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Related Concept Videos

Chronic Obstructive Pulmonary Disease I: Introduction01:23

Chronic Obstructive Pulmonary Disease I: Introduction

Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...

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Related Experiment Video

Updated: May 10, 2026

Intratracheal Instillation of Stem Cells in Term Neonatal Rats
04:27

Intratracheal Instillation of Stem Cells in Term Neonatal Rats

Published on: May 4, 2020

Curcumin protects the developing lung against long-term hyperoxic injury.

R Sakurai1, P Villarreal, S Husain

  • 1Dept. of Pediatrics, Los Angeles Biomedical Research Institute at Harbor UCLA Medical Center, David Geffen School of Medicine at UCLA, 1124 West Carson St., Torrance, CA 90502. vrehan@labiomed.org.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|July 2, 2013
PubMed
Summary

Curcumin protects developing lungs from long-term hyperoxia-induced injury, a key factor in bronchopulmonary dysplasia (BPD). This study shows curcumin

Keywords:
apoptosisbrochopulmonary dysplasiacurcuminhyperoxiainflammation

Related Experiment Videos

Last Updated: May 10, 2026

Intratracheal Instillation of Stem Cells in Term Neonatal Rats
04:27

Intratracheal Instillation of Stem Cells in Term Neonatal Rats

Published on: May 4, 2020

Area of Science:

  • Neonatal physiology and lung development
  • Pharmacology of natural compounds
  • Molecular mechanisms of lung injury

Background:

  • Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants, often caused by prolonged exposure to oxygen.
  • Curcumin, a compound from turmeric, has known anti-inflammatory and antioxidant properties.
  • Previous studies indicated curcumin's acute protective effects against hyperoxia-induced lung injury, but long-term benefits for BPD were unknown.

Purpose of the Study:

  • To investigate the long-term protective effects of concurrent curcumin treatment against hyperoxia-induced lung injury in developing rats.
  • To determine if curcumin administration during the critical early postnatal period can prevent structural and functional lung damage associated with BPD.

Main Methods:

  • Neonatal rat pups were exposed to hyperoxia (95% O₂) or room air (21% O₂) for the first 5 days of life.
  • Curcumin (5 mg/kg) or a vehicle was administered daily during the hyperoxic exposure period.
  • Lung development, injury markers (apoptosis, gene expression), morphology, and molecular signaling (MAPK pathway) were assessed at postnatal day 21. In vitro studies used fetal rat lung fibroblasts.

Main Results:

  • Curcumin treatment significantly blocked hyperoxia-induced lung injury, improving lung morphology (radial alveolar count, septal thickness) and reducing markers of fibrosis (collagen III, fibronectin).
  • Curcumin prevented hyperoxia-induced apoptosis and modulated the expression of key genes like Bcl-2/Bax, vimentin, calponin, and elastin.
  • Mechanistically, curcumin inhibited hyperoxia-induced increases in cleaved caspase-3 and Erk1/2 phosphorylation in vitro.

Conclusions:

  • Concurrent curcumin treatment provides long-term protection against neonatal hyperoxia-induced lung injury, suggesting a potential therapeutic role in preventing BPD.
  • The protective effects of curcumin appear to be mediated through the modulation of apoptotic pathways and the MAPK/Erk1/2 signaling cascade.
  • Curcumin demonstrates significant structural and cytoprotective actions, highlighting its potential as an intervention for BPD.