Evidence map›Paper›PMID 36707848›Full record

ArticleEuropean journal of medical research2023

Icariin synergizes therapeutic effect of dexamethasone on adriamycin-induced nephrotic syndrome.

Juan Lv, Guozhong Xue, Yunxia Zhang, Xinbin Wang, Enlai Dai

Open access · goldAbstract read
In one paragraph

Article in European journal of medical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.8field-weighted citation impact, top 30% 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, 4 citations in OpenAlex.

No citing paper in PubMed yet.

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 2 institutions in 1 country.

Juan LvDepartment of Integrated Traditional Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, Gansu, China.
Guozhong XueDepartment of Nephrology, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Yunxia ZhangDepartment of Neurology, Gansu Provincial Hospital of TCM, Lanzhou, Gansu, China.
Xinbin WangDepartment of Integrated Traditional Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, Gansu, China.
Enlai DaiDepartment of Integrated Traditional Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, Gansu, China. 2409558212@qq.com.
Gansu University of Traditional Chinese Medicine · CNGansu Provincial Hospital of TCM · CN

Funding

Regional Science Foundation Project 81760799
6 · The paper itself

Abstract

backgroundGlomerular damage is a common clinical indicator of nephrotic syndrome. High-dose hormone treatment often leads to hormone resistance in patients. How to avoid resistance and improve the efficiency of hormone therapy draws much attention to clinicians.

methodsAdriamycin (ADR) was used to induce nephropathy model in SD rats. The rats were treated with dexamethasone (DEX), icariin (ICA), and DEX + ICA combination therapy. The changes in urinary protein (UP), urea nitrogen (BUN), and serum creatinine (SCR) contents in rats were detected by enzyme-linked immunosorbent assay (ELISA), and the degree of pathological injury and the expression level of podocin were detected by HE staining and immunohistochemistry, to test the success of the model and the therapeutic effects of three different ways. The effect of treatments on podocytes autophagy was evaluated via transfection of mRFP-GFP-LC3 tandem adenovirus in vitro.

resultsThe contents of UP, SCR, and BUN were significantly increased, the glomerulus was seriously damaged, and the expression of Nephrosis2 (NPHS2) was significantly decreased in the ADR-induced nephrotic syndrome rat model compared to that of the control group. DEX, ICA, and the DEX + ICA combined treatment significantly alleviated these above changes induced by ADR. The combined treatment of DEX + ICA exhibited better outcome than single treatment. The combined treatment also restored the podocyte autophagy, increased the expression of microtubule-associated protein light-chain 3II (LC3II), and reduced the expression of p62 in vitro. The combined treatment protects podocytes by mediating the PI3K/AKT/mTOR (rapamycin complex) signaling pathway.

conclusionICA enhances the therapeutic effect of DEX on the nephrotic syndrome.

Indexed as

Kidney DiseasesNephrotic SyndromeAnimalsDexamethasoneDoxorubicinFlavonoidsHormonesPhosphatidylinositol 3-KinasesRatsRats, Sprague-DawleyDexamethasoneDoxorubicinFlavonoidsHormonesicariinPhosphatidylinositol 3-KinasesAdriamycinAutophagyNephrotic syndromePodocyte injury

Identifiers

PMID36707848
PMCPMC9881371
OpenAlexW4318219037

What OpenQuestion holds

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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.