Evidence map›Paper›PMID 31117931›Full record

ArticleMolecular medicine (Cambridge, Mass.)2019

Astragalus polysaccharides suppresses high glucose-induced metabolic memory in retinal pigment epithelial cells through inhibiting mitochondrial dysfunction-induced apoptosis by regulating miR-195.

Ping Liu, Qing-Hua Peng, Ping Tong, Wen-Jie Li

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

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  17. The Role of microRNAs in Metabolic Syndrome-Related Oxidative Stress.International journal of molecular sciences · 2020
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  18. Article
  19. The Impact of miRNAs in Health and Disease of Retinal Pigment Epithelium.Frontiers in cell and developmental biology · 2020
    Review
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

4 authors at 4 institutions in 1 country.

Ping LiuDepartment of Ophthalmology, The Second Xiangya Hospital of Central South University, Changsha, 410011, People's Republic of China.
Qing-Hua PengHunan Provincial Key Laboratory of Ophthalmology and Otorhinolaryngology of Chinese Medicine, Changsha, 410007, People's Republic of China.
Ping TongDepartment of Ophthalmology, The Second Xiangya Hospital of Central South University, Changsha, 410011, People's Republic of China.
Wen-Jie LiDepartment of Ophthalmology, The Third Xiangya Hospital of Central South University, No.138, Tongzipo Road, Yuelu District, Changsha, 410013, Hunan Province, People's Republic of China. liwenjie1470@163.com.
Central South University · CNHunan University of Traditional Chinese Medicine · CNSecond Xiangya Hospital of Central South University · CNThird Xiangya Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetabolic memory contributes to the development of diabetic retinopathy (DR), which is the complication of diabetes. But it's still unknown how to prevent the metabolic memory to treat the DR. In our study, we want to examine the function of Astragalus polysaccharides (APS) in the metabolic memory of retinal pigment epithelium (RPE) pretreated with high glucose (HG).

methodsARPE-19 and PRPE cells were exposed to HG followed by normal glucose (NG) treatment with or without APS. QPCR was used to examine the levels of miR-195 and Bcl-2. MDA and SOD detection assays were used to examine the oxidative stress level. Western blotting and immunostaining were applied to detect the protein level of mitochondrial damage and apoptotic signaling pathway. Flow cytometry and TUNEL staining were used to analyze cell apoptosis. Luciferase assay was used to examine the direct target of miR-195.

resultsAPS treatment significantly decreased the expression of miR-195, while increased the expression of Bcl-2 with optimized dosages which were induced by HG treatment, even after replacing the HG with NG. And we found Bcl-2 was the direct target of miR-195. APS alleviated the oxidative stress, mitochondrial damage and cell apoptosis induced by HG and HG + NG treatments in RPE cells via regulating miR-195. Furthermore, we found overexpression of miR-195 abolished the alleviated effects of APS on the HG-treated RPE cells.

conclusionsAPS suppressed high glucose-induced metabolic memory in retinal pigment epithelial cells through inhibiting mitochondrial dysfunction-induced apoptosis by regulating miR-195.

Indexed as

AnimalsApoptosisAstragalus PlantBlotting, WesternCells, CulturedGlucoseHEK293 CellsHumansIn Situ Nick-End LabelingMalondialdehydeMembrane Potential, MitochondrialMicroRNAsMitochondriaPolysaccharidesRatsRetinal Pigment EpitheliumGlucoseMalondialdehydeMicroRNAsMIRN195 microRNA, humanPolysaccharidesSuperoxide DismutaseApoptosisAstragalus polysaccharidesDiabetic retinopathyMetabolic memorymiR-195Mitochondrial damage

Identifiers

PMID31117931
PMCPMC6530096
OpenAlexW2947247281

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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.