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Decrease in Long-Chain Acylcarnitine Tissue Content Determines the Duration of and Correlates with the
Janis Kuka1, Marina Makrecka-Kuka1, Helena Cirule1
1Laboratory of Pharmaceutical Pharmacology, Latvian Institute of Organic Synthesis, Riga, Latvia.
Basic & Clinical Pharmacology & Toxicology
|March 1, 2017
Summary
Long-term treatment with methyl-GBB, an OCTN2 inhibitor, reduces heart long-chain acylcarnitines (LCACs) and protects against ischaemia-reperfusion damage for at least two weeks after treatment cessation. This cardioprotective effect correlates with sustained LCAC reduction.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Pharmacology
Background:
- Ischaemia-reperfusion (IR) injury in the heart involves long-chain acylcarnitines (LCACs).
- Sustained reduction of carnitine and LCACs via pre-treatment mitigates IR damage, but post-treatment effects are unknown.
Purpose of the Study:
- To evaluate the post-treatment duration of cardioprotection and LCAC reduction by methyl-GBB, an OCTN2 inhibitor.
- To determine the correlation between LCAC levels and infarct size following methyl-GBB treatment.
Main Methods:
- Male Wistar rats received methyl-GBB (5 mg/kg) for 28 days.
- Cardiac acylcarnitine profiles and infarct sizes were assessed up to 28 days post-treatment.
- Langendorff-perfused hearts were used to evaluate anti-infarction effects.
Main Results:
- Methyl-GBB pre-treatment significantly decreased cardiac LCACs by 87% and infarct size by 57%.
- Cardioprotective effects and LCAC reduction persisted for at least 14 days post-treatment (69% LCAC decrease, 32% infarct size decrease).
- A significant correlation (r = 0.48, p = 0.026) was observed between infarct size and cardiac LCAC content.
Conclusions:
- The cardioprotective effect of methyl-GBB extends for at least two weeks post-treatment.
- A decrease of at least 70% in LCAC content is necessary for cardioprotection.
- Sustained LCAC reduction dictates the duration of the cardioprotective effect of OCTN2 inhibitors.
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