Hydrogen Attenuates Cognitive Impairment in Rat Models of Vascular Dementia by Inhibiting Oxidative Stress and NLRP3 Inflammasome Activation

Author:

Yang Congwen12,He Yuxuan1,Ren Shuang3,Ding Yiqin1,Liu Xinru1,Li Xue1,Sun Hao1,Jiao Dezhi1,Zhang Haolin1,Wang Yingshuai3,Sun Lin4ORCID

Affiliation:

1. School of Clinical Medicine Shandong Second Medical University Weifang Shandong 261053 China

2. The Second Clinical College of Guangzhou University of Chinese Medicine Guangzhou Guangdong 510006 China

3. Department of Bioscience and Technology Shandong Second Medical University Weifang Shandong 261053 China

4. School of Psychology Shandong Second Medical University Weifang Shandong 261053 China

Abstract

AbstractVascular dementia (VaD) is the second most common form of dementia worldwide. Oxidative stress and neuroinflammation are important factors contributing to cognitive dysfunction in patients with VaD. The antioxidant and anti‐inflammatory properties of hydrogen are increasingly being utilized in neurological disorders, but conventional hydrogen delivery has the disadvantage of inefficiency. Therefore, magnesium silicide nanosheets (MSNs) are used to release hydrogen in vivo in larger quantities and for longer periods of time to explore the appropriate dosage and regimen. In this study, it is observed that hydrogen improved learning and working memory in VaD rats in the Morris water maze and Y‐maze, which elicits improved cognitive function. Nissl staining of neurons shows that hydrogen treatment significantly improves edema in neuronal cells. The expression and activation of reactive oxygen species (ROS), Thioredoxin‐interacting protein (TXNIP), NOD‐like receptor protein 3 (NLRP3), caspase‐1, and IL‐1β in the hippocampus are measured via ELISA, Western blotting, real‐time qPCR, and immunofluorescence. The results show that oxidative stress indicators and inflammasome‐related factors are significantly decreased after 7dMSN treatment. Therefore, it is concluded that hydrogen can ameliorate neurological damage and cognitive dysfunction in VaD rats by inhibiting ROS/NLRP3/IL‐1β‐related oxidative stress and inflammation.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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