Evidence map›Paper›PMID 37817130›Full record

ArticleBMC complementary medicine and therapies2023

Astragalus polysaccharide restores insulin secretion impaired by lipopolysaccharides through the protein kinase B /mammalian target of rapamycin/glucose transporter 2 pathway.

Xiaodan Ren, Ying Dai, Mengya Shan, Jing Zheng, Zhongyi Zhang, Tao Shen

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in BMC complementary medicine and therapies, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Research Progress on Chemical Components ofMolecules (Basel, Switzerland) · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Xiaodan Ren *School of Basic Medicine, Chengdu University of Traditional Chinese Medicine, No. 37, Shi-er-qiao Road, Jinniu District, 610075, 610075, Chengdu, Chengdu, Sichuan, China.
Ying Dai *Department of Integrative Medicine, Xinqiao Hospital, Army Medical University, Chongqing, China.
Mengya ShanDepartment of Integrative Medicine, Xinqiao Hospital, Army Medical University, Chongqing, China.
Jing ZhengDepartment of Integrative Medicine, Xinqiao Hospital, Army Medical University, Chongqing, China.
Zhongyi ZhangSchool of Basic Medicine, Chengdu University of Traditional Chinese Medicine, No. 37, Shi-er-qiao Road, Jinniu District, 610075, 610075, Chengdu, Chengdu, Sichuan, China.
Tao ShenSchool of Basic Medicine, Chengdu University of Traditional Chinese Medicine, No. 37, Shi-er-qiao Road, Jinniu District, 610075, 610075, Chengdu, Chengdu, Sichuan, China. shentaotcm@aliyun.com.
Chengdu University of Traditional Chinese Medicine · CNXinqiao Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLipopolysaccharide (LPS)-induced dysfunction of pancreatic β-cells leads to impaired insulin (INS) secretion. Astragalus polysaccharide (APS) is a bioactive heteropolysaccharide extracted from Astragalus membranaceus and is a popular Chinese herbal medicine. This study aimed to elucidate the mechanisms by which APS affects INS secretion from β-cells under LPS stress.

methodsRat insulinoma (INS-1) cells were treated with LPS at a low, medium, or high concentration of APS. Glucose-stimulated insulin secretion (GSIS) was evaluated using an enzyme-linked immunosorbent assay (ELISA). Transcriptome sequencing was used to assess genome-wide gene expression. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was used to determine the signaling pathways affected by APS. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to evaluate the gene expression of glucose transporter 2 (GLUT2), glucokinase (GCK), pancreatic duodenal homeobox-1 (PDX-1), and INS. Western blot analysis was used to detect the protein expression of phosphorylated protein kinase B (p-Akt), total Akt (t-Akt), phosphorylated mammalian target of rapamycin (p-mTOR), total mTOR (t-mTOR), and GLUT2.

resultsLPS decreased GLUT2, GCK, PDX-1, and INS expression and reduced GSIS. These LPS-induced decreases in gene expression and GSIS were restored by APS treatment. In addition, transcriptome sequencing in combination with KEGG enrichment analysis revealed changes in the INS signaling pathway following APS treatment. LPS decreased p-Akt and p-mTOR expression, which was restored by APS treatment. The restorative effects of APS on GSIS as well as on the expression of GLUT2, GCK, PDX-1, and INS were abolished by treatment with the Akt inhibitor MK2206 or the mTOR inhibitor rapamycin (RPM).

conclusionsAPS restored GSIS in LPS-stimulated pancreatic β-cells by activating the Akt/mTOR/GLUT2 signaling pathway.

Indexed as

LipopolysaccharidesProto-Oncogene Proteins c-aktAnimalsGlucoseGlucose Transport Proteins, FacilitativeInsulin SecretionMammalsPolysaccharidesRatsSirolimusTOR Serine-Threonine KinasesGlucoseGlucose Transport Proteins, FacilitativeLipopolysaccharidesPolysaccharidesProto-Oncogene Proteins c-aktSirolimusTOR Serine-Threonine KinasesAstragalus polysaccharideGlucose transporter 2Insulin secretionLipopolysaccharides

Identifiers

PMID37817130
PMCPMC10563267
OpenAlexW4387501154

What OpenQuestion holds

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LicenceCC BY
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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.