S-Allyl cysteine alleviates inflammation by modulating the expression of NF-κB during chromium (VI)-induced hepatotoxicity in rats

Abstract

<jats:p> Hexavalent chromium (Cr (VI)) is a common environmental pollutant. Cr (VI) exposure can lead to severe damage to the liver, but the preventive measures to diminish Cr (VI)-induced hepatotoxicity need further study. S-allyl cysteine (SAC) is a constituent of garlic ( Allium sativum) and has many beneficial effects to humans and rodents. In this study, we intended to analyze the mechanistic role of SAC during Cr (VI)-induced hepatotoxicity. Male Wistar albino rats were induced with 17 mg/kg body weight to damage the liver. The Cr (VI)-induced rats were treated with 100 mg/kg body weight of SAC as an optimum dosage to treat hepatotoxicity. We observed that the levels of oxidants, lipid peroxidation and hydroxyl radical (OH<jats:sup>•</jats:sup>) were increased, and enzymatic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were found to be decreased in Cr (VI)-induced rats. While treated with SAC, the levels of oxidants were decreased and enzymatic antioxidants were significantly ( p &lt; 0.05) increased. Lysosomal enzyme activities were increased in Cr (VI)-induced rats and on treatment with SAC, the activities were significantly decreased. The expressions of nuclear factor-kappa B (p65-NF-κB), tumor necrosis factor α (TNF-α), and inducible nitric oxide synthase (iNOS) were increased during induction with Cr (VI). Subsequent administration of SAC to animals showed a decrease in the expressions of NF-κB, TNF-α, and iNOS. Results obtained from this study clearly demonstrated that SAC protects the liver cells from the Cr (VI)-induced free radical damage. </jats:p>

S‐allyl cysteine, an active ingredient of garlic, attenuates acute liver dysfunction induced by lipopolysaccharide/d‐galactosamine in mouse: Underlying mechanisms

“…To support our findings, it has been proved that a fraction of protective property of SAC during chromiuminduced hepatotoxicity is attributable to its inhibition of inflammation, partly mediated via modulating the expression of NF-κB in rats. [22] Additionally, SAC could reduce mucosal damage of the stomach due to non-steroidal anti-inflammatory drugs via inhibition of Cox 2 and exerting an anti-inflammatory effect. [64] Besides, it has shown that SAC downregulates TLR4 and NF-κB in LPS-induced model of acute kidney injury [23] and in this way has exerted its protective effect in this study.…”

“…[30,31] Animals in treatment groups were administered SAC (Sigma-Aldrich) per os using a gavage needle at mentioned doses (25 or 100 mg/kg/d) for 3 days till 1 hour before LPS/D-Gal challenge. SAC dose was taken from previous studies on its anti-inflammatory and defensive effects against hepatotoxicity due to chromium in rats [22] and its mitigation of oxidative injury and improvement of neurologic deficits in an animal model of focal cerebral ischemia. [32] In addition, renoprotective effect of oral SAC at doses of 25, 50 and 100 mg/kg has been evaluated in the LPS-induced model of acute kidney injury in the C57BL/6 mouse and SAC at a dose of 100 mg/kg was most effective.…”

“…SAC is a promising medicinal compound showing multiple beneficial effects in various models of human disorders. [20] SAC has shown a wide spectrum of beneficial properties including antiapoptotic, [21] acting as an antioxidant to counteract oxidative stress, [22,23] redox modulation, [24] and also exerting antiinflammatory effects. [25,26] Of related significance to our study, SAC could attenuate H 2 O 2 -induced oxidative damage and apoptotic changes through accentuating antioxidants signaling cascade in HepG2 cells, [27] is able to lower carbon tetrachloride-induced liver fibrosis that is partly mediated through its inhibition of inflammation and oxidative damage, [28] and could protect against fat-mediated liver dysfunction in adults.…”

“…[25,26] Of related significance to our study, SAC could attenuate H 2 O 2 -induced oxidative damage and apoptotic changes through accentuating antioxidants signaling cascade in HepG2 cells, [27] is able to lower carbon tetrachloride-induced liver fibrosis that is partly mediated through its inhibition of inflammation and oxidative damage, [28] and could protect against fat-mediated liver dysfunction in adults. [29] Furthermore, SAC can have protective effect on chromiuminduced model of hepatotoxicity [22] and is able to ameliorate LPSinduced liver damage and to suppress release of nitric oxide (NO) and myeloperoxidase (MPO) in lung tissue due to its antioxidant capacity. [21] Accordingly, we conducted this study to evaluate whether SAC could protect against LPS/D-Gal-induced ALI.…”

Sulfur‑containing amino acids in aged garlic extract inhibit inflammation in human gingival epithelial cells by suppressing intercellular adhesion molecule‑1 expression and IL‑6 secretion

“…ascribed, at least in part, to the anti-inflammatory (9,11) and/or antioxidant (12,13) activities of sulfur compounds in AGE.…”