Bee venom alleviates isoproterenol-induced cardiac hypertrophy via JAK2/NF-κB signaling cascade

Area of Science:

• Cardiovascular Research
• Pharmacology
• Toxicology

Background:

• Pathological cardiac hypertrophy (CH) is a precursor to heart failure, posing a significant global health risk.
• Animal venom peptides offer potential therapeutic avenues for cardiovascular diseases.

Purpose of the Study:

• To investigate the therapeutic potential and mechanism of bee venom (BV) in treating isoproterenol (ISO)-induced cardiac hypertrophy (CH).
• To identify the key active component of BV and its molecular targets against CH.

Main Methods:

• UPLC-Q/TOF-MS was used to identify melittin as the primary component in BV.
• In vivo studies utilized ISO-induced CH mouse models, assessing electrocardiogram, echocardiography, and histopathology.
• In vitro studies on hypertrophic cardiomyocytes examined the effects of BV on CH markers, ACE, IL-1β, and the JAK2/NF-κB signaling pathway.

Main Results:

• BV treatment attenuated cardiac hypertrophy, preventing electrocardiogram and echocardiography abnormalities in mice.
• Melittin was identified as the dominant component of BV.
• BV downregulated CH markers (β-MHC, ANP, BNP), ACE, and IL-1β, and inhibited the JAK2/NF-κB signaling pathway in vitro.

Conclusions:

• Bee venom (BV) effectively alleviates isoproterenol-induced cardiac hypertrophy (CH) in both in vivo and in vitro models.
• The therapeutic mechanism involves the inhibition of the JAK2/NF-κB signaling cascade.
• BV, particularly its component melittin, shows promise for the treatment of CH and potentially heart failure.