Velvet antler polypeptide prevents the disruption of hepatic tight junctions<i>via</i>inhibiting oxidative stress in cholestatic mice and liver cell lines

Li, Lihua; Yang, Fan; Jia, Rongjun; Yan, Pengfei; Ma, Liman

doi:10.1039/d0fo01899f

Cited by 14 publications

(3 citation statements)

References 43 publications

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“…Most O 2 · − is dismutated by MnSOD to form H 2 O 2 in mitochondria [ 8 ]. Subsequently, mitochondrial H 2 O 2 diffuses into the cytoplasm to enhance oxidative damage, which is presumed to exert critical effects on the development of liver diseases, including hepatic steatosis, cholestatic liver injury and liver fibrosis [ 4 , 29 , 30 ]. Based on accumulating evidence, H 2 O 2 induces ECM synthesis by directly promoting collagen gene transcription in activated HSCs [ 31 , 32 ], which suggests that interventions designed to reduce mitochondrial H 2 O 2 production might be effective strategies for preventing liver fibrosis.…”

Section: Discussionmentioning

confidence: 99%

The m6A reader YTHDF3-mediated PRDX3 translation alleviates liver fibrosis

Sun

Tian

et al. 2022

Redox Biology

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Section: Discussionmentioning

confidence: 99%

The m6A reader YTHDF3-mediated PRDX3 translation alleviates liver fibrosis

Sun

Tian

et al. 2022

Redox Biology

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“…It is well-accepted that the hepatic tight junction is involved in various processes of liver diseases. The hepatic tight junction, involving occludin and claudin-1 and ZO-1, serves as a barrier to keep bile away from the blood circulation on hepatocytes . Also, the liver–gut–liver circulation of bile acid is critical for the absorption of nutrients and the regulation of metabolism …”

Section: Introductionmentioning

confidence: 99%

Modulation of Disordered Bile Acid Homeostasis and Hepatic Tight Junctions Using Salidroside against Hepatocyte Apoptosis in Furan-Induced Mice

Wang

Liu

et al. 2022

J. Agric. Food Chem.

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Furan, a processing-induced food contaminant, has attracted great attention due to its hepatotoxicity. To further investigate the underlying mechanism of salidroside (SAL) alleviating furan-induced liver damage, we divided Balb/c mice into the control group, the furan (8 mg/kg/day) group, and three groups of three different doses of SAL (10/20/40 mg/kg/day) in the current research. The shifted serum profile was observed through untargeted metabonomics, to which the bile acid metabolism was related, and the alleviating effect of SAL against furan-induced apoptosis was caused by the metabolism. Target bile acid quantification for the liver and serum showed that SAL positively regulated the homeostasis of bile acids disturbed by furan. Meanwhile, SAL significantly upregulated the synthesis genes of bile acids (Cyp7a1, Cyp7b1, Cyp8b1, and Cyp27a1) and the uptake transport genes (Ntcp and Oatps) and downregulated the efflux transport genes (Bsep, Ost-α, Ost-β, Mrp2, and Mrp4). Transmission electron microscopy of the bile canaliculi and tight junctions and the levels of tight junction marker proteins (ZO-1, occludin, and claudin-1) confirmed that the disruption of the hepatic tight junction was inhibited by SAL. The connection between the apoptosis- and tight junction-related proteins was observed through the construction of a protein–protein interaction network. SAL suppressed the furan-induced hepatocyte apoptosis evidenced by the detection of TUNEL and Bax, Bcl-2, and caspase-3 levels. Taken together, SAL alleviated furan-induced hepatocyte apoptosis via altering the disordered homeostasis of bile acids and hepatic tight junctions.

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“…Furthermore, CES has shown antioxidant effects in murine models of obesity, rheumatoid arthritis, fatty liver, and nephrotoxicity [ 11 , 20 , 21 , 22 ], and previous studies, particularly those focusing on neurological disease, have reported that the methanol extracts of velvet antler ameliorate Parkinson’s disease by inhibiting oxidative stress and neuroinflammation [ 18 ]. Although these results were demonstrated in neuronal-like cell lines and various disease models, neurotherapeutic effects have not been directly observed in mature neurons.…”

Section: Introductionmentioning

confidence: 99%

Neurotherapeutic Potential of Cervus elaphus Sibericus on Axon Regeneration and Growth Cone Reformation after H2O2-Induced Injury in Rat Primary Cortical Neurons

Hong

Lee

Kim

et al. 2021

Biology

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Cervus elaphus sibericus (CES), commonly known as deer antler, has been used as a medicinal herb because of its various pharmacological activities, including its anti-infective, anti-arthritic, anti-allergic, and anti-oxidative properties. However, the precise mechanisms by which CES functions as a potent anti-oxidative agent remain unknown; particularly, the effects of CES on cortical neurons and its neurobiological mechanism have not been examined. We used primary cortical neurons from the embryonic rat cerebral cortex and hydrogen peroxide to induce oxidative stress and damage in neurons. After post-treatment of CES at three concentrations (10, 50, and 200 µg/mL), the influence of CES on the neurobiological mechanism was assessed by immunocytochemistry, flow cytometry, and real-time PCR. CES effectively prevented neuronal death caused by hydrogen peroxide-induced damage by regulating oxidative signaling. In addition, CES significantly induced the expression of brain-derived neurotrophic factor and neurotrophin nerve growth factor, as well as regeneration-associated genes. We also observed newly processing elongated axons after CES treatment under oxidative conditions. In addition, filopodia tips generally do not form a retraction bulb, called swollen endings. Thus, CES shows therapeutic potential for treating neurological diseases by stimulating neuron repair and regeneration.

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Velvet antler polypeptide prevents the disruption of hepatic tight junctionsviainhibiting oxidative stress in cholestatic mice and liver cell lines

Abstract: The aim of the present study was to examine the protective effects and mechanism of velvet antler polypeptide (VAP) against lithocholic acid (LCA)-induced cholestatic liver injury in mice. A 7.0...

Cited by 14 publications

References 43 publications

The m6A reader YTHDF3-mediated PRDX3 translation alleviates liver fibrosis

The m6A reader YTHDF3-mediated PRDX3 translation alleviates liver fibrosis

Modulation of Disordered Bile Acid Homeostasis and Hepatic Tight Junctions Using Salidroside against Hepatocyte Apoptosis in Furan-Induced Mice

Neurotherapeutic Potential of Cervus elaphus Sibericus on Axon Regeneration and Growth Cone Reformation after H2O2-Induced Injury in Rat Primary Cortical Neurons

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