Li Gaifen, Wu Qiong, Wang Chao, Deng Pin, Li Jiaxin, Zhai Zhiguang, Li Yubo
Institute of Basic Theory for Traditional Chinese Medicine, China Academy of Chinese Medical Sciences, No.16, Nanxiaojie, Dongzhimen, Dongcheng District, Beijing, 100700, China.
Sci Rep. 2025 Jan 7;15(1):1135. doi: 10.1038/s41598-024-82571-9.
Following prolonged exposure to hypoxic conditions, for example, due to ascent to high altitude, aging or stroke, cognitive deficits can develop. The exact nature and genesis of hypoxia-induced cognitive deficits remain unresolved. Curcumin has been reported to stimulate neurogenesis and reduce neuronal degeneration. This study aimed to investigate the effect of curcumin on cognitive deficits in hypoxic-brain injury mice and its potential mechanism. Eight-week-old male C57BL/6J mice were exposure to normobaric-hypoxia (13%O) 14 days to establish hypoxic-brain injury models. Morris water maze and novel object recognition were used to detect the cognitive function of each mouse. Immunofluorescence assays, including Fluoro-Jade C (FJC) and bromodeoxyuridine (BrdU), were used to detect neuronal degeneration and neurogenesis. Thy1-YFP transgenic mice were used to detect synapse plasticity. Our results showed that curcumin administration rescued the impaired cognition of mice, shown as enhanced BrdU and dendritic spine in hippocampus. At the molecular level, curcumin was found to promote the expression of brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95). The results of primary hippocampal neuron detection showed that curcumin could promote dendritic growth. In conclusion, our study indicates that curcumin, increased BDNF and PSD95 expression and contacted with interneurons, salvaged of interneurons may normalize ambient neuroplasticity, resulting in the preservation of neurogenesis processes as well as contributing to improve cognitive performance.
例如，由于攀登到高海拔、衰老或中风等原因，在长期暴露于缺氧条件下后，可能会出现认知缺陷。缺氧诱导的认知缺陷的确切性质和成因仍未得到解决。据报道，姜黄素可刺激神经发生并减少神经元变性。本研究旨在探讨姜黄素对缺氧性脑损伤小鼠认知缺陷的影响及其潜在机制。将8周龄雄性C57BL/6J小鼠暴露于常压缺氧（13%氧气）环境14天以建立缺氧性脑损伤模型。采用莫里斯水迷宫和新物体识别实验来检测每只小鼠的认知功能。免疫荧光分析，包括氟玉红C（FJC）和溴脱氧尿苷（BrdU），用于检测神经元变性和神经发生。利用Thy1-YFP转基因小鼠检测突触可塑性。我们的结果表明，给予姜黄素可挽救小鼠受损的认知，表现为海马体中BrdU增加和树突棘增多。在分子水平上，发现姜黄素可促进脑源性神经营养因子（BDNF）和突触后致密蛋白95（PSD95）的表达。原代海马神经元检测结果表明，姜黄素可促进树突生长。总之，我们的研究表明，姜黄素增加了BDNF和PSD95的表达并与中间神经元接触，中间神经元的挽救可能使周围神经可塑性正常化，从而保留神经发生过程并有助于改善认知表现。
