Abstract Title:

Cyanidin ameliorates endotoxin-induced myocardial toxicity by modulating inflammation and oxidative stress through mitochondria and other factors.

Abstract Source:

Food Chem Toxicol. 2018 Oct ;120:104-111. Epub 2018 May 25. PMID: 29803697

Abstract Author(s):

Fang Li, Fangfang Lang, Yidan Wang, Chunxiao Zhai, Chuanbei Zhang, Liping Zhang, Enkui Hao

Article Affiliation:

Fang Li


Cyanidin, an anthocyanin pigment, demonstrates anti-oxidant and anti-inflammatory properties. Here, we examined the mechanistic role of cyanidin in endotoxin induced myocardial injury in inflammation and oxidative stress. In lipopolysaccharide (LPS) induced myocardial injury model, cyanidin ameliorated cardiac injury (Lactate dehydrogenase or LDH, Creatine Kinase or CK, cardiac troponin I or cTnI and cardiac myosin light chains 1 or cMLC1), cell death (caspase 3 activity and PARP activity), and improved cardiac function (ejection fraction or EF and end diastolic left ventricular inner dimension or LVID). Cyanidin also attenuated endotoxin induced myocardial injury by modulating inflammatory cytokines (Tumor necrosis factor alpha or TNFα, Interleukin-1 beta or IL-1β, macrophage inflammatory protein 2 or MIP-2 and chemokine (C-C motif) ligand 2 also known as monocyte chemoattractant protein 1 or MCP1) and oxidative stress (protein nitration). Cyanidin modulated redox homeostasis through intracellular oxidized/reduced glutathione.The most striking properties of cyanidin in endotoxin induced mediated myocardial injury was the modulation of mitochondria, its oxidative damage and associated factor Opa1 and Trx1. Thus, our study demonstrated that cyanidin as a constituent of our food chain may be beneficial and has therapeuticpotential in sepsis treatment or other myocardial oxidative and/or inflammation induced injuries.

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