Scalp acupuncture alleviates remote hippocampal damage in MCAO rats by inhibiting neuroinflammation: A TMT-based proteomics analysis

被引:0
作者
Liu, Huacong [1 ]
Huang, Weijia [2 ]
Ding, Qian [3 ,4 ]
Huang, Yumeng [1 ]
Lai, Zhenyi [1 ]
Liu, Zhaoxing [1 ]
Li, Shaoxiong [5 ]
Peng, Xinyi [5 ]
Wu, Zhenhong [5 ]
Deng, Liangbin [6 ]
Huang, Yong [1 ,7 ]
Chen, Junqi [3 ]
机构
[1] Southern Med Univ, Sch Tradit Chinese Med, Guangzhou, Guangdong, Peoples R China
[2] Southern Med Univ, Affiliated Hosp 3, Dept Neurosurg, Guangzhou, Guangdong, Peoples R China
[3] Southern Med Univ, Affiliated Hosp 3, Dept Rehabil Med, Guangzhou, Guangdong, Peoples R China
[4] Xi An Jiao Tong Univ, Honghui Hosp, Xian, Shanxi, Peoples R China
[5] Southern Med Univ, Affiliated Hosp 3, Guangzhou, Guangdong, Peoples R China
[6] Guangzhou Zengcheng Dist Hosp Tradit Chinese Med, Guangzhou, Guangdong, Peoples R China
[7] Southern Med Univ, Nanfang Hosp, Guangzhou, Guangdong, Peoples R China
关键词
Scalp acupuncture; Ischemic stroke; MCAO; Remote damage; Neuroinflammation; Proteomics; MONOACYLGLYCEROL LIPASE; ISCHEMIC-STROKE; NEURODEGENERATION; INFLAMMATION;
D O I
10.1016/j.neuroscience.2024.11.008
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
While mounting evidence suggests that scalp acupuncture (SA) may be effective in alleviating neurological deficits in patients with acute ischemic stroke (IS), its effect on remote hippocampal damage in acute IS and the underlying mechanisms remain elusive. Thus, proteomics analysis was conducted to identify potential targets of SA therapy in acute IS. SA significantly reduced cerebral infarct volume and attenuated neuronal damage in the ischemic penumbra and hippocampus, as well as alleviated neurological deficits in rats with middle cerebral artery occlusion (MCAO). Moreover, 74 upregulated and 50 downregulated proteins were identified in the MCAO group compared to the sham group, whilst 52 up-regulated and 50 down-regulated proteins were identified in the SA group compared to the MCAO group. Bioinformatics analysis indicated that SA may exert neuroprotective effects by modulating the acute inflammatory response and microglial activation. Additionally, SA downregulated the expression levels of Iba-1, TNF-alpha, IL-1 beta, and IL-6, while up-regulating those of IL-4 and IL-10. Likewise, it downregulated the expression levels of three key proteins identified via proteomics analysis (Kng1, Brd9, and Magl) that may mediate the anti-inflammatory effects of SA. Overall, these results indicate that SA attenuates neuronal damage in the hippocampus and ischemic penumbra and ameliorates neurological deficits. Proteomic analysis suggested that this effect is related to the modulation of the acute inflammatory response. SA attenuated remote hippocampal damage after IS by inhibiting microglia activation and neuroinflammation. Lastly, Kng1, Brd9, and Magl were identified as potential targets that mediate the antiinflammatory effects of SA.
引用
收藏
页码:117 / 128
页数:12
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