Long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction

Background: Probucol has been shown to prevent cerebral capillary disturbances characterized by blood-to-brain extravasation of plasma derived proteins and neurovascular inflammation in mice maintained on western-styled diets for 12 weeks. However the effect of probucol on capillary integrity in agi...

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Main Authors: Takechi, Ryu, Pallebage-Gamarallage, Menuka, Lam, Virginie, Giles, Corey, Mamo, John
Format: Journal Article
Published: BioMed Central Ltd. 2014
Subjects:
Online Access:http://hdl.handle.net/20.500.11937/5769
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author Takechi, Ryu
Pallebage-Gamarallage, Menuka
Lam, Virginie
Giles, Corey
Mamo, John
author_facet Takechi, Ryu
Pallebage-Gamarallage, Menuka
Lam, Virginie
Giles, Corey
Mamo, John
author_sort Takechi, Ryu
building Curtin Institutional Repository
collection Online Access
description Background: Probucol has been shown to prevent cerebral capillary disturbances characterized by blood-to-brain extravasation of plasma derived proteins and neurovascular inflammation in mice maintained on western-styled diets for 12 weeks. However the effect of probucol on capillary integrity in aging models with capillary dysfunction is not known. Methods: Wild-type C57BL6 mice were randomized to a low-fat (LF); saturated-fat (SFA); or SFA + Probucol diet for up to12 months of intervention. Results: Mice fed the LF diet had substantially greater parenchymal abundance of plasma derived IgG and apo B lipoproteins at 12 months, compared to LF mice at 3 months of intervention. Markers of neurovascular inflammation were also greater at 12 months in LF fed mice compared to LF mice at 3 months. The SFA diet exacerbated the aging induced parenchymal abundance of IgG and of apo B lipoproteins and neurovascular inflammation at 12 months. The SFA effects were associated with increased production of intestinal lipoprotein amyloid-ß (Aß). The co-provision of probucol with the SFA completely abolished heightened inflammation at 12 months. Probucol attenuated SFA-induced capillary permeability but had only a modest inhibitory effect on parenchymal retention of apoB lipoproteins. The improvements in markers of inflammation and capillary integrity because of probucol correlated with enterocytic genesis of chylomicron Aß. Conclusion: In this long-term feeding study, probucol profoundly suppressed dietary SFA induced disturbances in capillary integrity but had a more modest effect on age-associated changes.
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spelling curtin-20.500.11937-57692017-09-13T15:36:21Z Long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction Takechi, Ryu Pallebage-Gamarallage, Menuka Lam, Virginie Giles, Corey Mamo, John Apolipoprotein B Probucol Brain capillaries Neuroinflammation Saturated fatty acids Amyloid-ß Blood–brain barrier Enterocytes Background: Probucol has been shown to prevent cerebral capillary disturbances characterized by blood-to-brain extravasation of plasma derived proteins and neurovascular inflammation in mice maintained on western-styled diets for 12 weeks. However the effect of probucol on capillary integrity in aging models with capillary dysfunction is not known. Methods: Wild-type C57BL6 mice were randomized to a low-fat (LF); saturated-fat (SFA); or SFA + Probucol diet for up to12 months of intervention. Results: Mice fed the LF diet had substantially greater parenchymal abundance of plasma derived IgG and apo B lipoproteins at 12 months, compared to LF mice at 3 months of intervention. Markers of neurovascular inflammation were also greater at 12 months in LF fed mice compared to LF mice at 3 months. The SFA diet exacerbated the aging induced parenchymal abundance of IgG and of apo B lipoproteins and neurovascular inflammation at 12 months. The SFA effects were associated with increased production of intestinal lipoprotein amyloid-ß (Aß). The co-provision of probucol with the SFA completely abolished heightened inflammation at 12 months. Probucol attenuated SFA-induced capillary permeability but had only a modest inhibitory effect on parenchymal retention of apoB lipoproteins. The improvements in markers of inflammation and capillary integrity because of probucol correlated with enterocytic genesis of chylomicron Aß. Conclusion: In this long-term feeding study, probucol profoundly suppressed dietary SFA induced disturbances in capillary integrity but had a more modest effect on age-associated changes. 2014 Journal Article http://hdl.handle.net/20.500.11937/5769 10.1186/1476-511X-13-91 BioMed Central Ltd. fulltext
spellingShingle Apolipoprotein B
Probucol
Brain capillaries
Neuroinflammation
Saturated fatty acids
Amyloid-ß
Blood–brain barrier
Enterocytes
Takechi, Ryu
Pallebage-Gamarallage, Menuka
Lam, Virginie
Giles, Corey
Mamo, John
Long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction
title Long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction
title_full Long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction
title_fullStr Long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction
title_full_unstemmed Long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction
title_short Long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction
title_sort long-term probucol therapy continues to suppress markers of neurovascular inflammation in a dietary induced model of cerebral capillary dysfunction
topic Apolipoprotein B
Probucol
Brain capillaries
Neuroinflammation
Saturated fatty acids
Amyloid-ß
Blood–brain barrier
Enterocytes
url http://hdl.handle.net/20.500.11937/5769