Pathogenesis of Abnormal Hepatic Lipid Metabolism Induced by Chronic Intermittent Hypoxia in Rats and the Therapeutic Effect of N-Acetylcysteine

Wang, Haipeng; Wang, Yan; Xia, Tongliang; Liu, Yaxuan; Liu, Ting; Shi, Xuemei; Li, Yanzhong

doi:10.12659/msm.907228

Cited by 9 publications

(5 citation statements)

References 25 publications

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“…The present results suggested that 4 weeks of CIH exposure induced liver fibrosis in the CIH and ciH-Vector groups, while the ciH-Vector group presented an inflammatory state with increased expression of IL-1β, il-8, McP-1, TnF-α, icaM-1 and VcaM-1. nF-κB is considered to be an oxidant-sensitive transcription factor, and activation of nF-κB promotes inflammation and multiple tissue injury in response to ciH and in liver disease conditions (31,32). Furthermore, the present results indicated that 4 weeks of ciH exposure increased nF-κB and Tlr4 expression levels in the liver.…”

Section: Discussionsupporting

confidence: 57%

TLR4 mediates inflammation and hepatic fibrosis induced by chronic intermittent hypoxia in rats

Lin

et al. 2020

Mol Med Rep

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obstructive sleep apnea syndrome (oSaS) is a common and complex disorder that is associated with liver injury. Moreover, previous studies have revealed that chronic intermittent hypoxia (ciH) is associated with the development of non-alcoholic fatty liver disease and hepatic fibrosis. However, the underlying molecular mechanisms remain largely unknown. The present study aimed to investigate whether chronic intermittent hypoxia induced hepatic fibrosis, in addition to determining its underlying mechanisms, in ciH model rats using immunohistochemistry, western blotting and reverse transcription-quantitative Pcr. The present results suggested that CIH caused hepatic fibrosis and increased the expression levels of interleukin (il)-1β, il-8, monocyte chemotactic-1, tumor necrosis factor-α, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the liver; these conditions could be reversed by Toll-like receptor 4 (Tlr4) short hairpin rna lentivirus treatment. Moreover, immunohistochemistry and western blotting results indicated that Tlr4 and nF-κB expression levels were significantly increased in the CIH and ciH-Tlr4 empty vector lentivirus group. However, protein expression levels of Tlr4, nF-κB, inhibitor of nF-κB and phosphorylated-mitogen-activated protein kinase (MaPK)-1 in the hypoxia/reoxygenation group were significantly higher compared with the control group (P<0.05), and these results were reversed by the MaPK inhibitor u0126 in vitro. collectively, the present preliminary results suggested that inflammation and the Tlr4/nF-κB/MaPK signaling pathway may be involved in CIH-induced liver fibrosis.

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Section: Discussionsupporting

confidence: 57%

TLR4 mediates inflammation and hepatic fibrosis induced by chronic intermittent hypoxia in rats

Lin

et al. 2020

Mol Med Rep

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“…These findings suggest that this type of IH can enhance the oxygen-carrying capacity and tolerance to ischemia and hypoxia of tissues, thus improving exercise endurance. Left ventricular function was assessed in isolated Abnormal liver lipid metabolism [10], liver injury [11],endothelial cell dysfunction [12], hypercholesterolemia, and lipid peroxidation [13] Positive (low-intensity IH): protects against myocardial ischemiareperfusion injury [14], prevents arrhythmia [15] Positive (low-intensity IH): prevents arrhythmia and myocardial infarction [16], improves myocardial contractile function [17], etc.…”

Section: Non-osa-ihmentioning

confidence: 99%

Intermittent Hypoxia and Atherosclerosis: From Molecular Mechanisms to the Therapeutic Treatment

Luo

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Intermittent hypoxia (IH) has a dual nature. On the one hand, chronic IH (CIH) is an important pathologic feature of obstructive sleep apnea (OSA) syndrome (OSAS), and many studies have confirmed that OSA-related CIH (OSA-CIH) has atherogenic effects involving complex and interacting mechanisms. Limited preventive and treatment methods are currently available for this condition. On the other hand, non-OSA-related IH has beneficial or detrimental effects on the body, depending on the degree, duration, and cyclic cycle of hypoxia. It includes two main states: intermittent hypoxia in a simulated plateau environment and intermittent hypoxia in a normobaric environment. In this paper, we compare the two types of IH and summarizes the pathologic mechanisms and research advances in the treatment of OSA-CIH-induced atherosclerosis (AS), to provide evidence for the systematic prevention and treatment of OSAS-related AS.

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“…Multiple pathologic conditions can induce tissue hypoxia, which is an important mediator of lipid metabolism [ 30 , 31 ]. Chronic and acute alcohol intake stimulates hepatic oxygen consumption, and subsequently causes hepatic hypoxia, leading to Hif pathway activation.…”

Section: Discussionmentioning

confidence: 99%

Hif-2α regulates lipid metabolism in alcoholic fatty liver disease through mitophagy

Zhang

Liu

et al. 2022

Cell Biosci

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Background Disordered lipid metabolism plays an essential role in both the initiation and progression of alcoholic fatty liver disease (AFLD), and fatty acid β-oxidation is increasingly considered as a crucial factor for controlling lipid metabolism. Hif-2α is a member of the Hif family of nuclear receptors, which take part in regulating hepatic fatty acid β-oxidation. However, its functional role in AFLD and the underlying mechanisms remain unclear. Results Hif-2α was upregulated in EtOH-fed mice and EtOH-treated AML-12 cells. Inhibition or silencing of Hif-2α led to increased fatty acid β-oxidation and BNIP3-dependent mitophagy. Downregulation of Hif-2α activates the PPAR-α/PGC-1α signaling pathway, which is involved in hepatic fatty acid β-oxidation, by mediating BNIP3-dependent mitophagy, ultimately delaying the progression of AFLD. Conclusions Hif-2α induces liver steatosis, which promotes the progression of AFLD. Here, we have described a novel Hif-2α-BNIP3-dependent mitophagy regulatory pathway interconnected with EtOH-induced lipid accumulation, which could be a potential therapeutic target for the prevention and treatment of AFLD.

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Pathogenesis of Abnormal Hepatic Lipid Metabolism Induced by Chronic Intermittent Hypoxia in Rats and the Therapeutic Effect of N-Acetylcysteine

Cited by 9 publications

References 25 publications

TLR4 mediates inflammation and hepatic fibrosis induced by chronic intermittent hypoxia in rats

TLR4 mediates inflammation and hepatic fibrosis induced by chronic intermittent hypoxia in rats

Intermittent Hypoxia and Atherosclerosis: From Molecular Mechanisms to the Therapeutic Treatment

Hif-2α regulates lipid metabolism in alcoholic fatty liver disease through mitophagy

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