Evidence map›Paper›PMID 30206804›Full record

ArticleNeurochemical research2018

Glycyrrhizic Acid Alleviates 6-Hydroxydopamine and Corticosterone-Induced Neurotoxicity in SH-SY5Y Cells Through Modulating Autophagy.

Guangyi Yang, Jing Li, Youli Cai, Zhonghua Yang, Rong Li, Wenjun Fu

Abstract read
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In one paragraph

Article in Neurochemical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

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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 2 institutions in 1 country.

Guangyi YangDepartment of Pharmacy, Shenzhen Bao'an Traditional Chinese Medical Hospital (Group), Shenzhen, 518000, Guangdong, China.
Jing LiDepartment of Cardiology, First Affiliated Hospital of Guangzhou University of Chinese Medicine, No.16, Jichang Road, Guangzhou, 510405, Guangdong, China.
Youli CaiSchool of Basic Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, China.
Zhonghua YangSouth China Research Center for Acupuncture and Moxibustion, School of Basic Medical Science, Guangzhou University of Chinese Medicine, No. 232, East Waihuan Road, Guangzhou, 510006, Guangdong, China.
Rong LiDepartment of Cardiology, First Affiliated Hospital of Guangzhou University of Chinese Medicine, No.16, Jichang Road, Guangzhou, 510405, Guangdong, China. lrhbs@126.com.
Wenjun FuSouth China Research Center for Acupuncture and Moxibustion, School of Basic Medical Science, Guangzhou University of Chinese Medicine, No. 232, East Waihuan Road, Guangzhou, 510006, Guangdong, China. fuqingzhu2006@163.com.
Guangzhou University of Chinese Medicine · CNFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CN

Funding

Elite Youth Education Program of Guangzhou University of Chinese Medicine QNYC20140104Hubei province technical innovation project 2017ACA176National Natural Science Foundation of China 81573922Natural Science Foundation of Guangdong Province 2017ZC0135
6 · The paper itself

Abstract

Recent researches have shown that autophagy is associated with the pathogenesis of neurodegenerative disorders, but there is no paper to investigate the effects of autophagy modulation on Parkinson's disease depression (PDD). In addition, glycyrrhizic acid (GA), the major bioactive ingredient of Radix glycyrrhizae, can induce autophagy and ease rotenone-induced Parkinson's disease (PD). However, there is also no paper to study the action and molecular mechanisms of GA on PDD. In this research, we built the injury model of SH-SY5Y cells through 6-hydroxydopamine (6-OHDA) and corticosterone (CORT). Then, our results showed that GA markedly increased the viability and decreased the apoptosis in SH-SY5Y cells after pre-treating with 6-OHDA and CORT. Moreover, GA notably decreased the expressions of α-Syn and p-S1292-LRRK2 proteins, and significantly increased the levels of CREB and BDNF proteins. Previous papers have suggested that CORT contributed to dopaminergic neurodegeneration via the glucocorticoid (GC)/glucocorticoid receptor (GR) interaction, and our results showed that GA reduced GC level and hypothalamic-pituitary-adrenal (HPA) activity in SH-SY5Y cells by regulating GR signaling pathway. Furthermore, mechanism investigations also showed that GA had the ability to up-regulate the conversion of LC3B II/I and the expression of Beclin-1, and induce autophagy in SH-SY5Y cells, which were reversed by the autophagy inhibitor 3-methyladenine (3-MA). Collectively, these findings proved that GA exerted efficient activity against neurotoxicity in SH-SY5Y cells induced by 6-OHDA and CORT via activation of autophagy, which should be developed as an efficient candidate for treating PDD in the future.

Indexed as

alpha-SynucleinApoptosisAutophagyBeclin-1Brain-Derived Neurotrophic FactorCell Line, TumorCell SurvivalCorticosteroneCyclic AMP Response Element-Binding ProteinGlycyrrhizic AcidHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Microtubule-Associated ProteinsNeuroprotective AgentsOxidopamineParkinson Disease, Secondaryalpha-SynucleinBDNF protein, humanBeclin-1BECN1 protein, humanBrain-Derived Neurotrophic FactorCorticosteroneCREB1 protein, humanCyclic AMP Response Element-Binding ProteinGlycyrrhizic AcidLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanMAP1LC3B protein, humanMicrotubule-Associated ProteinsNeuroprotective AgentsOxidopamineSNCA protein, humanAutophagyGlycyrrhizic acidNeurotoxicityParkinson’s disease depressionSH-SY5Y cells

Identifiers

PMID30206804
OpenAlexW2891150867

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.