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Your search keyword '"Weng Zhiying"' showing total 4 results
Start Over Author "Weng Zhiying" Topic dementia
4 results on '"Weng Zhiying"'

1. Donepezil down‐regulates propionylation, 2‐hydroxyisobutyrylation, butyrylation, succinylation, and crotonylation in the brain of bilateral common carotid artery occlusion‐induced vascular dementia rats

Author

Na Li, Chen Chen, Chuang Xiao, Xin Ma, Weng Zhiying, Jun Lu, Changhong Zhang, Zhituan Ding, Maoceng Zhu, Chunmei Wu, Guanrong Qiao, Wen-Cong Gao, Weimin Yang, Chang-Bo Zheng, and Hongyan Wang

Subjects
Male, 0301 basic medicine, Carotid Artery, Common, Physiology, medicine.drug_class, Morris water navigation task, Pharmacology, Hippocampus, 03 medical and health sciences, Cognition, 0302 clinical medicine, Physiology (medical), mental disorders, medicine, Animals, Hippocampus (mythology), Dementia, Donepezil, Maze Learning, Vascular dementia, Stroke, business.industry, Dementia, Vascular, Brain, medicine.disease, Rats, Disease Models, Animal, 030104 developmental biology, Acetylcholinesterase inhibitor, 030220 oncology & carcinogenesis, business, medicine.drug, Executive dysfunction
Abstract

Vascular dementia (VaD), caused by stroke or small vessel disease, is the second-most common type of dementia after Alzheimer's disease (AD). Donepezil is an acetylcholinesterase inhibitor that is currently used in patients with mild to moderate AD, and has recently been shown to improve cognitive performance in patients with VaD. In this study, we evaluated the effects of donepezil on VaD, and investigated the underlying molecular mechanisms of action. VaD was established by ligation of the bilateral common carotid artery occlusion (BCCAO). Executive function was tested by the Morris water maze (MWM) test and the attentional set shifting task (ASST). Our results showed that donepezil improved executive dysfunction and cognitive flexibility in BCCAO rats. In addition, we showed that donepezil treatment decreased the level of Aβ1-42 in BCCAO rats by enzyme-linked immunosorbent assay. Post-translational modifications (PTMs) are known to be critical mechanisms in the regulation of various cellular processes. Furthermore, PTMs have been linked to the central nervous system, which highlights the importance of PTMs in neurodegenerative diseases. In this study, we used western blot analysis to identify several novel PTMs in the hippocampus of BCCAO rats that were treated with or without donepezil. The data revealed that lysine propionylation, 2-hydroxyisobutyrylation, butyrylation, succinylation, and crotonylation were elevated in the hippocampus of BCCAO rats when compared to sham rats. This increase was abolished by donepezil treatment. Taken together, we speculate that donepezil treatment improves cognitive function in our animal model of VaD, possibly by reducing aberrant acyl-PTMs.

Published
2020

2. Gastrodin Alleviates Vascular Dementia in a 2-VO-Vascular Dementia Rat Model by Altering Amyloid and Tau Levels

Author

Changhong Zhang, Chen Chen, Chang-bo Zheng, Tingyan Du, Weimin Yang, Chuang Xiao, Rui Shi, Zelan Dai, Hongyan Wang, Qiang Rao, Menghua Tian, Weng Zhiying, Bai-xi Ji, Chun-Yun Bai, Xianlun Yu, and Li Xian

Subjects
Male, medicine.medical_specialty, Amyloid, Morris water navigation task, tau Proteins, 030226 pharmacology & pharmacy, Hippocampus, Brain Ischemia, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Glucosides, Memory, Internal medicine, medicine, Dementia, Hippocampus (mythology), Animals, Carotid Stenosis, Gastrodin, Vascular dementia, Maze Learning, Benzyl Alcohols, Pharmacology, Neurons, Amyloid beta-Peptides, biology, business.industry, Dementia, Vascular, General Medicine, medicine.disease, biology.organism_classification, Gastrodia elata, Rats, Disease Models, Animal, Endocrinology, Neuroprotective Agents, chemistry, business, 030217 neurology & neurosurgery, Executive dysfunction
Abstract

Vascular dementia (VaD) is the second most common type of dementia and has become a major public health challenge as the global population ages. VaD is caused by cerebrovascular disease, and most patients with VaD have been reported to also have Alzheimer’s pathologies, which is the formation of neurofibrillary tangles and amyloid plaques that are mainly composed of hyperphosphorylated Tau and amyloid β (Aβ) respectively. However, the mechanisms of VaD are not completely understood, and very few drugs are available to treat this condition. Gastrodin (Gas) is the main bioactive component of the traditional Chinese herbal plant named Tian Ma (Gastrodia elata), and it has been used to treat neurasthenia in the clinical practice of Chinese Medicine for many years. Here, we hypothesize that Gas alleviates VaD in a rat model of permanent bilateral common carotid artery occlusion (2-VO)-induced VaD. Based on the results of the Morris water maze test and attention set shift test, either 22.5 or 90 mg/kg/day Gas improved the executive dysfunction and memory impairment of 2-VO rats following an intragastric administration for 4 weeks. Both 22.5 and 90 mg/kg/day Gas reduced Aβ1–40 and Aβ1–42 plaques in plasma and hippocampus of 2-VO rats. Mechanistically, in 2-VO rats, treatment with Gas (90 mg/kg/day) suppressed Aβ plaque deposition by decreasing the hippocampus levels of phosphorylated Tau. Thus, Gas ameliorated the cognitive deficits of 2-VO rats by inhibiting the abnormal phosphorylation of Aβ and Tau.

