Augmenter of liver regeneration (ALR) restrains concanavalin A-induced hepatitis in mice

Mu, Mao; Zhang, Zhenwei; Cheng, Yi; Liu, Guangze; Chen, Xiusheng; Wu, Xin; Zhuang, Caifang; Liu, Bing-Ying; Kong, Xiangping; You, Song

doi:10.1016/j.intimp.2016.03.040

Cited by 9 publications

(8 citation statements)

References 43 publications

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“…Gandhi et al found that liver-specific deletion of ALR caused hepatocellular necrosis, hepatic inflammation and fibrosis at 4-8 weeks after birth, which suggested that ALR is required for the development of liver [8]. Mu et al found that ALR treatment reduced pro-inflammatory cytokines, chemokines and iNOS in mice with concanavalin A (ConA)-induced hepatitis [9]. However, the protective mechanism of ALR in liver injury needs to be further explored.…”

Section: Introductionmentioning

confidence: 99%

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting autophagy in mice

et al. 2017

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BackgroundAugmenter of liver regeneration (ALR) exerts strong hepatoprotective properties in various animal models of liver injury, but its protective mechanisms have not yet been explored. Autophagy is a recently recognized rudimentary cellular response to inflammation and injury. The aim of this study was to test the hypothesis that ALR may protect against acute liver injury through the autophagic pathway.MethodsThe level and role of ALR in liver injury were studied in a mouse model of acute liver injury induced by carbon tetrachloride (CCl4). The effect of ALR on autophagy was analyzed in vitro and in vivo. After autophagy was inhibited by 3-methyladenine (3-MA), apoptosis and proliferation were detected in the mouse model with acute liver injury. The ALR and autophagic levels were measured in patients with liver cirrhosis (LC) and acute liver failure (ALF), respectively.ResultsDuring the progression of acute liver injury, the ALR levels increased slightly in early stage and significantly decreased in late stage in mice Treatment with an ALR plasmid via tail vein injection protected mice against acute liver injury. The protective effect of ALR relied on the induction of autophagy, which was supported by the following evidence: (1) ALR overexpression directly induced autophagy flux in vitro and in vivo; and (2) ALR treatment suppressed apoptosis and promoted proliferation in mice exposed to CCl4, but the inhibition of autophagy reversed these effects. More importantly, the ALR levels decreased in patients with LC and ALF compared with normal controls.ConclusionWe demonstrated that ALR ameliorated liver injury via an autophagic mechanism, which indicates a potential therapeutic application for liver injury.

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Section: Introductionmentioning

confidence: 99%

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting autophagy in mice

et al. 2017

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“…Gandhi et al found that liver-specific Research Paper: Pathology deletion of ALR caused hepatocellular necrosis, hepatic inflammation and fibrosis at 4-8 weeks after birth, which suggested that ALR is required for the development of liver [8]. Mu et al found that ALR treatment reduced pro-inflammatory cytokines, chemokines and iNOS in mice with concanavalin A (ConA)-induced hepatitis [9]. However, the protective mechanism of ALR in liver injury needs to be further explored.…”

Section: Introductionmentioning

confidence: 99%

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting the autophagy in mice

Han¹,

Shi²,

Duan³

2017

Journal of Hepatology

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“…Hepatic stimulatory substance, hepatopoietin, also known as augmenter of liver regeneration (ALR), is a protein specifically produced and secreted from hepatocytes [18]. The ALR has immunoregulatory and cytoprotective effects of liver injury [19]. The ALR stimulates synthesis of TNFα, IL6 and nitric oxide in Kupffer cells [18, 20] which play important roles in repairing processes.…”

Section: Introductionmentioning

confidence: 99%

Psychosocial-Stress, Liver Regeneration and Weight Gain: a Conspicuous Pathophysiological Triad

Ishtiaq

Khan

Arshad

2018

Cell Physiol Biochem

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Psychosocial stress alters several physiological parameters resulting in multiple disorders, particularly compromising the immune system thereby provoking various diseases including liver disorders. However, the plausible underlying mechanisms remain elusive. Recent literature provides mechanistic evidences of detrimental effects of psychosocial stress on physiology of different body organs including liver. The data of stress-induced pathophysiological changes in liver functions and obesity were systematically collected from PubMed, ScienceDirect and the Web of Science Databases published in English. Stress and glucocorticoids (GCs) control food intake and energy expenditure through appetite stimulators neuropeptide Y (NYP) and agouti-related protein (AgRP) in hypothalamus. Principle effectors of the activated hypothalamic-pituitary-adrenal (HPA) axis in response to psychosocial stress are proopiomelanocortin (POMC)-derived adrenocorticotropic hormone (ACTH) and GCs. Stress-induced GCs hyper-secretion triggers glucocorticoid receptor (GR)-dependent transcriptional factor, nuclear factor kappa B (NFκB), which interferes TNFα-IL6 and keap1-Nrf2 pathways in liver regeneration and obesity through fine-tuning of TNFα, IL6 and Nrf2 signaling. In this review, it is contrived upon existing evidence to put forward a model whereby exposure to life-stress has a prominent impact over weight gain and can alter the regenerative mode of a damaged liver through Keap1-Nrf2 and TNFa-IL6 pathways.

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Augmenter of liver regeneration (ALR) restrains concanavalin A-induced hepatitis in mice

Cited by 9 publications

References 43 publications

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting autophagy in mice

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting autophagy in mice

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting the autophagy in mice

Psychosocial-Stress, Liver Regeneration and Weight Gain: a Conspicuous Pathophysiological Triad

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