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  • 1
    Online Resource
    Online Resource
    PRDX6 inhibits hepatic stellate cells activation and fibrosis via promoting MANF secretion
    Elsevier BV ; 2022
    In:  Biomedicine & Pharmacotherapy Vol. 156 ( 2022-12), p. 113931-
    Details
    In: Biomedicine & Pharmacotherapy, Elsevier BV, Vol. 156 ( 2022-12), p. 113931-
    Type of Medium: Online Resource
    ISSN: 0753-3322
    URL: Article
    DOI: 10.1016/j.biopha.2022.113931
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1501510-5
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  • 2
    Online Resource
    Online Resource
    Myeloid FoxO1 depletion attenuates hepatic inflammation and prevents nonalcoholic steatohepatitis
    American Society for Clinical Investigation ; 2022
    In:  Journal of Clinical Investigation Vol. 132, No. 14 ( 2022-7-15)
    Details
    In: Journal of Clinical Investigation, American Society for Clinical Investigation, Vol. 132, No. 14 ( 2022-7-15)
    Type of Medium: Online Resource
    ISSN: 1558-8238
    URL: Article
    URL: Article
    DOI: 10.1172/JCI154333
    DOI: 10.1172/JCI154333DS1
    Language: English
    Publisher: American Society for Clinical Investigation
    Publication Date: 2022
    detail.hit.zdb_id: 2018375-6
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  • 3
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    Online Resource
    Hepatocyte‐derived MANF alleviates hepatic ischaemia‐reperfusion injury via regulating endoplasmic reticulum stress‐induced apoptosis in mice
    Wiley ; 2021
    In:  Liver International Vol. 41, No. 3 ( 2021-03), p. 623-639
    Details
    In: Liver International, Wiley, Vol. 41, No. 3 ( 2021-03), p. 623-639
    Abstract: Endoplasmic reticulum (ER) perturbations are novel subcellular effectors involved in the ischaemia‐reperfusion injury. As an ER stress‐inducible protein, mesencephalic astrocyte‐derived neurotrophic factor (MANF) has been proven to be increased during ischaemic brain injury. However, the role of MANF in liver ischaemia reperfusion (I/R) injury has not yet been studied. Methods To investigate the role of MANF in the process of liver ischaemia‐reperfusion, Hepatocyte‐specific MANF knockout (MANF hep−/− ) mice and their wild‐type (WT) littermates were used in our research. Mice partial (70%) warm hepatic I/R model was established by vascular occlusion. We detected the serum levels of MANF in both liver transplant patients and WT mice before and after liver I/R injury. Recombinant human MANF (rhMANF) was injected into the tail vein before 1 hour occlusion. AST, ALT and Suzuki score were used to evaluate the extent of I/R injury. OGD/R test was performed on primary hepatocytes to simulate IRI in vitro. RNA sequence and RT‐PCR were used to detect the cellular signal pathway activation while MANF knockout. Results We found that MANF expression and secretion are dramatically up‐regulated during hepatic I/R. Hepatocyte‐specific MANF knockout aggravates the I/R injury through the over‐activated ER stress. The systemic administration of rhMANF before ischaemia has the potential to ameliorate I/R‐triggered UPR and liver injury. Further study showed that MANF deficiency activated ATF4/CHOP and JNK/c‐JUN/CHOP pathways, and rhMANF inhibited the activation of the two proapoptotic pathways caused by MANF deletion. Conclusion Collectively, our study unravels a previously unknown relationship among MANF, UPR and hepatic I/R injury.
