI后24小时）后，记录神经评分、脑含水量和大脑皮质中的神经元细胞死亡情况。在进行神经评分后收集脑样本进行进一步分析。THC治疗减轻了脑水肿，减轻了TBI诱导的神经元细胞凋亡，并改善了神经行为功能。此外，TBI后核因子E2相关因子2（Nrf2）表达上调。这些结果表明，THC可能通过激活Nrf2信号通路改善TBI后的神经功能结局。
