Evidence map›Paper›PMID 26608500›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2016

Anti-inflammatory effects of fimasartan via Akt, ERK, and NFκB pathways on astrocytes stimulated by hemolysate.

Xiu-Li Yang, Chi Kyung Kim, Tae Jung Kim, Jing Sun, Doeun Rim, Young-Ju Kim, Sang-Bae Ko, Hyunduk Jang, Byung-Woo Yoon

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

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  12. K(+) channel blocker-induced neuroinflammatory response and neurological disorders: immunomodulatory effects of astaxanthin.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
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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

9 authors at 1 institution in 2 countries.

Xiu-Li YangDepartment of Neurology, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Chi Kyung KimDepartment of Neurology, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Tae Jung KimDepartment of Neurology, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Jing SunBiomedical Research Institute, Seoul National University Hospital, Seoul, 03080, Republic of Korea.
Doeun RimDepartment of Neurology, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Young-Ju KimDepartment of Neurology, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Sang-Bae KoDepartment of Neurology, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Hyunduk JangDepartment of Neurology, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea.
Byung-Woo YoonDepartment of Neurology, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea. bwyoon@snu.ac.kr.
Seoul National University Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe aim of this study was to investigate whether fimasartan, a novel angiotensin II receptor blocker, modulates hemolysate-induced inflammation in astrocytes.

methodsWe stimulated astrocytes with hemolysate to induce hemorrhagic inflammation in vitro. Astrocytes were pretreated with fimasartan and then incubated with hemolysate at different durations. Anti-inflammatory cell signaling molecules including Akt, extracellular signal regulated kinase (ERK), NFκB and cyclooxygenase-2 (COX-2) were assessed by western blotting. Pro-inflammatory mediators were evaluated by real-time RT-PCR and ELISA.

resultsThe stimulation by hemolysate generated a robust activation of inflammatory signaling pathways in astrocytes. Hemolysate increased the phosphorylation of Akt at 1 h, and ERK1/2 at 20 min compared with the control group and promoted the degradation of IκBα. Pretreated fimasartan significantly decreased hemolysate-induced phosphorylation of Akt and ERK1/2. In addition, fimasartan also suppressed NFκB-related inflammatory pathways induced by hemolysate, including reduction of the gene expression of NFκB, and decreased nuclear translocation of NFκB and degradation of IκB. This reduction of inflammatory upstream pathways decreased the expression of inflammatory end-products: COX-2 and interleukin-1 (IL-1β). Furthermore, the expression of COX-2 was attenuated by both Akt inhibitor (LY294002) and ERK inhibitor (U0126), and IκBα degradation was suppressed by LY294002.

conclusionsThese results demonstrate that pretreatment with fimasartan to astrocytes suppresses the inflammatory responses induced by hemolysate. Akt, ERK and NFκB were associated with hemolysate-induced COX-2 and IL-1β expression. Based on these mechanisms, fimasartan could be a candidate anti-inflammatory regulator for the treatment of intracerebral hemorrhage.

Indexed as

Angiotensin II Type 2 Receptor BlockersAnimalsAnti-Inflammatory AgentsAstrocytesBiphenyl CompoundsCells, CulturedCyclooxygenase 2Extracellular Signal-Regulated MAP KinasesHemorrhageI-kappa B ProteinsInterleukin-1betaMiceNF-kappa BNF-KappaB Inhibitor alphaProto-Oncogene Proteins c-aktPyrimidinesAngiotensin II Type 2 Receptor BlockersAnti-Inflammatory AgentsBiphenyl CompoundsCyclooxygenase 2Extracellular Signal-Regulated MAP KinasesfimasartanI-kappa B ProteinsInterleukin-1betaNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, mouseNfkbia protein, ratProto-Oncogene Proteins c-aktPtgs2 protein, mousePyrimidinesRNA, MessengerTetrazolesAstrocyteFimasartanHemolysateInflammationIntracerebral hemorrhage

Identifiers

PMID26608500
OpenAlexW2269041121

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.