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Free radicals upregulate complement expression in rabbit isolated heart.
E J Tanhehco1, K Yasojima, P L McGeer
1Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA.
Summary
Free radicals can increase complement production in heart tissue, potentially causing injury. Antioxidants can reduce this effect, suggesting a link between free radicals and complement-mediated tissue damage.
Area of Science:
- Cardiovascular Biology
- Immunology
- Free Radical Research
Background:
- Free radicals and complement activation are known mediators of tissue injury.
- The specific impact of free radicals on myocardial complement production remains unclear.
Purpose of the Study:
- To investigate whether free radicals influence complement production in the myocardium.
- To explore the potential role of complement activation in free radical-induced tissue damage.
Main Methods:
- Isolated rabbit hearts were perfused using a Langendorff apparatus.
- A free radical-generating system (xanthine/xanthine oxidase) was applied to the hearts.
- Complement gene expression (mRNA) and protein deposition were analyzed, along with cardiac function and perfusion pressure.
Main Results:
- Exposure to the free radical system significantly increased the transcription of complement components (C1q, C1r, C3, C8, C9) and membrane attack complex deposition.
- Xanthine/xanthine oxidase treatment led to increased coronary perfusion pressure, left ventricular end-diastolic pressure, and decreased left-ventricular developed pressure.
- Antioxidant treatment (N-(2-mercaptopropionyl)-glycine and SC-52608) significantly reduced complement mRNA upregulation and ameliorated functional deterioration.
Conclusions:
- Free radicals can upregulate complement production in the myocardium.
- Complement activation may be a key mechanism through which free radicals cause tissue injury.
- Antioxidant interventions show promise in mitigating free radical-induced complement-mediated cardiac damage.