Allicin

Allicin (diallyl thiosulfinate) is a mustard oil glycoside which, like sinigrin (allyl isothiocyanate), belongs to the glucosinolate family (AITC) and occurs naturally in garlic, onions and horseradish. Allicin is responsible for their typical odor, among other things. Allicin is excreted through the breath and skin.

Allicin has cytotoxic properties, but these have no effect when eaten, as it is very quickly broken down into non-toxic substances. Allicin has an antibacterial effect in the stomach (even in 100,000-fold dilution) on both gram-positive and gram-negative bacteria. Due to a lipid-lowering effect (although this has been disputed in recent studies), allicin (and therefore also garlic) has previously been attributed a positive therapeutic effect in arteriosclerosis. However, a reduction in LDL cholesterol (low density lipoprotein) could not be proven in a double-blind study with fresh garlic, garlic powder, garlic extract and placebos in 192 patients with slightly elevated cholesterol levels. The cytostatic effect of allicin is currently being investigated in animal experiments.

Allicin (diallyl thiosulfinate) is formed from the non-proteinogenic amino acid S-allylcysteine sulphoxide (alliin), catalyzed by the enzyme alliinase. Allicin inhibits proliferation in keratinocytes and psoriatic lesions by inducing G2/M cell cycle arrest. Furthermore, allicin induces keratinocyte apoptosis in vivo and in vitro (Zhang L et al. 2023). It can be assumed that allicin downregulates IL-17-associated inflammatory genes and thus the IL-17 signaling pathway. Animal experiments have shown that allicin reduces the release of inflammatory factors and the infiltration of immune cells (Zhang L et al. 2023).

Allicin reduces the mRNA serum levels of IL-17A . Allicin also reduces the mRNA expression of IL-17F, IL-12, IL-20 and IL-22, which are involved in the immune response to psoriasis. Allicin has also been shown to reduce the infiltration of ^CD3+, ^MPO+ and ^F4/80+ cells in psoriatic skin lesions. These results indicate that allicin not only reduces IL-17 secretion, but also inhibits keratinocyte viability and cell cycle progression and promotes apoptosis . Mechanistically, allicin inhibits IL-17-induced transcription of NF-κB, which triggered the expression of psoriasis-related target genes encoding CCL20 and S100a8/9. Allicin has been shown to inhibit the activation of the MAPK/NF-κB signaling pathway and the NLRP3 inflammasome (Li et al. 2020; Wang et al. 2017) and thus has an anti-inflammatory effect. Transcriptome analysis of mouse lesions treated with allicin shows a significant downregulation of IL-17-dependent gene expression (Zhang L et al. 2023).

^Kwai® Coblic Lozenges; ^AllicinMED® Capsules;

1. Caporaso et al. (1983) Antifungal activity in human urine and serum after ingestion of garlic (Allium sativum). Antimicrobial Agents and Chemotherapy 23: 700-702
2. Li et al. (2020) Allicin alleviates inflammation of diabetic macroangiopathy via the Nrf2 and NF-kB pathway. European Journal of Pharmacology 876: 173052.
3. Wang L et al. (2017) Allicin alleviates reticuloendotheliosis virus-induced immunosuppression via ERK/mitogen-activated protein kinase pathway in specific pathogen-free chickens. Frontiers in Immunology 8: 1856.
4. Zhang L et al. (2023) Allicin ameliorates imiquimod-induced psoriasis-like skin inflammation via disturbing the interaction of keratinocytes with IL-17A. Br J Pharmacol 180:628-646.
5. Zhang et al. (2006)Inducing apoptosis and upregulation of Bax and Fas ligand expression by allicin in hepatocellular carcinoma in Balb/c nude mice. Chinese Medical Journal 119: 422-426