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S‐allyl cysteine, an active ingredient of garlic, attenuates acute liver dysfunction induced by lipopolysaccharide/ d ‐galactosamine in mouse: Underlying mechanisms
Author(s) -
Rousta AliMohammad,
Mirahmadi SeyedMohamadSadegh,
Shahmohammadi Alireza,
Ramzi Samira,
Baluchnejadmojarad Tourandokht,
Roghani Mehrdad
Publication year - 2020
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22518
Subject(s) - chemistry , oxidative stress , malondialdehyde , superoxide dismutase , reactive oxygen species , pharmacology , myeloperoxidase , alkaline phosphatase , tumor necrosis factor alpha , lipopolysaccharide , inflammation , tlr4 , biochemistry , endocrinology , medicine , receptor , enzyme
In the present study, beneficial effect of S‐allyl cysteine (SAC) was evaluated in the lipopolysaccharide/ d ‐galactosamine (LPS/ d ‐Gal) model of acute liver injury (ALI). To mimic ALI, LPS and d ‐Gal (50 μg/kg and 400 mg/kg, respectively) were intraperitoneally administered and animals received SAC per os (25 or 100 mg/kg/d) for 3 days till 1 hour before LPS/ d ‐Gal injection. Pretreatment of LPS/ d ‐Gal group with SAC‐lowered activities of alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase and partially reversed inappropriate alterations of hepatic oxidative stress‐ and inflammation‐related biomarkers including liver reactive oxygen species, malondialdehyde, and hepatic activity of the defensive enzyme superoxide dismutase, ferric reducing antioxidant power (FRAP), toll‐like receptor‐4 (TLR4), cyclooxygenase 2, NLR family pyrin domain containing 3 (NLRP3), caspase 1, nuclear factor κB (NF‐κB), interleukin 1β (IL‐1β), IL‐6, tumor necrosis factor‐α, and myeloperoxidase activity. Additionally, SAC was capable to ameliorate apoptotic biomarkers including caspase 3 and DNA fragmentation. In summary, SAC can protect liver against LPS/ d ‐Gal by attenuation of neutrophil infiltration, oxidative stress, inflammation, apoptosis, and pyroptosis which is partly linked to its suppression of TLR4/NF‐κB/NLRP3 signaling.