Evidence map›Paper›PMID 31548878›Full record

ArticleCell & bioscience2019

BabaoDan attenuates high-fat diet-induced non-alcoholic fatty liver disease via activation of AMPK signaling.

Dandan Sheng, Shanmin Zhao, Lu Gao, Huifei Zheng, Wenting Liu, Jing Hou, Yuxiang Jin, Fei Ye, Qiudong Zhao, Rong Li and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 100 citations in OpenAlex.

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  14. IREB2 Knockdown Alleviates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease by TLR4/NF-κB Signaling Inactivation.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025
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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

14 authors at 1 institution in 1 country.

Dandan Sheng *1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Shanmin Zhao *1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Lu Gao *1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Huifei Zheng1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Wenting Liu1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Jing Hou1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Yuxiang Jin1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Fei Ye1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Qiudong Zhao1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Rong Li1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Naping Zhao2Department of Pharmacy, Changhai Hospital, Second Military Medical University, Shanghai, 200433 China.
Li Zhang2Department of Pharmacy, Changhai Hospital, Second Military Medical University, Shanghai, 200433 China.
Zhipeng Han1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.
Lixin Wei1Tumor Immunology and Gene Therapy Center, Third Affiliated Hospital of Second Military Medical University, NO. 225 Changhai Road, Shanghai, 200438 China.ORCID 0000-0002-6383-7452
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBabaodan (BBD), a traditional Chinese medicine, has been shown to have protective effects during liver injury and ameliorate liver disease progression, but little is known about its effect on non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the effects of BBD on obesity-induced NAFLD.

methodsC57BL/6 J mice were fed with normal diet, high fat diet (HFD) or HFD + BBD for 8 weeks. Weights of all mice were recorded every 3 days. At the end of the experiments, the level of livers, kidneys and adipose tissues of each animal was weighed. Blood serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C) cholesterol, low density lipoprotein cholesterol (LDL-C), glucose and leptin were detected with appropriate test kits. Haematoxylin-eosin (HE), Masson trichrome and Oil Red O staining of the liver were performed. We applied immunohistochemical analysis to investigate the expression of TNF-α, IL-6 and leptin in liver tissue. The expression of genes related lipid anabolism (SREBP1-c, ACC, SCD-1, LXRα and CD36) and ß-oxidation (CPT-1 and PPARα) in liver and adipose tissues was determined by RT-PCR. The expression of AMPK and p-AMPK was determined by western blot analysis.

resultsWe found the weight of bodies and tissues (retroperitoneal fat pads, kidneys and livers) of mice fed with HFD + BBD were significantly lower than that of HFD-fed mice. And liver injury induced by HFD was relieved in mice treated with BBD, accompanied with significant reduction were observed in serum ALT/AST activities and alleviated pathological damage. The levels of glucose, TG, TC, HDL-C and LDL-C in the liver or serum were significantly decreased on HFD + BBD group compared with HFD group. Furthermore, BBD treatment reduced the level of TNF-α and IL-6 induced by HFD. The level of leptin in the liver and serum were reduced in mice fed with HFD + BBD than that of HFD-fed mice. Several lipid synthesis genes (SREBP1-c, ACC, SCD-1, LXRα and CD36) were down-regulated and that of ß-oxidation (CPT-1 and PPARα) up-regulated in HFD + BBD group compared with HFD group. In addition, BBD increased the expression of p-AMPK compared with untreated HFD group, which suggested BBD improved the activation of AMPK pathway.

conclusionIn summary, our results indicate that BBD has potential applications in the prevention and treatment of NAFLD, which may be closely related to its effect on lipid metabolism via activation of AMPK signaling.

Indexed as

AMPK pathwayBabaodanLipid metabolismNon-alcoholic fatty liver disease

Identifiers

PMID31548878
PMCPMC6751621
OpenAlexW2973408003

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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.