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  • Li, Chun Guang  (5)
  • Zhou, Xian  (5)
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  • 1
    In: Journal of Neurochemistry, Wiley, Vol. 156, No. 2 ( 2021-01), p. 249-261
    Abstract: Neuroinflammation is believed to play a primary role in the pathogenesis of most neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and schizophrenia. Currently, suitable in vitro neuroinflammation models for studying cellular interactions and inflammatory mechanisms at the neurovascular unit are still scarce. In this study, we established an experimentally flexible tri‐culture neuroinflammation model combining murine microglial cells (N11), mouse neuroblastoma Nuro2A cell lines and brain microvascular endothelial MVEC(B3) cells in a transwell co‐culture system stimulated with lipopolysaccharides. Neuroinflammation was induced in this tri‐culture model as manifested by activated N11 cells via toll‐like receptor 4, resulting in increased release of proinflammatory mediators (nitric oxide, interleukin‐6 and tumour necrosis factor‐α) through the activation of nuclear factor‐κB signalling pathway. The released inflammatory cytokines from N11 in turn, damaged the tight junction in microvascular endothelial MVEC(B3) cells, increased permeability of endothelial barrier, and induced tau phosphorylation and up‐regulated caspase‐3 expression in mouse neuroblastoma Nuro2A cell lines, leading to neuroinflammation injury. In summary, this tri‐culture inflammation model mimics the microenvironment, the cellular crosstalk and the molecular events that take place during neuroinflammation. It provides a robust in vitro model for studying neuroinflammation mechanisms and screening for potential therapeutics to treat various neurodegenerative diseases. image
    Type of Medium: Online Resource
    ISSN: 0022-3042 , 1471-4159
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2020528-4
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2022
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 49, No. 2 ( 2022-02), p. 302-310
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 49, No. 2 ( 2022-02), p. 302-310
    Abstract: This study aimed to elucidate the role of transcription factor EB (TFEB) in protecting C2C12 myotubes against palmitate (PA)‐induced insulin resistance (IR) and explored its mechanism associated with autophagy. PA treatment significantly decreased insulin sensitivity in myotubes and downregulated TFEB protein expression. TFEB overexpression significantly reversed the PA‐suppressed glucose transporter 4 ( GLUT4) protein expression and improved intracellular glucose uptake and consumption, and also alleviated the decrease of autophagy markers induced by PA. The effect of TFEB overexpression on GLUT4 was also abolished by the autophagy inhibitor 3‐MA. In addition, AMPKɑ2‐DN inhibited or abolished the effects of TFEB overexpression on upregulation of GLUT4 and PA‐induced decrease of autophagy marker expressions. Taken together, our data demonstrated that upregulation of TFEB improved PA‐induced IR in C2C12 myotubes by enhancing autophagy and upregulating AMPK activity. TFEB, as a critical regulator of glucose homeostasis in skeletal muscle cells, may be a potential therapeutic target for IR and Type 2 diabetes.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2020033-X
    SSG: 15,3
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  • 3
    In: Biomedicine & Pharmacotherapy, Elsevier BV, Vol. 138 ( 2021-06), p. 111445-
    Type of Medium: Online Resource
    ISSN: 0753-3322
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 1501510-5
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  • 4
    In: Frontiers in Endocrinology, Frontiers Media SA, Vol. 13 ( 2022-8-18)
    Abstract: Endothelial dysfunction is an early pathological event in diabetic angiopathy which is the most common complication of diabetes. This study aims to investigate individual and combined actions of Curcumin (Cur) and Baicalein (Bai) in protecting vascular function. The cellular protective effects of Cur, Bai and Cur+Bai (1:1, w/w ) were tested in H 2 O 2 (2.5 mM) impaired EA. hy926 cells. Wistar rats were treated with vehicle control as the control group, Goto-Kakizaki rats (n=5 each group) were treated with vehicle control (model group), Cur (150 mg/kg), Bai (150 mg/kg), or Cur+Bai (75 mg/kg Cur + 75 mg/kg Bai, OG) for 4 weeks after a four-week high-fat diet to investigate the changes on blood vessel against diabetic angiopathy. Our results showed that Cur+Bai synergistically restored the endothelial cell survival and exhibited greater effects on lowering the fasting blood glucose and blood lipids in rats comparing to individual compounds. Cur+Bai repaired the blood vessel structure in the aortic arch and mid thoracic aorta. The network pharmacology analysis showed that Nrf2 and MAPK/JNK kinase were highly relevant to the multi-targeted action of Cur+Bai which has been confirmed in the in vitro and in vivo studies. In conclusion, Cur+Bai demonstrated an enhanced activity in attenuating endothelial dysfunction against oxidative damage and effectively protected vascular function in diabetic angiopathy rats.
    Type of Medium: Online Resource
    ISSN: 1664-2392
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2592084-4
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  • 5
    Online Resource
    Online Resource
    Wiley ; 2022
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 49, No. 4 ( 2022-04), p. 536-543
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 49, No. 4 ( 2022-04), p. 536-543
    Abstract: Previous studies reported inconsistent findings on autophagy activation in skeletal muscles after acute exercise. In this study, we investigated the effect of a single bout of exhaustive treadmill exercise on AMPK and autophagy activations in mice gastrocnemius muscle in vivo. Male ICR/CD‐1 mice were randomly divided into the control and exercise groups. The later was subjected to a single bout of exhaustive treadmill exercise. Changes of AMPK, phosphorylation of AMPK Thr172 (pAMPK Thr172 ), and autophagy markers including Beclin1, LC3II/LC3I and p62 mRNA and protein expressions in gastrocnemius muscle at different times (0, 6, 12, 24 h) after the exercise were analysed by quantitative real‐time PCR and western blot. Our results demonstrated that a single bout of exhaustive treadmill exercise significantly induced AMPK content and AMPK activity at 0, 6 and 12 h after the exercise, and changed the expressions of autophagy markers at different time points in the recovery period, respectively. Moreover, we observed positive correlations between expressions of LC3II/LC3I ratio and pAMPK Thr172 or AMPK, and a negative correlation between expressions of p62 and AMPK or pAMPK Thr172 . In conclusion, a single bout of exhaustive treadmill exercise in mice caused a prolonged activation of AMPK and improved autophagy in the gastrocnemius muscle. The regulation of autophagic markers were related to enhanced AMPK activity. The findings indicate that acute exercise enhanced AMPK‐related autophagy activation may be the underlying molecular mechanism that regulates cellular energy metabolism during exercise.
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2020033-X
    SSG: 15,3
    Location Call Number Limitation Availability
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