Evidence map›Paper›PMID 29386886›Full record

ArticleDrug design, development and therapy2018

Renal-protective effect of thalidomide in streptozotocin-induced diabetic rats through anti-inflammatory pathway.

Hongxia Zhang, Yanlan Yang, Yanqin Wang, Baodong Wang, Rongshan Li

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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  13. Renal and cerebral RAS interaction contributes to diabetic kidney disease.American journal of translational research · 2019
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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 1 institution in 1 country.

Hongxia ZhangDepartment of Nephrology.
Yanlan YangDepartment of Endocrinology, Affiliated People's Hospital of Shanxi Medical University, Shanxi Provincial People's Hospital, Taiyuan, Shanxi, People's Republic of China.
Yanqin WangDepartment of Nephrology.
Baodong WangDepartment of Nephrology.
Rongshan LiDepartment of Nephrology.
Shanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic nephropathy (DN) is a major microvascular complication in diabetes. An increasing body of evidence has shown that DN is related to chronic inflammation, kidney hypertrophy, and fibrosis. While thalidomide has been shown to have anti-inflammatory and antifibrotic effects, the effects of thalidomide on the pathogenesis of DN are unclear. This study was undertaken to explore whether thalidomide has renal-protective effects in diabetic rats.

methodsMale Sprague Dawley rats were injected intraperitoneally with 50 mg/kg streptozotocin to induce diabetes. Diabetic rats were treated with thalidomide (200 mg/kg/d) for 8 weeks, and then blood and urine were collected for measurement of renal function-related parameters. Histopathology, immunohistochemistry, enzyme-linked immunosorbent assay, and Western blot analyses were performed to assess renal proinflammatory cytokines, fibrotic protein, and related signaling pathways.

resultsDiabetic rats exhibited obvious renal structural and functional abnormalities, as well as renal inflammation and fibrosis. Compared with diabetic control rats, those treated with thalidomide showed significantly improved histological alterations and biomarkers of renal function, as well as reduced expression of renal inflammatory cytokines, including NF-κB and MCP-1. Furthermore, renal fibrotic proteins, such as TGF-β1, TβRII, TβRI, smad3, collagen IV, and fibronectin were also remarkably suppressed. Treatment with thalidomide markedly stimulated the phosphorylation of AMPKα.

conclusionIn this study, thalidomide suppressed the inflammatory and fibrotic processes in DN. These effects were partly mediated by the activation of AMPKα, and inhibition of the NF-κB/MCP-1 and TGF-β1/Smad signaling pathways. These results suggest that thalidomide may have therapeutic potential in diabetic renal injury through the anti-inflammatory pathway.

Indexed as

StreptozocinAMP-Activated Protein KinasesAnimalsAnti-Inflammatory AgentsCytokinesCytoprotectionDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisInflammation MediatorsKidneyMaleNephritisNF-kappa BPhosphorylationProtein Serine-Threonine KinasesAMP-Activated Protein KinasesAnti-Inflammatory AgentsCytokinesInflammation MediatorsNF-kappa BProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IISmad3 ProteinSmad3 protein, ratStreptozocinTgfb1 protein, ratTgfbr1 protein, ratThalidomideTransforming Growth Factor beta1AMPKdiabetic nephropathyNF-κBTGF-β1thalidomide

Identifiers

PMID29386886
PMCPMC5765978
OpenAlexW2783753677

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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.