Vitamin C alleviates alcoholic liver injury by suppressing neutrophil infiltration in senescence marker protein 30-knockout mice irrespective of its antioxidant effects

Baek, Su-Min; Lee, Seoung-Woo; Lee, Young Jin; Choi, Seong‐Kyoon; Seo, Min–Soo; Sung, Soo-Eun; Lee, A-Rang; Kim, Tae-Un; Han, Se‐Hyeon; Son, Jun‐Hyeok; Park, Sang-Joon; Kim, Tae‐Hwan; Jeong, Kyu‐Shik; Park, Jin-Kyu

doi:10.1016/j.lfs.2021.120228

Cited by 8 publications

(4 citation statements)

References 47 publications

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“…Inflammation plays an indispensable role in the pathological process of WMI (Back, 2017), which was verified in our study by upregulation of the inflammatory factor TNF‐α after chronic hypoxia and increased infiltration of microglia cells (Iba‐1 positive) in the corpus callosum. Previous studies have shown VC to have potent anti‐inflammatory effects on multiple organ systems (Back, 2017; Baek et al., 2022; He et al., 2021; Straaten, 2014). In our study, the protective effect of AS‐2P against chronic hypoxia‐induced WMI was also associated with an anti‐inflammatory effect through downregulated TNF‐α expression and reduced microglia cell infiltration.…”

Section: Discussionmentioning

confidence: 99%

L‐ascorbyl‐2‐phosphate alleviates white matter injury caused by chronic hypoxia through the PRMT5/P53/NF‐κB pathway

Ding,

Lou,

Qin

et al. 2024

Journal of Neurochemistry

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White matter injury (WMI) is one of the most serious complications associated with preterm births. Damage to oligodendrocytes, which are the key cells involved in WMI pathogenesis, can directly lead to myelin abnormalities. L‐ascorbyl‐2‐phosphate (AS‐2P) is a stable form of vitamin C. This study aimed to explore the protective effects of AS‐2P against chronic hypoxia‐induced WMI, and elucidate the underlying mechanisms. An in vivo chronic hypoxia model and in vitro oxygen–glucose deprivation (OGD) model were established to explore the effects of AS‐2P on WMI using immunofluorescence, immunohistochemistry, western blotting, real‐time quantitative polymerase chain reaction, Morris water maze test, novel object recognition test, beaming‐walking test, electron microscopy, and flow cytometry. The results showed that AS‐2P resulted in the increased expression of MBP, Olig2, PDGFRα and CC1, improved thickness and density of the myelin sheath, and reduced TNF‐α expression and microglial cell infiltration to alleviate inflammation in the brain after chronic hypoxia. Moreover, AS‐2P improved the memory, learning and motor abilities of the mice with WMI. These protective effects of AS‐2P may involve the upregulation of protein arginine methyltransferase 5 (PRMT5) and downregulation of P53 and NF‐κB. In conclusion, our study demonstrated that AS‐2P attenuated chronic hypoxia‐induced WMI in vivo and OGD‐induced oligodendrocyte injury in vitro possibly by regulating the PRMT5/P53/NF‐κB pathway, suggesting that AS‐2P may be a potential therapeutic option for WMI.

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Section: Discussionmentioning

confidence: 99%

L‐ascorbyl‐2‐phosphate alleviates white matter injury caused by chronic hypoxia through the PRMT5/P53/NF‐κB pathway

Ding,

Lou,

Qin

et al. 2024

Journal of Neurochemistry

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“…The accumulation of excessive levels of cholesterol in RGN −/− hepatocytes appears to be responsible for this impotency of SREBP1c in this case. Asc dramatically attenuates ethanol-mediated liver injury in ethanol-fed RGN −/− mice by suppressing the infiltration of neutrophils which is accompanied by less CD68-positive cell infiltration [ 156 ]. Thus, Asc appears to play pivotal roles in lipid homeostasis and the development of nonalcoholic liver disease (NAFLD), although further studies will be required to reveal the complete picture.…”

