Evidence map›Paper›PMID 28445528›Full record

ArticlePloS one2017

Baicalein protects rat insulinoma INS-1 cells from palmitate-induced lipotoxicity by inducing HO-1.

Hyun Jeong Kwak, Dongki Yang, Yongha Hwang, Hee-Sook Jun, Hyae Gyeong Cheon

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

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  6. Synthesis and Characterization of Baicalein-loaded Aquasomes: AnCurrent drug discovery technologies · 2024
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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

5 authors at 1 institution in 1 country.

Hyun Jeong KwakDepartment of Pharmacology, Gachon University College of Medicine, Incheon, Republic of Korea.
Dongki YangDepartment of Physiology, Gachon University College of Medicine, Incheon, Republic of Korea.
Yongha HwangCollege of Pharmacy and Gachon Institute of Pharmaceutical Science, Gachon University, Incheon, Republic of Korea.
Hee-Sook JunCollege of Pharmacy and Gachon Institute of Pharmaceutical Science, Gachon University, Incheon, Republic of Korea.
Hyae Gyeong CheonDepartment of Pharmacology, Gachon University College of Medicine, Incheon, Republic of Korea.ORCID http://orcid.org/0000-0003-3090-1988
Gachon University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveβ-Cell dysfunction plays a central role in the pathogenesis of type 2 diabetes (T2D), and the identification of novel approaches to improve β-cell function is essential to treat this disease. Baicalein, a flavonoid originally isolated from the root of Scutellaria Baicalensis, has been shown to have beneficial effects on β-cell function. Here, the authors investigated the molecular mechanism responsible for the protective effects of baicalein against palmitate (PA)-induced impaired β-cell function, and placed focus on the role of heme oxygenase (HO)-1.

methodsRat pancreatic β-cell line INS-1 cells or mouse pancreatic islets were cultured with PA (500 μM) to induce lipotoxicity in the presence or absence of baicalein (50 μM), and the expressions of the ER stress markers, ATF-3, CHOP and GRP78 were detected by Western blotting and/or qPCR. The involvement of HO-1 was evaluated by HO-1 siRNA transfection and using the HO-1 inhibitor ZnPP.

resultsBaicalein reduced PA-induced ER stress and inflammation and enhanced insulin secretion, and these effects were associated with the induction of HO-1. Furthermore, these protective effects were attenuated by ZnPP and by HO-1 siRNA. Pretreatment of PD98059 (an ERK inhibitor) significantly inhibited the protective effects of baicalein and blocked HO-1 induction. On the other hand, CO production by RuCO (a CO donor) ameliorated PA-induced ER stress, suggesting that CO production followed by HO-1 induction may contribute to the protective effects of baicalein against PA-induced β-cell dysfunction.

conclusionBaicalein protects pancreatic β-cells from PA-induced ER stress and inflammation via an ERK-HO-1 dependent pathway. The authors suggest HO-1 induction in pancreatic β-cells appears to be a promising therapeutic strategy for T2D.

Indexed as

AnimalsCells, CulturedCell SurvivalCytokinesDNA FragmentationEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressExtracellular Signal-Regulated MAP KinasesFlavanonesFlavonoidsHeat-Shock ProteinsHeme Oxygenase-1InsulinomaInsulin-Secreting CellsMaleMice2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-onebaicaleinCytokinesEndoplasmic Reticulum Chaperone BiPExtracellular Signal-Regulated MAP KinasesFlavanonesFlavonoidsHeat-Shock ProteinsHeme Oxygenase-1Hspa5 protein, mousePalmitatesProtective AgentsProtoporphyrinszinc protoporphyrin

Identifiers

PMID28445528
PMCPMC5405981
OpenAlexW2609812423

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.