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    URL: Article
    DOI: 10.1111/liv.v41.3
    DOI: 10.1111/liv.14697
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2124684-1
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  • 4
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    Online Resource
    Synergistic Effects of Artemisia vulgaris, Ocimum tenuiflorum, Azadirachta indica and Castanopsis indica Extracts against Methicillin-Resistant Staphylococcus aureus
    Nepal Journals Online (JOL) ; 2017
    In:  Himalayan Biodiversity Vol. 5, No. 1 ( 2017-12-28), p. 38-44
    Details
    In: Himalayan Biodiversity, Nepal Journals Online (JOL), Vol. 5, No. 1 ( 2017-12-28), p. 38-44
    Abstract: Staphylococcus aureus is a major public health concern. Methicillin resistant Staphylococcus aureus is not only resistant to methicillin and other β-lactam antibacterial agents but also to other antibacterial agents. Therefore, new agents are needed to treat Methicillin Resistant Staphylococcus aureus (MRSA). The main aim of the present research was to study the antibacterial activity of four plants extract against clinical isolates of Staphylococcus aureus at the purpose of overcoming its infection. The current investigation was carried out at Pokhara Bigyan tatha Prabidhi Campus based on the evaluation of traditional plants on its antibacterial activity against MRSA. Antibacterial activity of the medicinal plant extract was observed by mixing 100 g powder of collected leaves in 70% methanol making 1000 sml. After performed processes, extract was filtered and methanol was evaporated. Antibacterial activity of the medicinal plant extract was determined using agar well diffusion assay method. Methanol leaf extracts may have the potential to act against MRSA and could be a possible source to obtain new and effective herbal medicines to treat infections caused by methicillin resistant strains of microorganisms from community as well as hospital settings. The synergistic effect was clearly observed among all four medicinal herbs.
    Type of Medium: Online Resource
    ISSN: 2382-5200
    URL: Article
    DOI: 10.3126/hebids.v5i1.36152
    Language: Unknown
    Publisher: Nepal Journals Online (JOL)
    Publication Date: 2017
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  • 5
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    Online Resource
    1574-P: FoxO1 Links Insulin Resistance to Hepatic Inflammation and Catalyzes the Evolution of Benign Steatosis to Nonalcoholic Steatohepatitis
    American Diabetes Association ; 2023
    In:  Diabetes Vol. 72, No. Supplement_1 ( 2023-06-20)
    Details
    In: Diabetes, American Diabetes Association, Vol. 72, No. Supplement_1 ( 2023-06-20)
    Abstract: Hepatic inflammation is intertwined with insulin resistance and is a causative factor for the transition of benign steatosis to nonalcoholic steatohepatitis (NASH). We found that FoxO1 was markedly upregulated in hepatic macrophages, coinciding with hepatic inflammation and steatosis in dietary obese mice. We generated myeloid-conditional FoxO1-transgenic and FoxO1-knockout mice, two complementary models for determining the effect of FoxO1 gain- vs. loss-of-function on macrophage activation in response to insulin resistance. We found that myeloid FoxO1 gain-of-function aggravated hepatic inflammation in mice in response to overnutrition or endotoxin. In contrast, myeloid FoxO1 loss-of-function skewed macrophage polarization from pro-inflammatory M1 to anti-inflammatory M2 phenotypes, accompanied by the reduction of macrophage infiltration in liver. This effect contributed to the suppression of hepatic inflammation and improvement of insulin sensitivity. Despite fat-induced obesity, myeloid-conditional FoxO1-deficient mice were protected from developing hyperglycemia, hyperinsulinemia and glucose intolerance. Furthermore, the improvement in hepatic inflammation and insulin resistance translated into a significant beneficial effect on NASH, culminating in the reduction of hepatic steatosis and fibrosis in myeloid FoxO1-deficient mice on NASH-inducing diet. Human FOXO1 expression was upregulated in inflammatory macrophages in liver, correlating with hepatic inflammation, steatosis and fibrosis in patients with NASH. Mechanistically, FoxO1 counteracts Stat6 to skew macrophage polarization from M2 toward M1 signatures with pro-inflammatory profiles. We concluded that myeloid FoxO1 dysregulation is culpable for linking insulin resistance to abnormal macrophage activation. This effect perpetuates hepatic inflammation and catalyzes the evolution of simple steatosis to NASH. Disclosure S.Lee: None. T.Usman: None. G.Chhetri: None. X.Wang: None. H.Dong: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db23-1574-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2023