Published
2019

3. Tianma Formula Alleviates Dementia via ACER2-Mediated Sphingolipid Signaling Pathway Involving Aβ.

Author

Lin, Haochang, Wu, Sha, Weng, Zhiying, Wang, Hongyan, Shi, Rui, Tian, Menghua, Wang, Youlan, He, Haiyan, Wang, Yuchuan, Liu, Xuan, Jian, Zhimin, Wei, Fuqin, Wang, Peng, Zhang, Liuyi, Liu, Yi, Guo, Qiuzhe, Chen, Chen, and Yang, Weimin

Subjects
DIAGNOSIS of dementia, IN vivo studies, STAINS & staining (Microscopy), ANIMAL experimentation, CELLULAR signal transduction, GENE expression, DEMENTIA, ENZYME-linked immunosorbent assay, GENE expression profiling, MESSENGER RNA, POLYMERASE chain reaction, COMPUTER-assisted molecular modeling, CHINESE medicine, ANIMALS, MICE
Abstract

Objective. To reveal the molecular mechanism of the antagonistic effect of traditional Chinese medicine Tianma formula (TF) on dementia including vascular dementia (VaD) and Alzheimer's disease (AD) and to provide a scientific basis for the study of traditional Chinese medicine for prevention and treatment of dementia. Method. The TF was derived from the concerted application of traditional Chinese medicine. We detected the pharmacological effect of TF in VaD rats. The molecular mechanism of TF was examined by APP/PS1 mice in vivo, Caenorhabditis elegans (C. elegans) in vitro, ELISA, pathological assay via HE staining, and transcriptome. Based on RNA-seq analysis in VaD rats, the differentially expressed genes (DEGs) were identified and then verified by quantitative PCR (qPCR) and ELISA. The molecular mechanisms of TF on dementia were further confirmed by network pharmacology and molecular docking finally. Results. The Morris water maze showed that TF could improve the cognitive memory function of the VaD rats. The ELISA and histological analysis suggested that TF could protect the hippocampus via reducing tau and IL-6 levels and increasing SYN expression. Meanwhile, it could protect the neurological function by alleviating Aβ deposition in APP/PS1 mice and C. elegans. In the RNA-seq analysis, 3 sphingolipid metabolism pathway-related genes, ADORA3, FCER1G, and ACER2, and another 5 nerve-related genes in 45 key DEGs were identified, so it indicated that the protection mechanism of TF was mainly associated with the sphingolipid metabolism pathway. In the qPCR assay, compared with the model group, the mRNA expressions of the 8 genes mentioned above were upregulated, and these results were consistent with RNA-seq. The protein and mRNA levels of ACER2 were also upregulated. Also, the results of network pharmacology analysis and molecular docking were consistent with those of RNA-seq analysis. Conclusion. TF alleviates dementia by reducing Aβ deposition via the ACER2-mediated sphingolipid signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2021
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4. Gastrodin Alleviates Vascular Dementia in a 2-VO-Vascular Dementia Rat Model by Altering Amyloid and Tau Levels.

Author

Shi, Rui, Zheng, Chang-bo, Wang, Hongyan, Rao, Qiang, Du, Tingyan, Bai, Chunyun, Xiao, Chuang, Dai, Zelan, Zhang, Changhong, Chen, Chen, Li, Xian, Tian, Menghua, Yu, Xianlun, Ji, Baixi, Weng, Zhiying, and Yang, Weimin

Subjects
VASCULAR dementia, AMYLOID, DEMENTIA, CEREBROVASCULAR disease, NEUROFIBRILLARY tangles, SCOPOLAMINE, TROPANES, TAU proteins
Abstract

Vascular dementia (VaD) is the second most common type of dementia and has become a major public health challenge as the global population ages. VaD is caused by cerebrovascular disease, and most patients with VaD have been reported to also have Alzheimer's pathologies, which is the formation of neurofibrillary tangles and amyloid plaques that are mainly composed of hyperphosphorylated Tau and amyloid β (Aβ) respectively. However, the mechanisms of VaD are not completely understood, and very few drugs are available to treat this condition. Gastrodin (Gas) is the main bioactive component of the traditional Chinese herbal plant named Tian Ma (Gastrodia elata), and it has been used to treat neurasthenia in the clinical practice of Chinese Medicine for many years. Here, we hypothesize that Gas alleviates VaD in a rat model of permanent bilateral common carotid artery occlusion (2-VO)-induced VaD. Based on the results of the Morris water maze test and attention set shift test, either 22.5 or 90 mg/kg/day Gas improved the executive dysfunction and memory impairment of 2-VO rats following an intragastric administration for 4 weeks. Both 22.5 and 90 mg/kg/day Gas reduced Aβ1–40 and Aβ1–42 plaques in plasma and hippocampus of 2-VO rats. Mechanistically, in 2-VO rats, treatment with Gas (90 mg/kg/day) suppressed Aβ plaque deposition by decreasing the hippocampus levels of phosphorylated Tau. Thus, Gas ameliorated the cognitive deficits of 2-VO rats by inhibiting the abnormal phosphorylation of Aβ and Tau. [ABSTRACT FROM AUTHOR]

Published
2020
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