Section: In Vivo Antioxidative Action Of Asc Revealed By Animal Studiesmentioning

confidence: 99%

Ascorbate Is a Primary Antioxidant in Mammals

Fujii

Osaki

2022

Molecules

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Ascorbate (vitamin C in primates) functions as a cofactor for a number of enzymatic reactions represented by prolyl hydroxylases and as an antioxidant due to its ability to donate electrons, which is mostly accomplished through non-enzymatic reaction in mammals. Ascorbate directly reacts with radical species and is converted to ascorbyl radical followed by dehydroascorbate. Ambiguities in physiological relevance of ascorbate observed during in vivo situations could be attributed in part to presence of other redox systems and the pro-oxidant properties of ascorbate. Most mammals are able to synthesize ascorbate from glucose, which is also considered to be an obstacle to verify its action. In addition to animals with natural deficiency in the ascorbate synthesis, such as guinea pigs and ODS rats, three strains of mice with genetic removal of the responsive genes (GULO, RGN, or AKR1A) for the ascorbate synthesis have been established and are being used to investigate the physiological roles of ascorbate. Studies using these mice, along with ascorbate transporter (SVCT)-deficient mice, largely support its ability in protection against oxidative insults. While combined actions of ascorbate in regulating epigenetics and antioxidation appear to effectively prevent cancer development, pharmacological doses of ascorbate and dehydroascorbate may exert tumoricidal activity through redox-dependent mechanisms.

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“…Vitamin C (Fig. 4l), also called ascorbic acid, is rich in vegetables and fruits [302]. In rat BDL model, vitamin C weakens the liver fibrosis through its antioxidant effects [150].…”

Section: Natural Compounds Derived From Edible Plantsmentioning

confidence: 99%

“…Moreover, vitamin C exerts protection against choline-deficient diet-induced liver injury in rats, which is related to inhibiting oxidative stress and liver steatosis [303]. In alcohol-induced liver injury model in mice, vitamin C produces hepatoprotective effects by reducing neutrophil infiltration and modulating iron metabolism in the liver [302,304]. Vitamin C deficiency worsens TAA-induced liver fibrosis and oxidative stress in gulo −/− mice that cannot synthesize vitamin C, and impedes the recovery of NASH in the guinea pig, supporting its protection against liver fibrosis and injury [305,306].…”

Section: Natural Compounds Derived From Edible Plantsmentioning

confidence: 99%

A review of edible plant-derived natural compounds for the therapy of liver fibrosis

Wang

Niu

et al. 2022

European Journal of Gastroenterology &Amp; Hepatology

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Liver fibrosis has a high incidence worldwide and is the common pathological basis of many chronic liver diseases. Liver fibrosis is caused by the excessive deposition of extracellular matrix and concomitant collagen accumulation in livers and can lead to the development of liver cirrhosis and even liver cancer. A large number of studies have provided evidence that liver fibrosis can be blocked or even reversed by appropriate medical interventions. However, the antifibrosis drugs with ideal clinical efficacy are still insufficient. The edible plant-derived natural compounds have been reported to exert effective antifibrotic effects with few side-effects, representing a kind of promising source for the treatment of liver fibrosis. In this article, we reviewed the current progress of the natural compounds derived from dietary plants in the treatment of liver fibrosis, including phenolic compounds (capsaicin, chlorogenic acid, curcumin, ellagic acid, epigallocatechin-3-gallate, resveratrol, sinapic acid, syringic acid, vanillic acid and vitamin E), flavonoid compounds (genistein, hesperidin, hesperetin, naringenin, naringin and quercetin), sulfur-containing compounds (S-allylcysteine, ergothioneine, lipoic acid and sulforaphane) and other compounds (betaine, caffeine, cucurbitacin B, lycopene, α-mangostin, γ-mangostin, ursolic acid, vitamin C and yangonin). The pharmacological effects and related mechanisms of these compounds in in-vivo and in-vitro models of liver fibrosis are focused.

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Vitamin C alleviates alcoholic liver injury by suppressing neutrophil infiltration in senescence marker protein 30-knockout mice irrespective of its antioxidant effects

Cited by 8 publications

References 47 publications

L‐ascorbyl‐2‐phosphate alleviates white matter injury caused by chronic hypoxia through the PRMT5/P53/NF‐κB pathway

L‐ascorbyl‐2‐phosphate alleviates white matter injury caused by chronic hypoxia through the PRMT5/P53/NF‐κB pathway

Ascorbate Is a Primary Antioxidant in Mammals

A review of edible plant-derived natural compounds for the therapy of liver fibrosis

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