Evidence map›Paper›PMID 30830898›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

Calycosin Ameliorates Diabetes-Induced Renal Inflammation via the NF-κB Pathway In Vitro and In Vivo.

Ying-Ying Zhang, Rui-Zhi Tan, Xiao-Qin Zhang, Ying Yu, Chen Yu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 68 citations in OpenAlex.

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  8. Research Progress on the Treatment of Related Diseases WithDrug design, development and therapy · 2025
    Review
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  10. Calycosin inhibited MIF-mediated inflammatory chemotaxis of macrophages to ameliorate ischemia reperfusion-induced acute kidney injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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  16. Experimental and therapeutic medicine · 2023
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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 3 institutions in 1 country.

Ying-Ying ZhangDepartment of Nephrology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Rui-Zhi TanResearch Center of Combined Traditional Chinese and Western Medicine, Affiliated Traditional Medicine Hospital, Southwest Medical University, Luzhou, Sichuan, China (mainland).
Xiao-Qin ZhangDepartment of Nephrology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Ying YuDepartment of Nephrology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Chen YuDepartment of Nephrology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China (mainland).
Tongji Hospital · CNTongji University · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Diabetic nephropathy (DN), which is one of the primary causes of end-stage renal disease (ESRD), is increasingly diagnosed in patients due to the continuous increase in the prevalence of diabetic mellitus (DM). Astragali Radix, a traditional Chinese herb, is widely administrated to ameliorate the symptoms of diabetes and diabetic nephropathy, but its mechanism is still not yet fully defined. Calycosin (C₁₆H₁₂O₅) is the major active component of Astragali Radix. In this study, we analyzed the role of calycosin in diabetic nephropathy and explored its underlying mechanism. MATERIAL AND METHODS Cell activation, inflammatory cytokines expression and secretion, and protein levels were analyzed in cultured mouse tubular epithelial cells (mTEC). db/db mice were intraperitoneally injected with 10 mg/(kg·d) calycosin or control saline for 4 weeks, followed by analysis of structure injury, inflammation, and NF-κB signaling activity. RESULTS Our results indicated that TNF-α and IL-1β were significantly induced by advanced glycation end-products (AGEs), but calycosin remarkably reduced the expression of TNF-α and IL-1β in the cultured mouse tubular epithelial cells (mTEC). Calycosin effectively alleviated kidney injury in diabetic kidneys of db/db mice during the progression of diabetic renal injury, indicated by the reduction of histological injury and immunohistochemical of inflammatory cytokines. Mechanistically, we identified calycosin inhibited diabetes-induced inflammation in kidneys by suppressing the phosphorylation of IKBa and NF-κB p65 in vitro and in vivo. CONCLUSIONS Calycosin significantly ameliorated diabetes-induced renal inflammation in diabetic renal injury by inhibition of the NF-κB-dependent signaling pathway in vivo and in vitro.

Indexed as

AnimalsAstragalus propinquusCell Culture TechniquesCytokinesDiabetes Mellitus, ExperimentalDiabetic NephropathiesDisease Models, AnimalDrugs, Chinese HerbalEpithelial CellsInflammationInterleukin-1betaIsoflavonesKidneyMaleMiceNephritis7,3'-dihydroxy-4'-methoxyisoflavoneCytokinesDrugs, Chinese HerbalHuang QiIL1B protein, mouseInterleukin-1betaIsoflavonesNF-kappa BTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID30830898
PMCPMC6413560
OpenAlexW2918633862

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.