Evidence map›Paper›PMID 40234956›Full record

ArticleChinese medicine2025

Huang-Lian-Jie-Du decoction alleviates cognitive deficits in Alzheimer's disease model 5xFAD mice by inhibiting Trem2/Dap12 signaling pathway.

Rui-Kang Pang, Jia Shi, Xiang-Yu Peng, Shan Su, Jia-Yi Zheng, Kai Le, Vincent W Keng, Shi-Jie Zhang, Xiao-Xiao Li

Abstract read
In one paragraph

Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Rui-Kang Pang *State Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Jia Shi *State Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Xiang-Yu Peng *State Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Shan SuState Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Jia-Yi ZhengState Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Kai LeDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, No.17 Yongwaizheng Street, Nanchang, 330006, Jiangxi, China.
Vincent W KengDepartment of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong, China. vincent.keng@polyu.edu.hk.
Shi-Jie ZhangState Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China. shijiezhang@gzucm.edu.cn.
Xiao-Xiao LiCollege of Life Science, Zhuhai College of Science and Technology, Zhuhai, China. 15901357r@connect.polyu.hk.ORCID http://orcid.org/0000-0002-3529-6222

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder predominantly affecting the elderly population. It is characterized by cognitive deficits associated with the accumulation of amyloid-beta plaques and neurofibrillary tangles. Huang-Lian-Jie-Du (HLJD) decoction, recognized as a representative formulation with heat-clearing and detoxification effects, has been demonstrated to be effective in treating AD. However, the underlying mechanisms require further investigation.

methods5xFAD mice were administrated low and high doses of HLJD. The Morris water maze test was conducted to assess the effects of HLJD. Aβ42 and total tau protein levels were evaluated. Additionally, network pharmacology analysis was performed to identify therapeutic targets of HLJD's active components and their relevance to AD. ELISA, qPCR, Western Blot, and immunofluorescence assays were employed to confirm the identified pathways. Finally, primary microglia isolated from 5xFAD mice were used to validate the candidate targets of HLJD.

resultsHLJD improved cognitive deficits in 5xFAD mice and reduced amyloid plaque deposition and tau protein levels. Network pharmacology analysis indicated that HLJD influences the neuroinflammatory response, particularly through the Dap12 signaling pathway. This was confirmed by reduced levels of neuroinflammation markers, including TNF-α, IL-1β, IL-6, and indicators of microglial activation and polarization. The expression of Trem2 and Dap12 in the hippocampus (HIP) of 5xFAD mice, as well as in the isolated primary microglia, were downregulated following HLJD treatment.

conclusionOur study indicates that HLJD alleviates cognitive deficits in AD by suppressing the Trem2/Dap12 signaling pathway in the HIP of 5xFAD mice, thereby inhibiting microglial neuroinflammation.

Indexed as

Alzheimer’s diseaseDap12Huang-Lian-Jie-Du decoctionMicrogliaNeuroinflammationTrem2

Identifiers

PMID40234956
PMCPMC11998141

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