Allium sativum L./garlic (Allium sativum) and Allium fistulosum
2-Propene-1-sulfinothioic acid, S-2-propenyl ester (9CI)/AllS(O)SAll/S-Allyl prop-2-ene-1-sulfinothioate/Allisure Liquid/Allicin/alliosan/AlliMed/ARICINE(P)/S-Allyl 2-propene-1-sulfinothioate/Allisatin/2-Propene-1-sulfinothioic acid, S-2-propen-1-yl ester/S-prop-2-en-1-yl prop-2-ene-1-sulfinothioate/S-2-propenyl 2-propenethiosulfinate/Allantolin Allicin/Allitrid/allyl 2-propenethiosulfinate/ALLICIN(SH)/allyl 2-propenylthiosulfinate/S-2-propen-1-yl 2-propene-1-sulfinothioate/Dianyctrsnlgide
Allicin (diallyl thiosulfinate), a highly potent natural antimicrobial activity substance, inhibits growth of a variety of microorganisms, among them antibiotic-resistant strains.
Chloroform; Ethyl Acetate
248.6±43.0 °C at 760 mmHg
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provides coniferyl ferulate(CAS#:539-86-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Mastitis, inflammation of the mammary gland, occurs in both humans and animals. Staphylococcus aureus is the most common infectious bacterial pathogen associated with mastitis. We investigated the effects of allicin on S. aureus-induced mastitis in mice. Pathological histology revealed that allicin inhibited S. aureus-induced pathological damage and myeloperoxidase activity in mammary tissues. Enzyme-linked immunosorbent assays demonstrated that allicin reduced the production of IL-1β and TNF-α as well as inhibited the NF-κB and mitogen-activated protein kinase pathway by reducing phosphorylation of p65, IκBα, p38, JNK, and ERK. Western blotting revealed that allicin reduced TLR2 and TLR6 expression in mammary tissues and cells but not in HEK293 cells. The lipid raft content was reduced by allicin, which inhibited signaling downstream of TLR2 and TLR6. Liver X receptor α (LXRα) luciferase reporter assays and LXRα interference experiments showed that allicin improved the LXRα activity and adenosine 5′-triphosphate-binding cassette G and A1 (ABCG and ABCA1) expression, thereby reducing the cholesterol level, lipid raft formation, and downstream TLR2 and TLR6 pathway activity. These results demonstrated that allicin exerted anti-inflammatory effects against S. aureus mastitis by improving the LXRα activity and reducing lipid raft formation.
S. aureus; TLRs; allicin; immunity; lipid rafts; mastitis
Allicin Inhibited Staphylococcus aureus -Induced Mastitis by Reducing Lipid Raft Stability via LxRα in Mice.
Chen Y1, Wang Y1, Yang M1, Guo MY1.
To explore the protective effect and underlying mechanism of allicin (ALC) on myocardial ischemia reperfusion (MI/R) injury in rats.
The model of MI/R injury in rats was induced by ligating the left anterior descending branch of the coronary artery. Thirty male Sprague-Dawley rats were randomly divided into 3 equal groups (n = 10): sham group, MI/R injury group, and ALC precondition group. Enzyme-linked immunosorbent assay was used to examine the expression of cardiac troponin I, CK-MB, interleukin-6, tumor necrosis factor-α, and interleukin-8 in the rats’ serum. Hematoxylin and eosin staining was used to observe the myocardial pathologic morphology. A physiological recorder was used to measure cardiac systolic and diastolic function. Western blot analysis was used for detecting the expression of p38 and p-p38 in myocardium. The content of malondialdehyde and the activity of superoxide dismutase, catalase, and glutathione peroxidase in myocardium were examined by automatic analysis with the thiobarbituric acid chromogenic and dinitrobenzoic acid methods, respectively.
ALC can significantly decrease the expression of cardiac troponin I, CK-MB, interleukin-6, tumor necrosis factor-α, and interleukin-8 in the serum and reduce the myocardial pathologic injury and the expression of malondialdehyde and p-p38 in myocardial tissue. Moreover, ALC can upregulate the activity of superoxide dismutase, catalase, and glutathione peroxidase and improve myocardial systolic and diastolic function with no influence on the expression of p38.
ALC can protect rats against MI/R injury by suppressing inflammation and oxidative stress. The mechanism is associated with alleviating the activation of p38 signaling.
Copyright © 2019. Published by Elsevier Inc.
Allicin Attenuates Myocardial Ischemia Reperfusion Injury in Rats by Inhibition of Inflammation and Oxidative Stress.
Liu S1, He Y2, Shi J3, Liu L3, Ma H3, He L3, Guo Y4.
2019 Jul - Au
The allicin pleiotropic effects, which include anti-inflammatory, anti-oxidant, anti-tumoral, and antibacterial actions, were well demonstrated and correlated with various molecular pathways. The immunostimulatory mechanism of allicin has not been elucidated; however, there is a possible cytokine stimulation from immunoglobulin release caused by allicin. In this study, when Wistar female rats and CD19+ lymphocytes were treated with three different doses of allicin, immunoglobulins, glutathione, and oxidative stress markers were assayed. Molecular docking was performed between S-allylmercaptoglutathione (GSSA)-a circulating form of allicin in in vivo systems formed by the allicin interaction with glutathione (GSH)-and scavenger receptors class A and B from macrophages, as well as CD19+ B lymphocytes. Our data demonstrated a humoral immunostimulatory effect of allicin in rats and direct stimulation of B lymphocytes by S-allyl-mercapto-glutathione, both correlated with decreased catalase (CAT) activity. The molecular docking revealed that S-allyl-mercapto-glutathione interacting with Colec12, MARCO (class A), and SCARB1 (class B) scavenger receptors in in vitro tests demonstrates a direct stimulation of immunoglobulin secretion by GSSA in CD19+ B lymphocytes. These data collectively indicate that GSSA stimulates immunoglobulin secretion by binding on scavenger receptors class B type 1 (SCARB1) from CD19+ B lymphocytes.
allicin; immunoglobulins; mechanism; scavenger receptors
New Aspects Towards a Molecular Understanding of the Allicin Immunostimulatory Mechanism via Colec12, MARCO, and SCARB1 Receptors.
Toma VA1,2,3, Tigu AB4,5, Farcaș AD4,6,7, Sevastre B8, Taulescu M8, Gherman AMR7,9, Roman I6, Fischer-Fodor E5,10, Parvu M4.
2019 Jul 24