Evidence map›Paper›PMID 37802148›Full record

ArticleJournal of advanced research2024

Alisol B 23-acetate broadly inhibits coronavirus through blocking virus entry and suppresses proinflammatory T cells responses for the treatment of COVID-19.

Qiaohui Du, Ronghui Liang, Meiling Wu, Minxiao Yang, Yubin Xie, Qing Liu, Kaiming Tang, Xiang Lin, Shuofeng Yuan, Jiangang Shen

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Alisols A-C and their acetate derivatives: a review of natural occurrence, pharmacology, semisynthesis, pharmacokinetics, and metabolism.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  2. Article
  3. 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

10 authors at 3 institutions in 2 countries.

Qiaohui DuSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong, Hong Kong Special Administrative Region; State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Pokfulam, Hong Kong, Hong Kong Special Administrative Region.
Ronghui LiangState Key Laboratory of Emerging Infectious Diseases, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Meiling WuSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong, Hong Kong Special Administrative Region.
Minxiao YangSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong, Hong Kong Special Administrative Region.
Yubin XieState Key Laboratory of Emerging Infectious Diseases, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Qing LiuSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong, Hong Kong Special Administrative Region.
Kaiming TangState Key Laboratory of Emerging Infectious Diseases, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region.
Xiang LinSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong, Hong Kong Special Administrative Region.
Shuofeng YuanState Key Laboratory of Emerging Infectious Diseases, Department of Microbiology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region; Centre for Virology, Vaccinology and Therapeutics, Hong Kong Science and Technology Park, Hong Kong Special Administrative Region; Department of Clinical Microbiology and Infection Control, The University of Hong Kong-Shenzhen Hospital, Shenzhen, Guangdong, China. Electronic address: yuansf@hku.hk.
Jiangang ShenSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, 3 Sassoon Road, Pokfulam, Hong Kong, Hong Kong Special Administrative Region; State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Pokfulam, Hong Kong, Hong Kong Special Administrative Region. Electronic address: shenjg@hku.hk.
University of Hong Kong · HKChinese University of Hong Kong · CNUniversity of Hong Kong - Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionEmerging severe acute respiratory syndrome (SARS) coronavirus (CoV)-2 causes a global health disaster and pandemic. Seeking effective anti-pan-CoVs drugs benefit critical illness patients of coronavirus disease 2019 (COVID-19) but also may play a role in emerging CoVs of the future.

objectivesThis study tested the hypothesis that alisol B 23-acetate could be a viral entry inhibitor and would have proinflammatory inhibition for COVID-19 treatment.

methodsSARS-CoV-2 and its variants infected several cell lines were applied to evaluate the anti-CoVs activities of alisol B 23-aceate in vitro. The effects of alisol B 23-acetate on in vivo models were assessed by using SARS-CoV-2 and its variants challenged hamster and human angiotensin-converting enzyme 2 (ACE2) transgenic mice. The target of alisol B 23-acetate to ACE2 was analyzed using hydrogen/deuterium exchange (HDX) mass spectrometry (MS).

resultsAlisol B 23-acetate had inhibitory effects on different species of coronavirus. By using HDX-MS, we found that alisol B 23-acetate had inhibition potency toward ACE2. In vivo experiments showed that alisol B 23-acetate treatment remarkably decreased viral copy, reduced CD4

conclusionAlisol B 23-acetate could be a promising therapeutic agent for COVID-19 treatment and its underlying mechanisms might be attributed to viral entry inhibition and anti-inflammatory activities.

Indexed as

Angiotensin-Converting Enzyme 2CholestenonesCOVID-19COVID-19 Drug TreatmentMice, TransgenicSARS-CoV-2Virus InternalizationAnimalsAntiviral AgentsChlorocebus aethiopsCricetinaeDisease Models, AnimalHumansMiceT-LymphocytesVero CellsACE2 protein, humanalisol B 23-acetateAngiotensin-Converting Enzyme 2Antiviral AgentsCholestenonesACE2Alisol B 23-acetateAnti-coronavirusAnti-immunoinflammatory activityCOVID-19

Identifiers

PMID37802148
PMCPMC11331179
OpenAlexW4387344504

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.