Evidence map›Paper›PMID 26693241›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2015

The Impact of Paeoniflorin on α-Synuclein Degradation Pathway.

Zenglin Cai, Xinzhi Zhang, Yongjin Zhang, Xiuming Li, Jing Xu, Xiaomin Li

Open access · hybridAbstract read
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 31% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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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

6 authors at 1 institution in 1 country.

Zenglin CaiLianyungang First People's Hospital Postdoctoral Innovative Practice Base, Nanjing Medical University Postdoctoral Research Station, Lianyungang 222002, China ; Department of Neurology, Affiliated Lianyungang Hospital of Xuzhou Medical College, Lianyungang 222002, China.ORCID 0000-0003-2884-1429
Xinzhi ZhangDepartment of Neurology, Affiliated Lianyungang Hospital of Xuzhou Medical College, Lianyungang 222002, China.ORCID 0000-0002-7635-1662
Yongjin ZhangDepartment of Neurology, Affiliated Lianyungang Hospital of Xuzhou Medical College, Lianyungang 222002, China.ORCID 0000-0001-5553-2280
Xiuming LiDepartment of Neurology, Affiliated Lianyungang Hospital of Xuzhou Medical College, Lianyungang 222002, China.ORCID 0000-0002-1414-6559
Jing XuDepartment of Neurology, Affiliated Lianyungang Hospital of Xuzhou Medical College, Lianyungang 222002, China.ORCID 0000-0002-4498-772X
Xiaomin LiDepartment of Emergency, Affiliated Lianyungang Hospital of Xuzhou Medical College, Lianyungang 222002, China.ORCID 0000-0002-8494-7132
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paeoniflorin (PF) is the major active ingredient in the traditional Chinese medicine Radix. It plays a neuroprotective role by regulating autophagy and the ubiquitin-proteasome degradation pathway. In this study, we found PF significantly reduced cell damage caused by MPP+, returning cells to normal state. Cell viability significantly improved after 24 h exposure to RAPA and PF in the MPP+ group (all P < 0.01). CAT and SOD activities were significantly decreased after PF and RAPA treatment, compared with MPP+ (P < 0.001). In addition, MPP+ activated both LC3-II and E1; RAPA increased LC3-II but inhibited E1. PF significantly upregulated both LC3-II (autophagy) and E1 (ubiquitin-proteasome pathway) expression (P < 0.001), promoted degradation of α-synuclein, and reduced cell damage. We show MPP+ enhanced immunofluorescence signal of intracellular α-synuclein and LC3. Fluorescence intensity of α-synuclein decreased after PF treatment. In conclusion, these data show PF reversed the decline of proteasome activity caused by MPP+ and significantly upregulated both autophagy and ubiquitin-proteasome pathways, promoted the degradation of α-synuclein, and reduced cell damage. These findings suggest PF is a potential therapeutic medicine for neurodegenerative diseases.

Identifiers

PMID26693241
PMCPMC4674600
OpenAlexW2177513115

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Registered trials

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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.