Hemolysate-induced Expression of Intercellular Adhesion Molecule-1 and Monocyte Chemoattractant Protein-1 Expression in Cultured Brain Microvascular Endothelial Cells via Through ROS-dependent NF-κB Pathways

Lü, Hua; Shi, Jinjie; Zhang, Dongmei; Shen, Jie; Lin, Yingyan; Hang, Chun-Hua; Yin, Hong-Xia

doi:10.1007/s10571-008-9300-3

Cited by 8 publications

(4 citation statements)

References 29 publications

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“…NF-κB is one of the major transcription factors for inflammatory responses and triggers the secretion of pro-inflammatory cytokines including TNF-α and IL-1β. Elevated NF-κB expression and activity are also reported to promote cerebrovascular endothelial leukocyte infiltration by up-regulating expression of adhesion molecules through elevated inflammatory cytokines [ 26 - 28 ]. Similarly, augmentation of NF-κB subunits is involved in the suppression of tight junction proteins including occludin-1, claudin-5, ZO-1 and JAM-1 of BBB through increased pro-inflammatory cytokines [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Blood–brain barrier dysfunction developed during normal aging is associated with inflammation and loss of tight junctions but not with leukocyte recruitment

et al. 2015

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BackgroundFunctional loss of blood–brain barrier (BBB) is suggested to be pivotal to pathogenesis and pathology of vascular-based neurodegenerative disorders such as Alzheimer’s disease. We recently reported in wild-type mice maintained on standard diets, progressive deterioration of capillary function with aging concomitant with heightened neuroinflammation. However, the mice used in this study were relatively young (12 months of age) and potential mechanisms for loss of capillary integrity were not investigated per se. The current study therefore extended the previous finding to investigate the effect of aging on BBB integrity in aged mice at 24 months and its potential underlying molecular mechanisms.ResultsImmunomicroscopy analyses confirmed significantly increased capillary permeability with heightened neuroinflammation in naturally aged 24-month old mice compared to young control at 3 months of age. Aged mice showed significant attenuation in the expression of BBB tight junction proteins, occludin-1 and to lesser extent ZO-1 compared to young mice. In addition, TNF-α in cerebral endothelial cells of aged mice was significantly elevated compared to controls and this was associated with heightened peripheral inflammation. The expression of ICAM-1 and VCAM-1 remained unelevated, and no sign of leukocyte recruitment was observed in aged mice.ConclusionThe BBB breakdown that occurs during ordinary aging is associated with inflammation and disruption of tight junction complex assembly but not through leukocyte trafficking.Electronic supplementary materialThe online version of this article (doi:10.1186/s12979-015-0029-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Blood–brain barrier dysfunction developed during normal aging is associated with inflammation and loss of tight junctions but not with leukocyte recruitment

et al. 2015

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“…The generation of intracellular reactive oxygen species (ROS) was measured using the DCFH-DA method [37]. Briefly, SH-SY5Y cells were cultured in 96-well plates (1 × 10 4 cells per well).…”

Section: Methodsmentioning

confidence: 99%

Triterpenes and Aromatic Meroterpenoids with Antioxidant Activity and Neuroprotective Effects from Ganoderma lucidum

et al. 2019

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Reactive oxygen/nitrogen species generated in the human body can cause oxidative damage associated with many degenerative diseases such as atherosclerosis, dementia, coronary heart diseases, aging, and cancer. There is a great interest in developing new antioxidants from Ganoderma fungus due to its low toxicity. As part of our ongoing search for antioxidative constituents from the fruiting bodies of Ganoderma lucidum, the chemical constituents were investigated and seven secondary metabolites, including one new lanostane triterpene (1), two known aromatic meroterpenoids (6–7), and four known triterpenes (2–5), were isolated by a series of chromatographic methods. The structures of the seven compounds were elucidated by spectroscopic techniques. The isolated compounds were tested in vitro for antioxidant potencies and neuroprotective activities against H2O2 and aged Aβ-induced cell death in SH-SY5Y cells. As a result, compounds 1, 6, and 7 exhibited potent antioxidant and neuroprotective activities. Additionally, all isolated compounds were tested for radical scavenging activities. Compounds 6 and 7 showed the comparable free radical scavenging activities with the standard drug in both ABTS (2, 2’-azobis (3-ethylbenzothiazole-6-sulfonaic acid)) and ORAC (oxygen radical absorbance capacity) experiments. The results from this study suggested that G. lucidum and its metabolites (especially the meroterpenoids) may be potential functional food ingredients for the antioxidation and prevention of neurogenerative diseases.

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“…Intracellular reactive oxygen species (ROS) level was measured using the 2 0 ,7 0 -dichlorofluorescin diacetate (DCFH-DA) method (Lu et al 2009). DCFH-DA is a nonfluorescent compound, and it can be enzymatically converted to highly fluorescent compound, DCF, in the presence of ROS.…”

Section: Measurement Of Intracellular Ros Levelmentioning

confidence: 99%

Protective Effects of Paeoniflorin Against Glutamate-Induced Neurotoxicity in PC12 Cells via Antioxidant Mechanisms and Ca2+ Antagonism

et al. 2010

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Preclinical and clinical investigations have shown hippocampal neuronal atrophy and destruction were observed in patients with depression, which could be ameliorated by the treatment with antidepressants. Therefore, neuroprotection has been proposed to be one of the acting mechanisms of antidepressant. Paeoniflorin, a monoterpene glycoside, has been reported to display antidepressant-like effects in animal models of behavioral despair. The present study aimed to examine the protective effect of paeoniflorin on glutamate-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The results showed that pretreatment with paeoniflorin elevated cell viability, inhibited apoptosis, decreased levels of intracellular reactive oxygen species and malondialdehyde, and enhanced activity of superoxide dismutase in glutamate-treated PC12 cells. Pretreatment with paeoniflorin also reversed the increased intracellular Ca(2+) concentration and the reduced Calbindin-D28K mRNA level caused by glutamate in PC12 cells. The results suggest that paeoniflorin exerts a neuroprotective effect on glutamate-induced neurotoxicity in PC12 cells, at least in part, via inhibiting oxidative stress and Ca(2+) overload. This neuroprotective effect may be one of the action pathways accounting for the in vivo antidepressant activity of paeoniflorin.

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Hemolysate-induced Expression of Intercellular Adhesion Molecule-1 and Monocyte Chemoattractant Protein-1 Expression in Cultured Brain Microvascular Endothelial Cells via Through ROS-dependent NF-κB Pathways

Cited by 8 publications

References 29 publications

Blood–brain barrier dysfunction developed during normal aging is associated with inflammation and loss of tight junctions but not with leukocyte recruitment

Blood–brain barrier dysfunction developed during normal aging is associated with inflammation and loss of tight junctions but not with leukocyte recruitment

Triterpenes and Aromatic Meroterpenoids with Antioxidant Activity and Neuroprotective Effects from Ganoderma lucidum

Protective Effects of Paeoniflorin Against Glutamate-Induced Neurotoxicity in PC12 Cells via Antioxidant Mechanisms and Ca2+ Antagonism

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