Evidence map›Paper›PMID 41034926›Full record

ArticleChinese medicine2025

Amygdalin regulated vasoactive intestinal peptide receptor to protect alveolar epithelial barrier against lung injury induced by influenza a virus.

Xueyue Song, Ting Wang, Miao Ye, Xunlong Shi, Daofeng Chen, Yan Lu, Haiyan Zhu

Abstract read
In one paragraph

Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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.

Xueyue Song *Department of Biological Medicines & Shanghai Engineering Research Center of ImmunoTherapeutics, School of Pharmacy, Fudan University, 826# Zhangheng Rd., Pudong District, Shanghai, 201203, China.
Ting Wang *Center for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Miao YeDepartment of Biological Medicines & Shanghai Engineering Research Center of ImmunoTherapeutics, School of Pharmacy, Fudan University, 826# Zhangheng Rd., Pudong District, Shanghai, 201203, China.
Xunlong ShiDepartment of Biological Medicines & Shanghai Engineering Research Center of ImmunoTherapeutics, School of Pharmacy, Fudan University, 826# Zhangheng Rd., Pudong District, Shanghai, 201203, China.
Daofeng ChenDepartment of Natural Medicine, School of Pharmacy, Fudan University, Shanghai, 201203, China.
Yan LuDepartment of Natural Medicine, School of Pharmacy, Fudan University, Shanghai, 201203, China.
Haiyan ZhuDepartment of Biological Medicines & Shanghai Engineering Research Center of ImmunoTherapeutics, School of Pharmacy, Fudan University, 826# Zhangheng Rd., Pudong District, Shanghai, 201203, China. haiyanzhu@fudan.edu.cn.

Funding

National Natural Science Foundation of China 82141219,82030113
6 · The paper itself

Abstract

backgroundBitter apricot kernel is a common traditional Chinese medicine used for lung diseases. Previous studies showed that Xuanbai-Chengqi decoction (XCD) containing bitter apricot kernel protected the alveolar and intestinal barriers in influenza-infected mice. However, the specific contribution of bitter apricot kernel and its active substances in viral pneumonia remain unclear. PURPOSE: This study aimed to identify the main active ingredient in bitter apricot kernel and investigate its mechanism in protecting the alveolar epithelial barrier in viral pneumonia.

methodBitter apricot kernel was evaluated based on the efficacy differences between XCD and XCD without bitter apricot kernel. Amygdalin was identified through in vitro activity tests and verified in vivo. Immunohistochemistry, RT-qPCR, and WB were used to assess barrier protection and anti-inflammatory effects. The molecular mechanisms were explored using SPR/LC/MS and validated experimentally.

resultRemoving bitter apricot kernel significantly weakened XCD's protective effect in influenza A virus-infected mice. Amygdalin showed anti-inflammatory, anti-hypoxia anti-influenza virus activities, and promoted endothelial cell migration in vitro. Amygdalin at 100 mg/kg effectively mitigated pulmonary injury and attenuated excessive inflammatory responses by regulating IL-6 and IL-10 in IAV-infected murine models. Oseltamivir is more effective than amygdalin in inhibiting the replication of influenza viruses and upregulating the expression level of IL-10. Amygdalin protected the alveolar barrier by restoring alveolar type II cells (AT2) and promoting alveolar regeneration, while upregulating surfactant protein A (SP-A) and aquaporin protein-5 (AQP5). Amygdalin bound selectively to vasoactive intestinal peptide receptor 1 (VIPR1) thereby upregulating cyclic adenosine monophosphate (cAMP) levels and the protein expression levels of Protein kinase A (PKA) and Phosphor-protein kinase A (p-PKA).

conclusionAmygdalin is the key bioactive component of bitter apricot kernel, which exhibits protective effects in an IAV-induced pneumonia mouse model by activating the cAMP/PKA/p-PKA signaling cascade and recapitulating the biological effects of vasoactive intestinal peptide (VIP).

Indexed as

Alveolar epithelial barrierAmygdalinInfluenza virusVasoactive intestinal peptide receptorViral pneumonia

Identifiers

PMID41034926
PMCPMC12490164

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.