Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases

• Published in: Life sciences (1973) 2020-05, Vol.249, p.117513-117513, Article 117513
• Main Authors: Mocayar Marón, Feres José, Camargo, Alejandra Beatriz, Manucha, Walter
• Format: Article
• Language: English
• Subjects: Allicin; Anti-Inflammatory Agents - therapeutic use; Cardiotonic Agents - therapeutic use; Cardiovascular Diseases - drug therapy; Cardiovascular disorders; Garlic; Humans; Inflammation - drug therapy; Mitochondria; Nervous System Diseases - drug therapy; Neuroprotection; Neuroprotective Agents - therapeutic use; Organosulfur compounds; Oxidative stress; Sulfinic Acids - therapeutic use
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2020.117513

According to investigations in phytomedicine and ethnopharmacology, the therapeutic properties of garlic (Allium sativum) have been described by ancestral cultures. Notwithstanding, it is of particular concern to elucidate the molecular mechanisms underlying this millenary empirical knowledge. Allicin (S-allyl prop-2-ene-1-sulfinothioate), a thioester of sulfenic acid, is one of the main bioactive compounds present in garlic, and it is responsible for the particular aroma of the spice. The pharmacological attributes of allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others). The primary goal of the present article is to review and clarify the common molecular mechanisms by which allicin and its derivates molecules may perform its therapeutic effects on cardiovascular diseases and neuroinflammatory processes. The intricate interface connecting the cardiovascular and nervous systems suggests that the impairment of one organ could contribute to the dysfunction of the other. Allicin might target the cornerstone of the pathological processes underlying cardiovascular and neuroinflammatory disorders, like inflammation, renin-angiotensin-aldosterone system (RAAS) hyperactivation, oxidative stress, and mitochondrial dysfunction. Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes. Finally, allicin represents an attractive therapeutic alternative targeting the complex interaction between cardiovascular and neuroinflammatory disorders. [Display omitted]