Evidence map›Paper›PMID 41287775›Full record

ArticleJournal of inflammation research2025

Mechanistic Insights Into the Modulation of Gut Microbiota and ERK Signaling by Morusin in Juvenile Rats with Post-Infectious Cough.

Jing Luo, Dan Zhang, Miaomiao Zhang, Yiqiang Chen, Yi Ding

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Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Jing LuoDepartment of Chinese Medicine, Shenzhen Qianhai Shekou Free Trade Zone Hospital, Shenzhen, Guangzhou, People's Republic of China.
Dan ZhangDepartment of Chinese Medicine, Shenzhen Qianhai Shekou Free Trade Zone Hospital, Shenzhen, Guangzhou, People's Republic of China.
Miaomiao ZhangDepartment of Chinese Medicine, Shenzhen Qianhai Shekou Free Trade Zone Hospital, Shenzhen, Guangzhou, People's Republic of China.
Yiqiang ChenDepartment of Chinese Medicine, Shenzhen Qianhai Shekou Free Trade Zone Hospital, Shenzhen, Guangzhou, People's Republic of China.
Yi DingDepartment of Physical Medicine and Rehabilitation, Changsha Social Work College, Changsha, Hunan, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Post-infectious cough (PIC) is a leading cause of chronic cough in children, often persisting after respiratory infections and significantly impairing quality of life. Current therapies, such as montelukast sodium (MAS), offer only partial symptom relief and do not target the underlying inflammatory and microbiota-driven mechanisms. Emerging evidence suggests that the lung-gut axis, ERK pathway activation, and cytokine-microbiota interactions are central to PIC pathogenesis. Morusin, a prenylated flavonoid from Morus alba, possesses anti-inflammatory and barrier-protective activities and may uniquely modulate both ERK signaling and gut microbiota, offering mechanistic advantages over conventional treatments. Methods: A juvenile rat model of PIC was induced by smoke exposure, lipopolysaccharide nasal instillation, and capsaicin atomization. Rats were assigned to control, model, morusin, or MAS groups. Physiological outcomes, histology, and immunostaining were assessed, including body weight, airway resistance, goblet cells, cytokines (IL-4, IL-6, IL-10), and phosphorylated ERK1/2 (p-ERK1/2) in lung and colon tissues. Gut microbiota was profiled via 16S rRNA sequencing, with correlation analyses linking microbial changes to cytokine and signaling profiles. Results: Morusin improved systemic parameters (body weight, salivary flow, skin hydration), reduced airway hyperreactivity, and normalized anxiety-like behaviors, effects not observed with MAS. Both morusin and MAS reduced lung goblet cell hyperplasia and inflammatory cytokines, but only morusin suppressed p-ERK1/2 in both lung and colon tissues and reshaped the gut microbiota. Morusin enriched beneficial genera (Lactobacillus, Akkermansia) and reduced pro-inflammatory taxa (Ruminococcus, Lachnospiraceae_NK4A136_group). Correlation analyses confirmed strong links between microbial shifts, cytokine balance, and ERK modulation. Conclusion: Morusin alleviates PIC through systemic, mucosal, and behavioral improvements, combined with unique modulation of gut microbiota and ERK signaling across the lung-gut axis. These findings highlight morusin's novel mechanistic advantage over MAS and support its potential as a translational therapy for pediatric PIC.

Indexed as

air way inflammationgut microbiotamorusinp-ERKpost-infectious cough

Identifiers

PMID41287775
PMCPMC12640600

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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.