Evidence map›Paper›PMID 38498259›Full record

ArticlePharmacological reports : PR2024

Protective effect of hygrolansamycin C against corticosterone-induced toxicity and oxidative stress-mediated via autophagy and the MAPK signaling pathway.

Jongtae Roh, Jun-Pil Jang, Taehoon Oh, Jihong Kim, Byeongsan Lee, Young-Soo Hong, Jae-Hyuk Jang, Sung-Kyun Ko

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In one paragraph

Article in Pharmacological reports : PR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 96% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Jongtae Roh *Chemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea.
Jun-Pil Jang *Chemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea.
Taehoon OhChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea.
Jihong KimChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea.
Byeongsan LeeChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea.
Young-Soo HongChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea.
Jae-Hyuk JangChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea. jangjh@kribb.re.kr.
Sung-Kyun KoChemical Biology Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju, 28116, Korea. ksk1230@kribb.re.kr.ORCID http://orcid.org/0000-0002-8202-1205
Korea Research Institute of Bioscience and Biotechnology · KRChungbuk National University · KR

Funding

Korea Research Institute of Bioscience and Biotechnology KGM1222413Korea Research Institute of Bioscience and Biotechnology KGM5292423the National Research Council of Science & Technology CAP23011-300the National Research Foundation of Korea 2017R1C1B2002602
6 · The paper itself

Abstract

backgroundExcessive stress, a major problem in modern societies, affects people of all ages worldwide. Corticosterone is one of the most abundant hormones secreted during stressful conditions and is associated with various dysfunctions in the body. In particular, we aimed to investigate the protective effects of hygrolansamycin C (HYGC) against corticosterone-induced cellular stress, a manifestation of excessive stress prevalent in contemporary societies.

methodsWe isolated HYGC from Streptomyces sp. KCB17JA11 and subjected PC12 cells to corticosterone-induced stress. The effects of HYGC were assessed by measuring autophagy and the expression of mitogen-activated protein kinase (MAPK) phosphorylation-related genes. We used established cellular and molecular techniques to analyze protein levels and pathways.

resultsHYGC effectively protected cells against corticosterone-induced injury. Specifically, it significantly reduced corticosterone-induced oxidative stress and inhibited the expression of autophagy-related proteins induced by corticosterone, which provided mechanistic insight into the protective effects of HYGC. At the signaling level, HYGC suppressed c-Jun N-terminal kinase and extracellular signal-regulated kinase phosphorylation and p38 activation.

conclusionsHYGC is a promising candidate to counteract corticosterone-induced apoptosis and oxidative stress. Autophagy and MAPK pathway inhibition contribute to the protective effects of HYGC. Our findings highlight the potential of HYGC as a therapeutic agent for stress-related disorders and serve as a stepping stone for further exploration and development of stress management strategies.

Indexed as

Corticosteronep38 Mitogen-Activated Protein KinasesAnimalsApoptosisAutophagyExtracellular Signal-Regulated MAP KinasesHumansMAP Kinase Signaling SystemOxidative StressRatsSignal TransductionCorticosteroneExtracellular Signal-Regulated MAP Kinasesp38 Mitogen-Activated Protein KinasesAutophagyCorticosteroneHygrolansamycin CMitogen-activated protein kinaseOxidative stress

Identifiers

PMID38498259
OpenAlexW4392919121

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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.