Assessment reveals C60 fullerene improves contractile activity and mechanokinetics of musculus soleus, indicating its antioxidant potential post-stroke.
The results of our previous study revealed that ischemic stroke (IS) is accompanied by an increased concentration of plasma peptides, furthermore, circulatory IS-related peptides may trigger the progression of IS-associated complications. The goal of the current study was twofold: (1) to evaluate the effect of the peptides isolated from the blood plasma of patients with cardioembolic (CIS) and atherothrombotic (AIS) ischemic stroke on the mechanokinetic of rat musculus soleus contraction; and (2) to explore the effect of C60 fullerene as an antioxidant on the skeletal muscle dysfunction caused by ischemic peptides. The peptide fractions were administered intravenously at a dose of 0.1 mg/kg of animal weight. Control animals were injected with a peptide pool isolated from the blood plasma of healthy volunteers at the same dose. C60 fullerene aqueous solution (C60FAS) was administered intraperitoneally at a dose of 1 mg/kg of animal weight 1 h after the peptide injection. The biomechanical parameters were investigated using the strain gauge method. It was shown that intravenous injection of peptides isolated from both AIS and CIS patients (at the acute phase) caused a faster transition of musculus soleus to the stage of complete tetanic contraction compared to control. The analysis of force mechanograms revealed a significant acceleration of muscle fatigue onset and a decrease in the integrated power value after peptide fraction administration (isolated during the acute phase as well as 1 year after the acute phase). It was found that the administration of peptide fraction from the blood plasma of AIS patients has a higher influence on the mechanokinetics of musculus soleus contraction compared to the effects of CIS peptide fraction. The application of C60FAS stabilized the mechanokinetics of rat musculus soleus contraction. Consequently, C60 fullerene is able to prevent the occurrence of dysfunction in the active muscle and thus maintain it within the physiologically normal range throughout the contraction process.
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Nozdrenko et al. (2025) studied this question.
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