Related Experiment Video
Updated: Feb 17, 2026
A Rat Lung Transplantation Model of Warm Ischemia/Reperfusion Injury: Optimizations to Improve Outcomes
Published on: October 28, 2021
Methylene Blue Protects the Isolated Rat Lungs from Ischemia-Reperfusion Injury by Attenuating Mitochondrial
Wen-Fang Tian1, Si Zeng2, Qiong Sheng1
1Wuxi School of Medicine, Jiangnan University, No.1800 Lihu Road, 214122, Wuxi, China.
Introduction:
Impaired mitochondrial function is a key factor attributing to the lung ischemia reperfusion injury (LIRI). Methylene blue (MB) has been reported to attenuate brain and renal ischemia-reperfusion injury. We hypothesized that MB also could have a protective effect against LIRI by preventing mitochondrial oxidative damage.
Methods:
Isolated rat lungs were assigned to the following four groups (n = 6): a sham group: perfusion for 105 min without ischemia; I/R group: shutoff of perfusion and ventilation for 45 min followed by reperfusion for 60 min; and I/R + MB group and I/R + glutathione (GSH) group: 2 mg/kg MB or 4 μM glutathione were intraperitoneally administered for 2 h, and followed by 45 min of ischemia and 60 min of reperfusion.
Results:
MB lessened pulmonary dysfunction and severe histological injury induced by ischemia-reperfusion injury. MB reduced the production of reactive oxygen species and malondialdehyde and enhanced the activity of superoxide dismutase. MB also suppressed the opening of the mitochondrial permeability transition pore and partly preserved mitochondrial membrane potential. Moreover, MB inhibited the release of cytochrome c from the mitochondria into the cytosol and decreased apoptosis. Additionally, MB downregulated the mRNA expression levels of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-18).
Conclusion:
MB protects the isolated rat lungs against ischemia-reperfusion injury by attenuating mitochondrial damage.
Insights
Methylene blue (MB) protects isolated rat lungs from ischemia-reperfusion injury by preventing mitochondrial damage and reducing inflammation. This study demonstrates MB
Area of Science:
- Mitochondrial function and oxidative stress in lung ischemia-reperfusion injury (LIRI).
- Pharmacological interventions for organ protection during ischemia-reperfusion.
- Molecular mechanisms of apoptosis and inflammation in LIRI.
Background:
- Impaired mitochondrial function is a primary driver of lung ischemia-reperfusion injury (LIRI).
- Methylene blue (MB) has shown protective effects in other organ systems against ischemia-reperfusion injury.
- The potential of MB to mitigate LIRI by targeting mitochondrial oxidative damage requires investigation.
Purpose of the Study:
- To investigate the protective effects of Methylene blue (MB) against lung ischemia-reperfusion injury (LIRI) in an isolated rat lung model.
- To determine if MB attenuates LIRI by preventing mitochondrial oxidative damage.
- To evaluate the impact of MB on mitochondrial function, oxidative stress markers, and inflammatory responses in LIRI.
Main Methods:
- Isolated rat lungs underwent sham operation, ischemia-reperfusion (I/R) alone, or I/R with Methylene blue (MB) or glutathione (GSH) administration.
- Pulmonary function and histological injury were assessed.
- Mitochondrial oxidative stress markers, mitochondrial permeability transition pore opening, mitochondrial membrane potential, cytochrome c release, apoptosis, and pro-inflammatory cytokine mRNA expression were analyzed.
Main Results:
- Methylene blue (MB) significantly reduced pulmonary dysfunction and histological damage caused by ischemia-reperfusion injury.
- MB decreased reactive oxygen species and malondialdehyde, while increasing superoxide dismutase activity.
- MB suppressed mitochondrial permeability transition pore opening, preserved mitochondrial membrane potential, inhibited cytochrome c release, reduced apoptosis, and downregulated pro-inflammatory cytokines.
Conclusions:
- Methylene blue (MB) exerts a protective effect on isolated rat lungs against ischemia-reperfusion injury.
- MB mitigates LIRI by attenuating mitochondrial damage, reducing oxidative stress, and inhibiting apoptosis and inflammation.
- MB represents a potential therapeutic agent for managing lung ischemia-reperfusion injury.
More Related Videos
06:27Rodent Heart and Brain Tissue Preparation for Digital Macro Photography after Ischemia-reperfusion
Published on: February 1, 2022
09:48Quantification of Neurovascular Protection Following Repetitive Hypoxic Preconditioning and Transient Middle Cerebral Artery Occlusion in Mice
Published on: May 4, 2015