Ascorbic Acid Deficiency Stimulates Hepatic Expression of Inflammatory Chemokine, Cytokine-Induced Neutrophil Chemoattractant-1, in Scurvy-Prone ODS Rats

Horio, Fumihiko; Kiyama, Keiichiro; Kobayashi, Misato; Kawai, Kenichiro; Tsuda, Takanori

doi:10.3177/jnsv.52.28

Cited by 20 publications

(16 citation statements)

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“…Furthermore, keeping ODS rats on a VitC free diet for 14 days resulted in increased cytokine-induced neutrophil chemoattractant-1 (CINC-1), a potent inflammatory chemokine, in serum, liver and spleen. Thus, VitC deficiency may mediate the infiltration and accumulation of neutrophils with subsequent inflammatory damage in some tissues [ 97 ].…”

Section: Does Vitamin C Deficiency Promote Nafld?mentioning

confidence: 99%

Does Vitamin C Deficiency Promote Fatty Liver Disease Development?

2014

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Obesity and the subsequent reprogramming of the white adipose tissue are linked to human disease-complexes including metabolic syndrome and concurrent non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). The dietary imposed dyslipidemia promotes redox imbalance by the generation of excess levels of reactive oxygen species and induces adipocyte dysfunction and reprogramming, leading to a low grade systemic inflammation and ectopic lipid deposition, e.g., in the liver, hereby promoting a vicious circle in which dietary factors initiate a metabolic change that further exacerbates the negative consequences of an adverse life-style. Large epidemiological studies and findings from controlled in vivo animal studies have provided evidence supporting an association between poor vitamin C (VitC) status and propagation of life-style associated diseases. In addition, overweight per se has been shown to result in reduced plasma VitC, and the distribution of body fat in obesity has been shown to have an inverse relationship with VitC plasma levels. Recently, a number of epidemiological studies have indicated a VitC intake below the recommended daily allowance (RDA) in NAFLD-patients, suggesting an association between dietary habits, disease and VitC deficiency. In the general population, VitC deficiency (defined as a plasma concentration below 23 μM) affects around 10% of adults, however, this prevalence is increased by an adverse life-style, deficiency potentially playing a broader role in disease progression in specific subgroups. This review discusses the currently available data from human surveys and experimental models in search of a putative role of VitC deficiency in the development of NAFLD and NASH.

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Section: Does Vitamin C Deficiency Promote Nafld?mentioning

confidence: 99%

Does Vitamin C Deficiency Promote Fatty Liver Disease Development?

2014

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“…Through this mechanism, ascorbic acid inhibits necroinflammatory activity. For that, the concentration of inflammatory chemokine and cytokineinduced neutrophil chemoattractant-1 is elevated in rats with ascorbic acid deficiency (Horio et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, ascorbic acid and vitamin E supplementation improve liver function, and prevent fibrosis in patients with non-alcoholic steatohepatitis (Harrison et al, 2003). Furthermore, ascorbic acid alone reduces hepatic injury in an experimental model of acute ischemia in rats (Huseyin et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Role of Ascorbic Acid Versus Silymarin in Amelioration of Hepatotoxicity Induced by Acrylamide in Adult Male Albino Rats: Histological and Immunohistochemical Study

2020

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Acrylamide (ACR) is a cytotoxic and carcinogenic material. It is a product of a Maillard reaction during the cooking of many types of fried fast food, e.g. potato chip fries, and chicken nuggets. ACR has a severe toxic effect on different body organs. This study investigates the hepatotoxic effect of ACR, and the protective effect of ascorbic acid and silymarin. For this purpose, forty adult, male, albino rats were divided into four groups and received the following treatments for fourteen days: Group I: (the control) normal saline; Group II: ACR only; Group III: ACR and ascorbic acid; and Group IV: ACR and silymarin. Under a light microscope, the liver from rats treated with ACR only presented disturbed liver architecture, degenerated hepatocytes, reduced glycogen contents, congested central vein, and increased collagen fibres with areas of fibrosis. Immunohistochemical examination revealed an increased mean number of CD68-, and α-SMA-positive cells. This indicates the presence of large numbers of stellate macrophages (Kupffer cells) and Hepatic stellate cells (HSCs). The combination of ACR with either ascorbic acid or silymarin resulted in less hepatic degeneration, less fibrosis and fewer CD68 and α-SMA positive cells compared to the ACR only group. In conclusion, treatment with silymarin or ascorbic acid along with ACR appears to alleviate ACR-induced hepatotoxicity with more protection in silymarin treated rats.

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“…Recently, vitamin C was reported to depress T-cellmediated acute liver injury in Gulo(-/-) mice (Bae et al, 2013b). In addition, vitamin C deficiency elevated the serum concentrations of inflammatory chemokine, cytokine-induced neutrophil chemoattractant-1 in rats (Horio et al, 2006). Thus, vitamin C might have a physiological potency to suppress necroinflammatory process by reducing chemotaxis of neutrophil granulocytes through lowering the concentrations of inflammatory chemokine (Horio et al, 2006).…”

Section: Discussionmentioning

confidence: 99%