Evidence map›Paper›PMID 29959134›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2018

Glycyrrhizin Alleviates Nonalcoholic Steatohepatitis via Modulating Bile Acids and Meta-Inflammation.

Tingting Yan, Hong Wang, Lijuan Cao, Qiong Wang, Shogo Takahashi, Tomoki Yagai, Guolin Li, Kristopher W Krausz, Guangji Wang, Frank J Gonzalez and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. [Construction norms for the tiered diagnosis and treatment and standardized management center of metabolic-associated fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Guideline
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article
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

11 authors at 5 institutions in 2 countries.

Tingting YanState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Hong WangState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Lijuan CaoState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Qiong WangState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Shogo TakahashiState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Tomoki YagaiState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Guolin LiState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Kristopher W KrauszState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Guangji WangState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.).
Frank J GonzalezState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.) gonzalef@mail.nih.gov haipinghao@cpu.edu.cn.
Haiping HaoState Key Laboratory of Natural Medicines, Key Laboratory of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, Nanjing, Jiangsu, China (Ti. Y., H.W., L.C., G.W., H.H.); and Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health National Cancer Institute, Bethesda, Maryland (Ti. Y., Q.W., S.T., To.Y., G.L., K.W.K., F.J.G.) gonzalef@mail.nih.gov haipinghao@cpu.edu.cn.
State Key Laboratory of Natural MedicineChina Pharmaceutical University · CNCenter for Cancer Research · USNational Cancer Institute · USNational Institutes of Health · US

Funding

Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
6 · The paper itself

Abstract

Nonalcoholic steatohepatitis (NASH) is the progressive stage of nonalcoholic fatty liver disease that may ultimately lead to cirrhosis and liver cancer, and there are few therapeutic options for its treatment. Glycyrrhizin (GL), extracted from the traditional Chinese medicine liquorice, has potent hepatoprotective effects in both preclinical animal models and in humans. However, little is currently known about its effects and mechanisms in treating NASH. To explore the effects of GL on NASH, GL or its active metabolite glycyrrhetinic acid (GA) was administered to mice treated with a methionine- and choline-deficient (MCD) diet-induced NASH model, and histologic and biochemical analyses were used to measure the degree of lipid disruption, liver inflammation, and fibrosis. GL significantly improved MCD diet-induced hepatic steatosis, inflammation, and fibrosis and inhibited activation of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome. GL significantly attenuated serum bile acid accumulation in MCD diet-fed mice partially by restoring inflammation-mediated hepatic farnesoid X receptor inhibition. In Raw 264.7 macrophage cells, both GL and GA inhibited deoxycholic acid-induced NLRP3 inflammasome-associated inflammation. Notably, both intraperitoneal injection of GL's active metabolite GA and oral administration of GL prevented NASH in mice, indicating that GL may attenuate NASH via its active metabolite GA. These results reveal that GL, via restoration of bile acid homeostasis and inhibition of inflammatory injury, can be a therapeutic option for treatment of NASH.

Indexed as

AnimalsAnti-Inflammatory AgentsBile Acids and SaltsGlycyrrhizic AcidHep G2 CellsHumansInflammationMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseRandom AllocationRAW 264.7 CellsAnti-Inflammatory AgentsBile Acids and SaltsGlycyrrhizic Acid

Identifiers

PMID29959134
PMCPMC6081736
OpenAlexW2811373928

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.