Related Experiment Video
Updated: Feb 18, 2026
Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry
Published on: May 5, 2022
Mitochondria Targeted Peptide Attenuates Mitochondrial Dysfunction, Controls Inflammation and Protects Against Spinal
Background/Aims:
Spinal cord injury (SCI) is a common and devastating disease, which results in systemic inflammatory response syndrome and secondary lung injury. Mitochondrial dysfunction and inflammation are closely related to lung injury in diverse disease models. No studies have demonstrated the effects of mitochondrial targeted peptide SS-31 in a mouse model of SCI-induced lung injury.
Methods:
Immediately after injury, mice in the treatment groups received a daily, single-dose intraperitoneal injection of SS-31 and for the next 2 days. The sham and SCI groups also received a daily single dose of vehicle (DMSO and 0.9% NaCl, 1: 3). The lung tissue of mice was examined after SCI, and tissue damage, apoptosis, inflammation, and mitochondrial dysfunction were recorded.
Results:
SS-31 treatment attenuated lung edema and tissue damage. Furthermore, SS-31 treatment reduced apoptosis of alveolar type II cells, the number of total macrophages and M1 macrophages, and neutrophil infiltration. Moreover, SS-31 treatment attenuated reactive oxygen species levels, reversed mitochondrial dysfunction and inhibited NLRP3 inflammasome activation.
Conclusions:
Collectively, our results demonstrate that SS-31 attenuates mitochondrial dysfunction, controls inflammatory responses, and alleviates the severity of lung damage in a mouse model of SCI-induced lung injury.
Insights
Mitochondrial targeted peptide SS-31 effectively reduced lung injury following spinal cord injury (SCI) in mice. SS-31 treatment mitigated inflammation, apoptosis, and mitochondrial dysfunction, offering a potential therapeutic strategy for SCI-induced lung damage.
Area of Science:
- Biomedical research
- Injury models
- Mitochondrial medicine
Background:
- Spinal cord injury (SCI) triggers systemic inflammation and secondary lung injury.
- Mitochondrial dysfunction and inflammation are key contributors to lung injury.
- The therapeutic potential of SS-31 for SCI-induced lung injury remains unexplored.
Purpose of the Study:
- To investigate the efficacy of mitochondrial-targeted peptide SS-31 in mitigating lung injury following SCI in a mouse model.
- To evaluate the impact of SS-31 on lung tissue damage, apoptosis, inflammation, and mitochondrial function post-SCI.
Main Methods:
- Mice received daily intraperitoneal injections of SS-31 or vehicle immediately after SCI induction.
- Lung tissues were analyzed for damage, apoptosis, inflammatory cell infiltration, and mitochondrial dysfunction markers.
- Specific assessments included reactive oxygen species levels and NLRP3 inflammasome activation.
Main Results:
- SS-31 treatment significantly attenuated lung edema and tissue damage.
- SS-31 reduced apoptosis in alveolar type II cells and decreased neutrophil and macrophage infiltration.
- The treatment reversed mitochondrial dysfunction, reduced reactive oxygen species, and inhibited NLRP3 inflammasome activation.
Conclusions:
- SS-31 effectively alleviates lung injury severity in a mouse model of SCI.
- The peptide's protective effects are linked to the attenuation of mitochondrial dysfunction and inflammatory responses.
- SS-31 demonstrates promise as a therapeutic agent for SCI-induced lung injury.
More Related Videos
Related Concept Videos
01:19Translocation of Proteins into the Mitochondria
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
01:39Mitochondrial Precursor Proteins
Most of the mitochondrial...