Evidence map›Paper›PMID 37872577›Full record

ArticleBMC endocrine disorders2023

Acteoside protects podocyte against apoptosis through regulating AKT/GSK-3β signaling pathway in db/db mice.

Xiaoya Li, Zhilong Liu, Zhixiu He, Xiaocheng Wang, Rongshan Li, Junwei Wang, Guiqiao Ma, Peipei Zhang, Chanjuan Ma

Open access · goldAbstract read
In one paragraph

Article in BMC endocrine disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Xiaoya LiDepartment of Nephrology, Shanxi Provincial People's Hospital, Taiyuan, China.
Zhilong LiuShanxi Provincial Key Laboratory of Kidney Disease, Shanxi Provincial People's Hospital, Taiyuan, China.
Zhixiu HeDepartment of Nephrology, Shanxi Provincial People's Hospital, Taiyuan, China.
Xiaocheng WangDepartment of Medical Record & Statistics, Shanxi Provincial People's Hospital, Taiyuan, China.
Rongshan LiDepartment of Nephrology, Shanxi Provincial People's Hospital, Taiyuan, China.
Junwei WangShanxi Provincial Key Laboratory of Kidney Disease, Shanxi Provincial People's Hospital, Taiyuan, China.
Guiqiao MaShanxi Provincial Key Laboratory of Kidney Disease, Shanxi Provincial People's Hospital, Taiyuan, China.
Peipei ZhangDepartment of Nephrology, Shanxi Provincial People's Hospital, Taiyuan, China.
Chanjuan MaDepartment of Nephrology, Shanxi Provincial People's Hospital, Taiyuan, China. mcj5670206@163.com.
Shanxi Medical University · CNShaanxi Provincial People's Hospital · CNShanxi University · CN

Funding

National Natural Science Foundation of China No. 81300698Research Project Supported by Shanxi Scholarship Council of China 2022-206the Fund Program for the Scientific Activities of Selected Returned Overseas Professionals in Shanxi Province No. 20220046the Natural Science Foundation of Shanxi Province No. 201901D111437
6 · The paper itself

Abstract

backgroundPodocyte apoptosis is one of the important pathological mechanisms of diabetic kidney disease (DKD). Acteoside (Act), a major active component of Rehmannia glutinosa leaves total glycoside, has a strong renoprotective action. Our study aims to demonstrate Act's renoprotective actions in db/db mice.

methodsWe adopted C57BLKS/J db/db mice as DKD animal models. After 8 weeks of Act administration, the 24-hour urine albumin, renal function index, and blood lipid levels were quantified using matching kits. Renal pathology was evaluated by HE and PAS staining. The podocyte damage and apoptosis-related signaling pathway were observed by using immunohistochemistry, western blot, and TUNEL staining.

resultsThe albuminuria of db/db mice was reduced from 391 ug/24 h to 152 ug/24 h, and renal pathology changes were alleviated after Act administration. The western blot and immunohistochemistry showed that Act treatment upregulated the synaptopodin and podocin expression compared with db/db mice, while the TUNEL staining indicated podocyte apoptosis was inhibited. The B-cell lymphoma-2 (Bcl-2) level was upregulated in the Act group, but cleaved caspase-3 and Bcl-2 associated X protein (Bax) expression declined, while the protein kinase B/glycogen synthase kinase-3β (AKT/GSK-3β) signaling pathway was repressed.

conclusionsBy inhibiting the AKT/GSK-3β signaling pathway, Act protected podocytes from apoptosis, decreasing the urine albumin of db/db mice and delaying the course of DKD.

Indexed as

Diabetic NephropathiesPodocytesAlbuminsAnimalsApoptosisGlucosidesGlycogen Synthase Kinase 3 betaMicePolyphenolsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Signal TransductionacteosideAlbuminsGlucosidesGlycogen Synthase Kinase 3 betaPolyphenolsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2ActeosideAKT/GSK-3β signaling pathwayApoptosisDiabetic Kidney Disease (DKD)Podocyte

Identifiers

PMID37872577
PMCPMC10591407
OpenAlexW4387877494

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.