    detail.hit.zdb_id: 1501252-9
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  • 6
    Online Resource
    Online Resource
    Role of Mesencephalic Astrocyte-Derived Neurotrophic Factor in Alcohol-Induced Liver Injury
    Hindawi Limited ; 2020
    In:  Oxidative Medicine and Cellular Longevity Vol. 2020 ( 2020-07-07), p. 1-15
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2020 ( 2020-07-07), p. 1-15
    Abstract: Consumption of alcohol in immoderate quantity induces endoplasmic reticulum (ER) stress response (alcohol-induced ER stress). Mesencephalic astrocyte-derived neurotrophic factor (MANF), an ER stress-inducible protein, works as an evolutionarily conserved regulator of systemic and liver metabolic homeostasis. In this study, the effects of MANF on alcohol-induced liver injury were explored by using hepatocyte-specific MANF-knockout mice (MANF Δ Hep ) in a chronic-plus-binge alcohol feeding model. We found that alcohol feeding upregulated MANF expression and MANF Δ Hep mice exhibited more severe liver injury with extra activated ER stress after alcohol feeding. In addition, we found that MANF deficiency activated iNOS and p65 and increased the production of NO and anti-inflammatory cytokines, which was further enhanced after alcohol treatment. Meanwhile, MANF deletion upregulated the levels of CYP2E1, 4-HNE, and MDA and downregulated the levels of GSH and SOD. These results indicate that MANF has potential protection on alcohol-induced liver injury, and the underlying mechanisms may be associated with meliorating the overactivated ER stress triggered by inflammation and oxidative stress via inhibiting and reducing NO/NF- κ B and CYP2E1/ROS, respectively. Therefore, MANF might be a negative regulator in alcohol-induced ER stress and participate in the crosstalk between the NF- κ B pathway and oxidative stress in the liver. Conclusions . This study identifies a specific role of MANF in alcohol-induced liver injury, which may provide a new approach for the treatment of ALI.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2020/9034864
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2455981-7
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  • 7
    Online Resource
    Online Resource
    199-OR: Beta-Cell IRS1 Deficiency Predisposes Female Mice to Developing Gestational Diabetes
    American Diabetes Association ; 2024
    In:  Diabetes Vol. 73, No. Supplement_1 ( 2024-06-14)
    Details
    In: Diabetes, American Diabetes Association, Vol. 73, No. Supplement_1 ( 2024-06-14)
    Abstract: Gestational diabetes mellitus (GDM) is characterized by glucose intolerance in pregnant women without previously diagnosed diabetes. To understand the mechanism of GDM, we characterized the role of IRS1 in β-cell compensation for pregnancy. We generated β-cell conditional IRS1-knockout (βIRS1-KO) mice. While virgin βIRS1-KO mice maintained normal metabolism, pregnant βIRS1-KO mice developed GDM, culminating in the onset of fasting hyperglycemia and glucose intolerance at gestational day 15.5. These effects were attributable to the reduction of glucose-stimulated insulin secretion in pregnant βIRS1-KO mice. Anti-insulin immunohistochemistry revealed that pregnant βIRS1-KO vs. WT mice had significantly diminished islet size and reduced β-cell mass. Anti-Ki67 immunostaining showed that βIRS1-KO vs. WT mice had minimal β-cell replication during pregnancy. Islet RNA transcriptome analysis demonstrated that IRS1-deficient islets were associated with a significant downregulation of GATA4 and its targets Reg1 and Reg3a, key factors critical for β-cell replication. In pregnant WT mice, β-cell IRS1 along with GATA4, Reg1 and Reg3a was upregulated in islets, coinciding with the physiological induction of β-cell mass expansion during pregnancy. These effects were totally abolished in IRS1-deficient islets, correlating with impaired β-cell compensation in pregnant βIRS1-KO mice. Mechanistically, IRS1 underwent prolactin-stimulated phosphorylation at Tyr632. This effect correlated with the induction of GATA4, Reg1 and Reg3a expression in islets of pregnant WT mice. We recapitulated these findings in INS1 cells in response to prolactin. Our studies uncovered a new IRS1-GATA4-Reg1/Reg3a signaling cascade in integrating gestational hormones to β-cell compensation, an adaptive mechanism that acts to overcome maternal insulin resistance and protect against GDM. Disclosure X. Wang: None. T. Usman: None. G. Chhetri: None. W. Zheng: None. H. Yeh: None. M.F. White: Board Member; Housey Pharmaceutical Research Laboratories. H. Dong: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db24-199-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2024
    detail.hit.zdb_id: 1501252-9
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