Allicin Alleviates Mitochondrial Dysfunction in Acrylamide-Induced Rat Kidney Involving the Regulation of SIRT1

Abstract

Acrylamide (AA), commonly formed in carbohydrate-rich thermally processed foods, exerts harmful effects on the kidney. Allicin, from crushed garlic cloves, exhibits strong biological activities. In the current study, the protection mechanisms of allicin against AA-caused nephrotoxicity were comprehensively examined using an in vivo rat model based on previous research that allicin plays a key role in improving renal function. The results showed that allicin attenuated histological changes of the kidney and ameliorated renal function. Damaged mitochondrial structures, upregulated voltage-dependent anion channel 1 expression, and decreased membrane potential and adenosine 5′-triphosphate levels were observed after AA treatment. Surprisingly, allicin notably reversed the adverse effects. Further, allicin effectively restored mitochondrial function via modulating mitochondrial biogenesis and dynamics, which might be associated with the upregulated expression of sirtuin 1 (SIRT1). Meanwhile, allicin dramatically activated the SIRT1 activity and subsequently inhibited p53 acetylation, prevented the translocation of cytochrome c to the cytoplasm, and reduced the caspase expression, thus further inhibiting mitochondrial apoptosis caused by AA. In summary, the relieving effect of allicin on AA-caused nephrotoxicity lies in its inhibition of mitochondrial dysfunction and mitochondrial apoptosis.

Lactobacillus reuteri JCM 1112 ameliorates chronic acrylamide-induced glucose metabolism disorder via the bile acid–TGR5–GLP-1 axis and modulates intestinal oxidative stress in mice

“…3–7 Toxicological data from in vivo and in vitro showed that AA caused multiple toxicities, including neurotoxicity, reproductive toxicity, carcinogenicity, genotoxicity, hepatotoxicity, nephrotoxicity, and cardiac toxicity. 8–12 Recently, our study confirmed that short term high-dose AA (30 mg per kg bw) can induce glucose metabolism disorders (GMDs). 13,14 However, the effects of prolonged low-dose AA exposure on host glucose homeostasis are still poorly understood.…”

“…Many substances, including polyphenols, terpenoids, alkaloids, quinones, vitamins, and inulin, were found to have protective functions against AA-induced neurotoxicity, reproductive toxicity, genotoxicity, hepatotoxicity, nephrotoxicity, cardiac toxicity, and intestinal barrier dysfunction. 2,10,17,18 These studies indicated that using exogenous substances to alleviate AA-induced toxicities was a promising and feasible strategy. However, it is still unclear whether exogenous substances can also alleviate AA-induced GMD.…”

Mini-encyclopedia of mitochondria-relevant nutraceuticals protecting health in primary and secondary care—clinically relevant 3PM innovation

“…In the model of intervertebral disc degeneration, allicin protected the nucleus pulposus cells against advanced oxidation protein product–modulated mitochondrial dysfunction and oxidative stress through the downregulation of the p38-MAPK signaling pathway [ 234 ]. Regarding nephroprotective effects, allicin improved mitochondrial dysfunction in acrylamide-induced nephrotoxicity in rats through the upregulation of the SIRT1 signaling pathway [ 235 ]. In another study evaluating the cardioprotective effects of allicin, the suppression of lipopolysaccharide-induced oxidative stress and inflammation was observed in human umbilical vein endothelial cells.…”