Sung Pi-Shan, Chen Pei-Wen, Yen Chia-Jui, Shen Meng-Ru, Chen Chih-Hung, Tsai Kuen-Jer, Lin Chou-Ching K
Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan 704, Taiwan.
Department of Neurology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan 704, Taiwan.
Cancers (Basel). 2021 Aug 19;13(16):4177. doi: 10.3390/cancers13164177.
Chemotherapy-induced cognitive impairment (CICI) is an adverse side effect of cancer treatment with increasing awareness. Hippocampal damage and related neurocognitive impairment may mediate the development of CICI, in which altered neurogenesis may play a role. In addition, increased inflammation may be related to chemotherapy-induced hippocampal damage. Memantine, an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist that may enhance neurogenesis and modulate inflammation, may be useful for treating CICI. To test this hypothesis, paclitaxel was administered to eight-week-old male B6 mice to demonstrate the relationship between CICI and impaired neurogenesis, and then, we evaluated the impact of different memantine regimens on neurogenesis and inflammation in this CICI model. The results demonstrated that both the pretreatment and cotreatment regimens with memantine successfully reversed impaired neurogenesis and spatial memory impairment in behavior tests. The pretreatment regimen unsuccessfully inhibited the expression of peripheral and central TNF-α and IL-1β and did not improve the mood alterations following paclitaxel treatment. However, the cotreatment regimen led to a better modulatory effect on inflammation and restoration of mood disturbance. In conclusion, this study illustrated that impaired neurogenesis is one of the mechanisms of paclitaxel-induced CICI. Memantine may serve as a potential treatment for paclitaxel-induced CICI, but different treatment strategies may lead to variations in the treatment efficacy.
化疗诱导的认知障碍(CICI)是癌症治疗中一种日益受到关注的不良副作用。海马损伤及相关神经认知障碍可能介导了CICI的发生发展,其中神经发生改变可能起一定作用。此外,炎症增加可能与化疗诱导的海马损伤有关。美金刚是一种非竞争性N-甲基-D-天冬氨酸(NMDA)受体拮抗剂,可能增强神经发生并调节炎症,或许可用于治疗CICI。为验证这一假设,对8周龄雄性B6小鼠给予紫杉醇,以证明CICI与神经发生受损之间的关系,然后,我们评估了不同美金刚给药方案对该CICI模型中神经发生和炎症的影响。结果表明,美金刚预处理和联合治疗方案均成功逆转了行为测试中神经发生受损和空间记忆障碍。预处理方案未能抑制外周和中枢肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的表达,也未改善紫杉醇治疗后的情绪改变。然而,联合治疗方案对炎症具有更好的调节作用,并能恢复情绪障碍。总之,本研究表明神经发生受损是紫杉醇诱导CICI的机制之一。美金刚可能是治疗紫杉醇诱导CICI的一种潜在药物,但不同的治疗策略可能导致治疗效果存在差异。