Evidence map›Paper›PMID 26563497›Full record

ArticleMolecular neurobiology2016

Suppressing Receptor-Interacting Protein 140: a New Sight for Salidroside to Treat Cerebral Ischemia.

Tong Chen, Zhanqiang Ma, Lingpeng Zhu, Wenjiao Jiang, Tingting Wei, Rui Zhou, Fen Luo, Kai Zhang, Qiang Fu, Chunhua Ma and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 68 citations in OpenAlex.

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  15. Preclinical Evidence and Possible Mechanisms ofFrontiers in pharmacology · 2021
    Review
  16. Article
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  20. Article
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

11 authors at 1 institution in 1 country.

Tong ChenState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Zhanqiang MaDepartment of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, 210009, China.
Lingpeng ZhuDepartment of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, 210009, China.
Wenjiao JiangState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Tingting WeiState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China.
Rui ZhouDepartment of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, 210009, China.
Fen LuoDepartment of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, 210009, China.
Kai ZhangDepartment of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, 210009, China.
Qiang FuDepartment of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, 210009, China.
Chunhua MaDepartment of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, 210009, China. machuanhua25@126.com.
Tianhua YanState Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, 210009, China. yantianhuabest@126.com.
China Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of the current study was to detect the effect of salidroside (Sal) on cerebral ischemia and explore its potential mechanism. Middle cerebral artery occlusion (MCAO) was performed to investigate the effects of Sal on cerebral ischemia. The rats were randomly divided into five groups: sham group, vehicle group, clopidogrel (7.5 mg/kg) group, Sal (20 mg/kg) group, and Sal (40 mg/kg) group. SH-SY5Y cells were exposed to ischemia-reperfusion (I/R) injury to verify the protective effect of Sal in vitro. We also built the stable receptor-interacting protein 140 (RIP140)-overexpressing SH-SY5Y cells. The results showed that Sal significantly reduces brain infarct size and cerebral edema. Sal could effectively decrease the levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in serum of the MCAO rats and supernatant of I/R-induced SH-SY5Y cells. Immunohistochemical and Western blot results demonstrated that Sal inhibited RIP140-mediated inflammation and apoptosis in the MCAO rats and SH-SY5Y cells. In addition, we further confirmed that RIP140/NF-κB signaling plays a crucial role by evaluating the protein expression in RIP140-overexpressing SH-SY5Y cells. Our findings suggested that Sal could be used as an effective neuroprotective agent for cerebral ischemia due to its significant effect on preventing neuronal cell injury after cerebral ischemia both in vivo and in vitro by the inhibitions of RIP140-mediated inflammation and apoptosis.

Indexed as

Animalsbcl-2-Associated X ProteinBrainBrain EdemaBrain IschemiaCell Line, TumorCell SurvivalCytokinesGlucosidesHumansMaleNF-kappa BNuclear Receptor Co-Repressor 1PhenolsRats, Sprague-DawleySignal Transductionbcl-2-Associated X ProteinCytokinesGlucosidesNF-kappa BNuclear Receptor Co-Repressor 1PhenolsrhodiolosideCerebral ischemiaInflammationRIP140Salidroside

Identifiers

PMID26563497
OpenAlexW2176658335

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.