Evidence map›Paper›PMID 34427852›Full record

ArticleInflammation2022

Glycyrrhizic Acid Alleviates Lipopolysaccharide (LPS)-Induced Acute Lung Injury by Regulating Angiotensin-Converting Enzyme-2 (ACE2) and Caveolin-1 Signaling Pathway.

Yangye Chen, Lihua Qu, Yi Li, Chao Chen, Wei He, Li Shen, Ran Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Anti-Inflammatory Effects ofLife (Basel, Switzerland) · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Glycyrrhizic Acid Protects Experimental Sepsis Rats against Acute Lung Injury and Inflammation.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  15. 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

7 authors at 3 institutions in 1 country.

Yangye Chen *Department of Physiology, Hunan Normal University School of Medicine, 371 TongZiPo Road, Changsha, 410013, Hunan, China.
Lihua Qu *Department of Physiology, Hunan Normal University School of Medicine, 371 TongZiPo Road, Changsha, 410013, Hunan, China.
Yi LiDepartment of Physiology, Hunan Normal University School of Medicine, 371 TongZiPo Road, Changsha, 410013, Hunan, China.
Chao ChenSchool of Medicine & Holistic Integrative Medicine, Nanjing University of Chinese Medicine, Nanjing, 210013, China.
Wei HeDepartment of Ultrasonography, The Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Li ShenDepartment of Physiology, Hunan Normal University School of Medicine, 371 TongZiPo Road, Changsha, 410013, Hunan, China. shenhunannu@163.com.ORCID http://orcid.org/0000-0002-4431-0006
Ran ZhangDepartment of Immunology, Hunan Normal University School of Medicine, 371 TongZiPo Road, Changsha, 410013, Hunan, China. zhangrankp@qq.com.
Hunan Normal University · CNCentral South University · CNNanjing University of Chinese Medicine · CN

Funding

Hunan Natural Science Foundation No. 2018JJ2255Hunan Natural Science Foundation Joint Project of Science and Health No. 2018JJ6052Hunan Provincial Innovation Foundation for Postgraduate CX20190406National Natural Science Foundation of China No. 81100054
6 · The paper itself

Abstract

Acute lung injury (ALI) is mainly caused by severe infection, shock, trauma, and burn, which causes the extensive release of inflammatory factors and other mediators. As a major bioactive constituent of traditional Chinese herb licorice, glycyrrhizic acid (GA) plays an important effect on inflammatory regulation. Nevertheless, the exact mechanism of this effect remains unclear. The present study aims to explore the potential protective effect of GA on LPS-induced ALI. Our results showed that GA significantly attenuated LPS-induced ALI and decreased the production of inflammatory factors, including IL-1β, MCP-1, COX2, HMGB1, and adhesion molecules, such as E-selectin, VCAM-1, and modulated expression of angiotensin-converting enzyme 2 (ACE2). Moreover, treatment of ACE2 inhibitor (MLN-4760) reversed the effects of GA on the secretion of pro-inflammatory factors in ALI. Additionally, GA exerts its protective effect by regulating the ACE2 and caveolin-1/NF-κB signaling pathway. In conclusion, this study showed that GA alleviated LPS-induced ALI by upregulating ACE2 and inhibiting the caveolin-1/NF-κB signaling pathway.

Indexed as

Acute Lung InjuryAngiotensin-Converting Enzyme 2AnimalsAnti-Inflammatory AgentsBiomarkersCaveolin 1Glycyrrhizic AcidHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesLungMaleMiceMice, Inbred BALB CSignal TransductionTreatment OutcomeACE2 protein, humanAce2 protein, mouseAngiotensin-Converting Enzyme 2Anti-Inflammatory AgentsBiomarkersCaveolin 1Glycyrrhizic AcidLipopolysaccharidesAcute lung injury (ALI)angiotensin converting enzyme 2 (ACE2)Caveolin-1glycyrrhizic acid (GA)NF-κB

Identifiers

PMID34427852
OpenAlexW3194039681

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.