Evidence map›Paper›PMID 29993180›Full record

ArticleJournal of cellular and molecular medicine2018

Gypenosides improve diabetic cardiomyopathy by inhibiting ROS-mediated NLRP3 inflammasome activation.

Hailong Zhang, Xi Chen, Beibei Zong, Hongmin Yuan, Zhizeng Wang, Yinxiang Wei, Xuance Wang, Guangchao Liu, Jun Zhang, Shulian Li and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
3.9field-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

98 citing papers in PubMed, 166 citations in OpenAlex.

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  9. Mechanisms of gypenosides in type 2 diabetes mellitus via regulation of m6A methylase METTL3/14 and demethylase FTO.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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  12. High glucose affects the cardiac function of diabetic Akita mice by inhibiting cardiac ATP synthase beta subunit.International journal of cardiology. Cardiovascular risk and prevention · 2025
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38 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Hailong ZhangJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.ORCID 0000-0003-3316-4290
Xi ChenDepartment of General Pathology, Huaihe Hospital, Henan University, Kaifeng, China.
Beibei ZongJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.
Hongmin YuanDepartment of Thyroid Breast Surgery, Huaihe Hospital, Henan University, Kaifeng, China.
Zhizeng WangJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.
Yinxiang WeiJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.
Xuance WangCentre for Translational Medicine, Huaihe Hospital, Henan University, Kaifeng, China.
Guangchao LiuJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.
Jun ZhangJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.
Shulian LiJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.
Guanchang ChengDepartment of Cardiac Surgery, Huaihe Hospital, Henan University, Kaifeng, China.
Yaohui WangJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.
Yuanfang MaJoint National Laboratory for Antibody Drug Engineering, Key Laboratory of Cellular and Molecular Immunology of Henan Province, School of Basic Medicine, Henan University, Kaifeng, China.
Henan University · CNHenan University Huaihe Hospital and Huaihe Clinical Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NLRP3 inflammasome activation plays an important role in diabetic cardiomyopathy (DCM), which may relate to excessive production of reactive oxygen species (ROS). Gypenosides (Gps), the major ingredients of Gynostemma pentaphylla (Thunb.) Makino, have exerted the properties of anti-hyperglycaemia and anti-inflammation, but whether Gps improve myocardial damage and the mechanism remains unclear. Here, we found that high glucose (HG) induced myocardial damage by activating the NLRP3 inflammasome and then promoting IL-1β and IL-18 secretion in H9C2 cells and NRVMs. Meanwhile, HG elevated the production of ROS, which was vital to NLRP3 inflammasome activation. Moreover, the ROS activated the NLRP3 inflammasome mainly by cytochrome c influx into the cytoplasm and binding to NLRP3. Inhibition of ROS and cytochrome c dramatically down-regulated NLRP3 inflammasome activation and improved the cardiomyocyte damage induced by HG, which was also detected in cells treated by Gps. Furthermore, Gps also reduced the levels of the C-reactive proteins (CRPs), IL-1β and IL-18, inhibited NLRP3 inflammasome activation and consequently improved myocardial damage in vivo. These findings provide a mechanism that ROS induced by HG activates the NLRP3 inflammasome by cytochrome c binding to NLRP3 and that Gps may be potential and effective drugs for DCM via the inhibition of ROS-mediated NLRP3 inflammasome activation.

Indexed as

AnimalsAntioxidantsBlood GlucoseCardiotonic AgentsCarrier ProteinsCell LineCytochromes cDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesGene Expression RegulationGynostemmaInflammasomesInterleukin-18Interleukin-1betaMaleMyocytes, CardiacAntioxidantsBlood GlucoseCardiotonic AgentsCarrier ProteinsCrp protein, ratCytochromes cgypenosideIL1B protein, ratInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratPlant ExtractsReactive Oxygen SpeciesStreptozocincytochrome cdiabetic cardiomyopathygypenosideshigh glucoseNLRP3 inflammasomeROS

Identifiers

PMID29993180
PMCPMC6111804
OpenAlexW2836826811

What OpenQuestion holds

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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 OpenQuestion graph.