Evidence map›Paper›PMID 33536742›Full record

ArticleDrug design, development and therapy2021

Physcion Protects Rats Against Cerebral Ischemia-Reperfusion Injury via Inhibition of TLR4/NF-kB Signaling Pathway.

Xiaobo Dong, Lei Wang, Guangrong Song, Xu Cai, Wenxin Wang, Jiaqi Chen, Gesheng Wang

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 55 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

7 authors at 1 institution in 1 country.

Xiaobo Dong *The Third Department of Encephalopathy, Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, People's Republic of China.
Lei Wang *The Third Department of Encephalopathy, Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, People's Republic of China.
Guangrong SongThe Third Department of Encephalopathy, Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, People's Republic of China.
Xu CaiThe Third Department of Encephalopathy, Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, People's Republic of China.
Wenxin WangThe Third Department of Encephalopathy, Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, People's Republic of China.
Jiaqi ChenThe Third Department of Encephalopathy, Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, People's Republic of China.
Gesheng WangThe Third Department of Encephalopathy, Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, People's Republic of China.
Beijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIschemic stroke (IS) is characterized by the rapid loss of brain function due to ischemia. Physcion has been found to have a neuroprotective effect against cerebral ischemia-reperfusion (I/R) injury. However, the mechanism by which physcion regulates cerebral I/R injury remains largely unknown.

methodsAn oxygen-glucose deprivation/reperfusion (OGD/R) model in SH-SY5Y cells and a rat cerebral ischemia-reperfusion (I/R) model were established, respectively. CCK-8 and flow cytometry assays were used to detect the viability and apoptosis of SH-SY5Y cells. Moreover, enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of SOD, MDA, GSH-Px, TNF-α, IL-1β, IL-6 and IL-10 in the supernatant of SH-SY5Y cells. Meanwhile, Western blot assay was used to detect the expressions of TLR4, p-p65 and p-IκB in SH-SY5Y cells and I/R rats.

resultsIn this study, physcion treatment significantly rescued OGD/R-induced neuronal injury. In addition, physcion decreased inflammatory response in SH-SY5Y cells after OGD/R insult, as shown by the decreased levels of the pro-inflammatory factors TNF-α, IL-1β, IL-6 and IL-10. Moreover, physcion attenuated the oxidative stress in OGD/R-treated SY-SY5Y cells, as evidenced by the increased SOD and GSH levels and the decreased ROS and MDA levels. Meanwhile, physcion significantly reduced cerebral infarction, attenuated neuronal injury and apoptosis in I/R rats. Furthermore, physcion markedly decreased the expressions of TLR4, p-NF-κB p65 and p-IκB in the brain tissues of rats subjected to I/R and in SH-SY5Y cells exposed to OGD/R.

conclusionIn conclusion, our study indicated that physcion protected neuron cells against I/R injury in vitro and in vivo by inhibition of the TLR4/NF-kB pathway; thus, physcion might serve as a promising therapeutic candidate for IS.

Indexed as

AnimalsBrain IschemiaCell Line, TumorEmodinHumansNF-kappa BProtective AgentsRatsRats, Sprague-DawleyReperfusion InjurySignal TransductionToll-Like Receptor 4EmodinNF-kappa BphyscioneProtective AgentsTLR4 protein, humanTlr4 protein, ratToll-Like Receptor 4ischemia-reperfusion injuryNF-κBphyscionstroke

Identifiers

PMID33536742
PMCPMC7847770
OpenAlexW3122717651

What OpenQuestion holds

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LicenceCC BY-NC
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.