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Chronic Obstructive Pulmonary Disease-II: Pathophysiology

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Oridonin Alleviates Cigarette Smoke-induced Nasal Polyp Formation By Promoting Autophagy.

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Oridonin Alleviates Cigarette Smoke-induced Nasal Polyp Formation By Promoting Autophagy.

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Oridonin alleviates cigarette smoke-induced nasal polyp formation by promoting autophagy.

Peiqiang Liu¹, Xiaomin Wu¹, Hao Lv¹

¹Department of Otolaryngology-Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, China; Department of Rhinology and Allergy, Renmin Hospital of Wuhan University, Wuhan, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie

|October 15, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Oridonin protects against nasal epithelial barrier damage in chronic rhinosinusitis with nasal polyps by promoting autophagy. This natural compound may offer a new therapeutic strategy for CRSwNP.

Keywords:

Autophagy Chronic rhinosinusitis with nasal polyp Cigarette smoke Epithelial barrier Oridonin

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Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Published on: January 16, 2015

Area of Science:

Immunology
Cell Biology
Pharmacology

Background:

Chronic rhinosinusitis with nasal polyps (CRSwNP) is an inflammatory airway disease.
Cigarette smoke (CS) exacerbates CRSwNP, causing polypoid changes and epithelial barrier dysfunction.
Oridonin, a natural compound, shows potential for treating inflammatory conditions.

Purpose of the Study:

To investigate the protective mechanism of oridonin in a mouse model of CRSwNP induced by cigarette smoke.
To elucidate the role of autophagy in oridonin's therapeutic effects on CRSwNP.
To explore the impact of oridonin on epithelial barrier integrity and inflammatory markers.

Main Methods:

Establishment of a CRSwNP mouse model using cigarette smoke exposure.
Administration of oridonin and an autophagy inhibitor (3-methyladenine) to mice.

In vitro studies using cigarette smoke extract (CSE) on epithelial cells.

Analysis of polypoid changes, goblet cell counts, tight junction proteins, inflammatory cytokines, and autophagy markers (LC3-II, Beclin-1, P62).

Main Results:

Oridonin reduced polypoid changes, goblet cell count, and inflammatory markers (IgE, IL-6, IFN-γ, IL-5, IL-13, IL-17A) in CS-treated mice.
Oridonin promoted tight junction protein expression (ZO-1, occludin, claudin-1) and autophagy (increased autophagosomes, LC3-II, Beclin-1; decreased P62).
Oridonin reversed CSE-induced epithelial barrier damage in vitro, linked to autophagy activation and the PI3K/AKT/mTOR pathway.

Conclusions:

Oridonin ameliorates CS-induced nasal epithelial barrier damage in CRSwNP by enhancing autophagy.
Autophagy plays a crucial role in the protective effects of oridonin against CRSwNP.
Oridonin represents a potential novel therapeutic agent for CRSwNP treatment.