Apigenin Protects Against Cisplatin-Induced Cardiotoxicity: Potential Involvement of CD38-Sirt3 Signaling in Rats

Area of Science:

• Cardiovascular Research
• Pharmacology
• Biochemistry

Background:

• Cisplatin chemotherapy can cause cardiotoxicity, linked to oxidative stress, inflammation, and apoptosis.
• The specific role of CD38-Sirt3 signaling in this process requires further elucidation.

Purpose of the Study:

• To investigate the cardioprotective effects of apigenin against cisplatin-induced cardiac injury.
• To determine if apigenin modulates CD38-Sirt3 signaling in the context of cisplatin cardiotoxicity.

Main Methods:

• Male Sprague Dawley rats were divided into control, cisplatin-treated, and apigenin + cisplatin groups.
• Evaluated left ventricular function, cardiac injury markers, oxidative stress, inflammation, apoptosis, and CD38-Sirt3 signaling proteins.

Main Results:

• Cisplatin impaired cardiac function and increased injury, oxidative stress, inflammation, and apoptosis, with altered CD38-Sirt3 signaling.
• Apigenin treatment significantly improved cardiac function, reduced injury markers, attenuated oxidative stress, suppressed inflammation, and inhibited apoptosis.
• Apigenin normalized SOD2 expression and reversed CD38-Sirt3 signaling alterations in cisplatin-exposed rats.

Conclusions:

• Cisplatin-induced cardiotoxicity involves significant alterations in CD38-Sirt3 signaling.
• Apigenin demonstrates cardioprotective effects against cisplatin toxicity, potentially via the CD38-Sirt3 pathway.
• Apigenin shows promise as a therapeutic agent to mitigate chemotherapy-induced heart damage.