Evidence map›Paper›PMID 24793312›Full record

ArticleActa pharmacologica Sinica2014

Telmisartan protects central neurons against nutrient deprivation-induced apoptosis in vitro through activation of PPARγ and the Akt/GSK-3β pathway.

Tao Pang, Li-Xin Sun, Tao Wang, Zhen-Zhou Jiang, Hong Liao, Lu-Yong Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 41 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.

Tao Pang1] New Drug Screening Center, China Pharmaceutical University, Nanjing 210009, China [2] State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China [3] Key Laboratory of Drug Quality Control and Pharmacovigilance (China Pharmaceutical University), Ministry of Education, Nanjing 210009, China.
Li-Xin SunNew Drug Screening Center, China Pharmaceutical University, Nanjing 210009, China.
Tao WangNew Drug Screening Center, China Pharmaceutical University, Nanjing 210009, China.
Zhen-Zhou JiangNew Drug Screening Center, China Pharmaceutical University, Nanjing 210009, China.
Hong Liao1] New Drug Screening Center, China Pharmaceutical University, Nanjing 210009, China [2] State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China.
Lu-Yong Zhang1] New Drug Screening Center, China Pharmaceutical University, Nanjing 210009, China [2] State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China.
China Pharmaceutical University · CNNational Center for Drug Screening · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo determine whether angiotensin II receptor blockers (ARBs) could protect central neurons against nutrient deprivation-induced apoptosis in vitro and to elucidate the underlying mechanisms.

methodsPrimary rat cerebellar granule cells (CGCs) underwent B27 (a serum substitute) deprivation for 24 h to induce neurotoxicity, and cell viability was analyzed using LDH assay and WST-1 assay. DNA laddering assay and TUNEL assay were used to detect cell apoptosis. The expression of caspase-3 and Bcl-2, and the phosphorylation of Akt and GSK-3β were detected using Western blot analysis. AT1a mRNA expression was determined using RT-PCR analysis.

resultsB27 deprivation significantly increased the apoptosis of CGCs, as demonstrated by LDH release, DNA laddering, caspase-3 activation and positive TUNEL staining. Pretreatment with 10 μmol/L ARBs (telmisartan, candesartan or losartan) partially blocked B27 deprivation-induced apoptosis of CGCs with telmisartan being the most effective one. B27 deprivation markedly increased the expression of AT1a receptor in CGCs, inhibited Akt and GSK-3β activation, decreased Bcl-2 level, and activated caspase-3, which were reversed by pretreatment with 1 μmol/L telmisartan. In addition, pretreatment with 10 μmol/L PPARγ agonist pioglitazone was more effective in protecting CGCs against B27 deprivation-induced apoptosis, whereas pretreatment with 20 μmol/L PPARγ antagonist GW9662 abolished all the effects of telmisartan in CGCs deprived of B27.

conclusionARBs, in particular telmisartan, can protect the nutrient deprivation-induced apoptosis of CGCs in vitro through activation of PPARγ and the Akt/GSK-3β pathway.

Indexed as

Angiotensin II Type 1 Receptor BlockersAnimalsApoptosisBenzimidazolesBenzoatesCells, CulturedCerebellumFemaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMaleNeuronsNeuroprotective AgentsPPAR gammaProto-Oncogene Proteins c-aktRatsAngiotensin II Type 1 Receptor BlockersBenzimidazolesBenzoatesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratNeuroprotective AgentsPPAR gammaProto-Oncogene Proteins c-aktTelmisartan

Identifiers

PMID24793312
PMCPMC4086392
OpenAlexW2019812235

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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.