Evidence map›Paper›PMID 31607744›Full record

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

Berberine (BBR) Attenuated Palmitic Acid (PA)-Induced Lipotoxicity in Human HK-2 Cells by Promoting Peroxisome Proliferator-Activated Receptor α (PPAR-α).

Yueyue Wu, Fangyuan Chen, Xinmei Huang, Rui Zhang, Zhiyan Yu, Zaoping Chen, Jun Liu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-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

7 citing papers in PubMed, 15 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

7 authors at 2 institutions in 1 country.

Yueyue WuDepartment of Endocrinology, Shanghai Fifth People's Hospital Affiliated to Fudan University, Shanghai, China (mainland).
Fangyuan ChenDepartment of Endocrinology, Shanghai Fifth People's Hospital Affiliated to Fudan University, Shanghai, China (mainland).
Xinmei HuangDepartment of Endocrinology, Shanghai Fifth People's Hospital Affiliated to Fudan University, Shanghai, China (mainland).
Rui ZhangDepartment of Endocrinology, Shanghai Fifth People's Hospital Affiliated to Fudan University, Shanghai, China (mainland).
Zhiyan YuDepartment of Endocrinology, Shanghai Fifth People's Hospital Affiliated to Fudan University, Shanghai, China (mainland).
Zaoping ChenDepartment of Endocrinology, Shanghai Fifth People's Hospital Affiliated to Fudan University, Shanghai, China (mainland).
Jun LiuDepartment of Endocrinology, Shanghai Fifth People's Hospital Affiliated to Fudan University, Shanghai, China (mainland).
Obstetrics and Gynecology Hospital of Fudan University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Berberine (BBR), a natural alkaloid isolated from Coptis chinensis, has frequently been reported as an antidiabetic reagent, partly due to its lipid-lowering activity. Evidence suggests that BBR ameliorates palmitate-induced lipid deposition and apoptosis in renal tubular epithelial cells (TECs), which tracks in tandem with the enhancement of peroxisome proliferator-activated receptor alpha (PPAR-alpha). The study aim was to investigate the roles of BBR in renal lipotoxicity in vitro, and investigate whether PPAR-alpha was the underlying mechanism. MATERIAL AND METHODS Human TECs (HK-2 cells) were injured with palmitic acid (PA), and then treated with BBR, BBR+PPAR-alpha inhibitor (GW6471), and PA+PPAR-alpha agonist (fenofibrate). Endoplasmic reticulum (ER) stress was assessed by measuring the expression of prospective evaluation of radial keratotomy (PERK), C/EBP-homologous protein (CHOP), and 78 kDa glucose-regulated protein (GRP78). Lipid metabolism was assessed by determining lipid anabolism-associated genes, including fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and lipoprotein lipase (LPL), as well as lipid catabolism-associated gene, including carnitine palmitoyl transferase 1 (CPT1). Inflammatory response of HK-2 cells was evaluated by measuring interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha. Cell apoptosis and protein levels of cleaved-caspase-3 were evaluated. RESULTS PA downregulated PPAR-alpha and induced server lipotoxicity in HK-2 cells by ER stress, increasing lipid deposition, and elevating inflammatory response of HK-2 cells accompanied with inducting cell apoptosis and cleaved-caspase-3, which were obviously reversed by additional treatment of BBR or PPAR-alpha agonist. However, the protective effect of BBR in PA-induced lipotoxicity in HK-2 cells was significantly ameliorated by PPAR-alpha inhibitor. CONCLUSIONS BBR attenuated PA-induced lipotoxicity via the PPAR-alpha pathway.

Indexed as

ApoptosisBerberineCell LineEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHumansInflammationPalmitic AcidPPAR alphaSignal TransductionUp-RegulationBerberineEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanPalmitic AcidPPAR alpha

Identifiers

PMID31607744
PMCPMC6812469
OpenAlexW2980676121

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.