Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases
Autor: | Alejandra Beatriz Camargo, Feres Jose Mocayar Maron, Walter Manucha |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Cardiotonic Agents Anti-Inflammatory Agents Mitochondrion Pharmacology medicine.disease_cause 030226 pharmacology & pharmacy Neuroprotection General Biochemistry Genetics and Molecular Biology 03 medical and health sciences chemistry.chemical_compound Phytomedicine 0302 clinical medicine Medicine Humans Disulfides General Pharmacology Toxicology and Pharmaceutics Neuroinflammation Inflammation Allicin business.industry General Medicine Sulfinic Acids 030104 developmental biology Neuroprotective Agents chemistry mitochondrial fusion Cardiovascular Diseases Sulfenic acid Nervous System Diseases business Oxidative stress |
Zdroj: | Life sciences. 249 |
ISSN: | 1879-0631 |
Popis: | 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. |
Databáze: | OpenAIRE |
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