Caprylic Acid Inhibits High Mobility Group Box-1-Induced Mitochondrial Damage in Myocardial Tubes.

Area of Science:

• Cardiology
• Oncology
• Biochemistry

Background:

• Myocardial damage is a significant concern in cancer patients, impacting prognosis.
• Mechanisms underlying cancer- and treatment-induced myocardial damage are not fully understood.
• Previous research indicated medium-chain fatty acids (MCFAs) can mitigate cancer-induced heart damage.

Purpose of the Study:

• To investigate the role of inflammatory cytokines in cancer-related myocardial damage.
• To evaluate the differential effects of caprylic acid (C8), capric acid (C10), and lauric acid (C12) on myocardial damage.
• To explore the potential of C8 in counteracting high-mobility group box-1 (HMGB1)-induced cardiac injury.

Main Methods:

• Utilized a mouse model of cancer-induced myocardial damage.
• Employed H9C2 cardiomyoblast cell line to study myocardial tube differentiation.
• Treated cells with high-mobility group box-1 (HMGB1), interleukin-6, and tumor necrosis factor-α, with and without MCFAs (C8, C10, C12) or beta-hydroxybutyrate.

Main Results:

• The caprylic acid (C8) diet demonstrated superior efficacy in ameliorating myocardial damage compared to C10 and C12 diets.
• High-mobility group box-1 (HMGB1) induced mitochondrial oxidative stress, reduced membrane potential, and inhibited myocardial tube differentiation.
• C8 treatment counteracted HMGB1-induced mitochondrial damage, enhanced autophagy, and promoted mitochondrial biogenesis and maturation.

Conclusions:

• High-mobility group box-1 (HMGB1) plays a crucial role in cancer-related myocardial damage.
• Caprylic acid (C8) effectively mitigates HMGB1-induced cardiac injury, offering a potential therapeutic strategy.
• Further clinical investigations are warranted to confirm the therapeutic benefits of C8 in cancer patients.