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Major Ozonated Autoheamotherapy Alleviates Skeletal Muscle Ischemia/Reperfusion Injury by Regulating Nrf2/HO-1
Hui-Zhuang Guo1,2, Sheng-Long Yu3, Han-Wei Chen1,4
1The First Affiliated Hospital of Jinan University, Guangzhou, China.
Abstract:
Skeletal muscle ischaemia/reperfusion (I/R) injury remains a clinically significant condition characterized by muscular dystrophy. Although ozone therapy has shown protective potential against I/R injury in animal models of various organs including skeletal muscle, its precise mechanistic underpinnings require further elucidation. This investigation evaluates the therapeutic potential of major ozonated autohemotherapy (MOAH) for skeletal muscle I/R injury management. Utilizing a rat femoral artery ligation/release model, we demonstrated that MOAH pretreatment substantially alleviated histopathological damage through hematoxylin-eosin/Masson staining analyzes, diminished skeletal muscle apoptosis via terminal deoxynucleotidyl transferase dUTP nick-end labeling and Western blot, and reduced tissue edema as quantified by wet weight ratios. Serum biomarker assessments confirmed decreased creatine kinase and lactate dehydrogenase levels with MOAH administration. In oxygen-glucose deprivation/reoxygenation (OGD/R)-treated L6 myoblast models, ozone pretreatment enhanced cellular proliferation capacity while attenuating apoptosis and mitochondrial dysfunction. Subsequent analyzes revealed ozone's regulatory effects on oxidative stress markers (MDA content, SOD and CAT activity) and inflammatory factors (TNF-α and IL-1β) across both in vivo and in vitro models. Mechanistic evaluations through Western blot and reverse transcription quantitative real-time polymerase chain reaction techniques identified MOAH-induced activation of the Nrf2/HO-1 signaling pathway, with observed abolition of protective efficacy under Nrf2 knockdown conditions. These results collectively establish that MOAH mitigates skeletal muscle I/R injury through Nrf2/HO-1 pathway modulation, providing substantive mechanistic justification for its clinical implementation in I/R injury therapeutics.
Insights
Major ozonated autohemotherapy (MOAH) effectively treats skeletal muscle ischemia/reperfusion (I/R) injury by reducing damage and inflammation. This therapy activates the Nrf2/HO-1 pathway, offering a promising treatment for I/R injury.
Area of Science:
- Biomedical Science
- Regenerative Medicine
- Molecular Biology
Background:
- Skeletal muscle ischemia/reperfusion (I/R) injury is a significant clinical issue causing muscular damage.
- Ozone therapy shows promise for I/R injury, but its mechanisms in skeletal muscle require detailed study.
- Major ozonated autohemotherapy (MOAH) is explored for its therapeutic potential in managing skeletal muscle I/R injury.
Purpose of the Study:
- To evaluate the therapeutic efficacy of MOAH in a rat model of skeletal muscle I/R injury.
- To elucidate the underlying molecular mechanisms of MOAH's protective effects.
- To assess MOAH's impact on cellular apoptosis, oxidative stress, and inflammation in I/R injury.
Main Methods:
- Established a rat femoral artery ligation/release model for skeletal muscle I/R injury.
- Administered MOAH pretreatment and assessed histopathological damage, apoptosis, and edema.
- Utilized oxygen-glucose deprivation/reoxygenation (OGD/R) in L6 myoblasts for in vitro analysis.
- Measured oxidative stress markers, inflammatory cytokines, and key signaling pathway proteins (Nrf2/HO-1).
Main Results:
- MOAH pretreatment significantly reduced histopathological damage, apoptosis, and edema in skeletal muscle I/R injury.
- MOAH decreased serum creatine kinase and lactate dehydrogenase levels.
- In vitro, ozone enhanced myoblast proliferation and attenuated apoptosis and mitochondrial dysfunction.
- MOAH modulated oxidative stress and inflammatory markers, activating the Nrf2/HO-1 pathway.
- Nrf2 knockdown abolished the protective effects of MOAH, confirming pathway involvement.
Conclusions:
- MOAH effectively mitigates skeletal muscle I/R injury by reducing cellular damage, apoptosis, and inflammation.
- The protective mechanism involves the activation of the Nrf2/HO-1 signaling pathway.
- MOAH demonstrates significant therapeutic potential for clinical application in managing skeletal muscle I/R injury.
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