Abstract
Cell-to-cell communication is a key element of microvascular blood flow control, including rapidly carrying signals through the vascular endothelium in response to local stimuli. This cell-to-cell communication is negatively impacted during inflammation through the disruption of junctional integrity. Such disruption is associated with promoting the onset of cardiovascular diseases as a result of altered microvascular blood flow regulation. Therefore, understanding the mechanisms how inflammation drives microvascular dysfunction and compounds that mitigate such inflammation and dysfunction are of great interest for development. As such we aimed to investigate extracts of mushrooms as potential novel compounds. Using intravital microscopy, the medicinal mushroom, Inonotus obliquus was observed, to attenuate histamine-induced inflammation conducted vasodilation in second-order arterioles in the gluteus maximus muscle of C57BL/6 mice. Mast cell activation by C48/80 similarly disrupted endothelial junctions and conducted vasodilation but only histamine was blocked by the histamine antagonist, pyrilamine not C48/80 suggesting the importance of mast cell activation. Data presented here supports that histamine induced inflammation is a major disruptor of junctional integrity, and highlights the important anti-inflammatory properties of Inonotus obliquus focusing future assessment of mast cells as putative target for Inonotus obliquus.
Highlights
Inflammation is a protective mechanism that is activated to combat invading pathogens or to reverse tissue injury
LPS was replaced by histamine to assess the effect of histamine in inducing TNF-α in RAW 264.7 macrophage cells
Previous work with Inonotus obliquus has demonstrated anti-inflammatory activity [5,7,8,9,10] and in this study, we showed that all four extracts of I. obliquus collected were able to significantly inhibit LPS-induced TNF-α production in RAW 264.7 mouse macrophage cells (Fig 1)
Summary
Inflammation is a protective mechanism that is activated to combat invading pathogens or to reverse tissue injury. The activation of inflammatory pathways stimulates the release of proinflammatory mediators including nitric oxide, reactive oxygen species, interleukins IL-1, I-L6), tumor necrosis factor-alpha (TNF-α), cyclo-oxygenase (COX-2), prostaglandins (PGE2), nuclear factor (NF-κβ)[1]. Anti-inflammation and mushrooms pathophysiology of various inflammatory mediated metabolic and neurodegenerative diseases. Mechanisms to attenuate aberrant inflammatory responses would be beneficial mitigating the onset of disease states
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