Evidence map›Paper›PMID 42163385›Full record

ArticleChinese medicine2026

Targeted degradation of aberrant Tau for the discovery of Pulsatilla chinensis in Alzheimer's disease.

Lan Deng, Can Yin, Xiaogang Zhou, Chi Feng, Jianming Wu, Xiaobing An, Jianing Mi, Lufen Huang, Dalian Qin, Lu Yu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Chinese medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Lan Deng *Sichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China.
Can Yin *Sichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China.
Xiaogang Zhou *Sichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China.
Chi Feng *Sichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China.
Jianming WuSichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China.
Xiaobing AnSichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China.
Jianing MiState Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, Guangdong, China.
Lufen HuangDepartment of Pharmacy, Jining Medical University, Rizhao, 276500, Shandong, China.
Dalian QinSichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China. dalianqin@swmu.edu.cn.
Lu YuSichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China. yulu863@swmu.edu.cn.
Ting ChenSchool of Pharmaceutical Sciences, China-Pakistan International Science and Technology Innovation Cooperation Base for Ethnic Medicine Development in Huna Province, Hunan University of Medicine, Huaihua, 418000, China. chenting@hnmu.edu.cn.
Anguo WuSichuan Key Medical Laboratory of New Drug Discovery and Drugability Evaluation, Department of Cardiology, School of Pharmacy, The Affiliated Hospital of Southwest Medical University and Key Laboratory of Medical Electrophysiology, Southwest Medical University, Luzhou, 646000, China. wuanguo1114@swmu.edu.cn.

Funding

Department of Science and Technology of Sichuan Province 2024YFHZ0361Joint Project of Luzhou Municipal People's Government and Southwest Medical University 2024LZXNYDJ026Natural Science Foundation of Henan Province 81903829State Key Laboratory of Traditional Chinese Medicine Syndrome SKLKY2024B0006
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is characterized by Tau aggregation, mitochondrial dysfunction, and oxidative stress, yet effective interventions targeting these pathological cascades remain limited. Therapeutic strategies that enhance autophagic and mitophagic clearance, attenuate Tau toxicity, and restore mitochondrial homeostasis are crucial for AD management.

methodsThis study investigated the neuroprotective effects of Pulsatilla chinensis extract (PCE) in SH-SY5Y neuronal cells and Caenorhabditis elegans (C. elegans) models of Tauopathy. Autophagic flux was evaluated by GFP-LC3 puncta formation, LC3-II conversion, and p62 degradation. Mitochondrial function was assessed through reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), and ultrastructural analysis. The roles of autophagy and mitophagy were examined using 3-methyladenine (3-MA) and the Parkin inhibitor AC220. In C. elegans, locomotion, Tau aggregation, oxidative stress, and mitophagosome formation were assessed, and pink-1 knockdown was used to confirm mitophagy dependence.

resultsPCE significantly enhanced autophagic flux, decreased total and phosphorylated Tau (p-Tau Ser404) levels, and improved neuronal viability. It significantly reduced ROS accumulation, maintained MMP, and preserved mitochondrial morphology under both Tau overexpression and H

conclusionPCE exerts potent neuroprotective effects by promoting mitophagy, reducing Tau phosphorylation and aggregation, and restoring mitochondrial integrity. These findings reveal a novel mechanism linking mitochondrial quality control with Tau proteostasis and highlight PCE as a promising natural therapeutic candidate for AD.

Indexed as

Alzheimer’s diseaseCaenorhabditis elegansMitophagyPulsatilla chinensis extractSH-SY5YTau

Identifiers

PMID42163385
PMCPMC13188461

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.