scholarly journals Luteolin ameliorates lipopolysaccharide-induced microcirculatory disturbance through inhibiting leukocyte adhesion in rat mesenteric venules

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jie Su ◽  
Han-Ting Xu ◽  
Jing-Jing Yu ◽  
Mei-Qiu Yan ◽  
Ting Wang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Blood Flow ◽  
Mast Cell ◽  
Small Intestine ◽  
Leukocyte Adhesion ◽  
Mast Cell Degranulation ◽  
Microcirculatory Disturbance ◽  
Hydrogen Peroxide Production ◽  
Intestinal Microcirculation ◽  
Pro Inflammatory Cytokines

Abstract Background Microcirculatory disturbance is closely associated with multiple diseases such as ischemic and septic stroke. Luteolin (3,4,5,7-tetrahydroxyflavone) is a vascular protective flavonoid present in several dietary foods. However, how luteolin plays a role in microcirculatory disturbance is still unknown. The purpose of this study was to find out the influence of luteolin on the lipopolysaccharide (LPS)-induced microcirculatory disturbance, focusing on its effect on leukocyte adhesion and the underlying mechanism of this effect. Methods After injecting LPS into rats, we used an inverted intravital microscope to observe the velocity of red blood cells in venules, numbers of leukocytes adherent to and emigrated across the venular wall, hydrogen peroxide production in venular walls and mast cell degranulation. Intestinal microcirculation blood flow was measured by High-resolution Laser Doppler Perfusion Imaging. Histological changes of small intestine and mesenteric arteries were evaluated. Additionally, cell adhesion stimulated by LPS was tested on EA.hy926 and THP-1 cells. The production of pro-inflammatory cytokines, adhesion molecules and the activation of TLR4/Myd88/NF-κB signaling pathway were determined. Results The results showed luteolin significantly inhibited LPS-induced leukocyte adhesion, hydrogen peroxide production and mast cell degranulation, and increased intestinal microcirculation blood flow and ameliorated pathological changes in the mesenteric artery and the small intestine. Furthermore, luteolin inhibited the release of pro-inflammatory cytokines, the expression of TLR4, Myd88, ICAM-1, and VCAM-1, the phosphorylation of IκB-α and NF-κB/p65 in LPS stimulated EA.hy926. Conclusions Our findings revealed that it is likely that luteolin can ameliorate microcirculatory disturbance. The inhibitory effects of luteolin on the leukocyte adhesion stimulated by LPS, which participates in the development of microcirculatory disturbance, are mediated through the regulation of the TLR4/Myd88/NF-κB signaling pathway.

Role of cardiac mast cells in complement C5a-induced myocardial ischemia

1993 ◽  
Vol 264 (5) ◽  
pp. H1346-H1354 ◽  
Author(s):  
B. R. Ito ◽  
R. L. Engler ◽  
U. del Balzo
Keyword(s):  
Blood Flow ◽  
Mast Cell ◽  
Myocardial Ischemia ◽  
Coronary Blood Flow ◽  
Cell Activation ◽  
Mast Cell Degranulation ◽  
Mast Cell Activation ◽  
Coronary Vein ◽  
Arterial Blood ◽  
Complement C5a

Activated complement component C5a causes myocardial ischemia mediated by thromboxane (Tx) A2 and leukotrienes C4/D4. Blood cells are not involved in either the mediator release or the myocardial effects of C5a, suggesting that a C5a-sensitive, cardiac resident inflammatory cell is responsible. The goals of this study were to determine whether 1) cardiac mast cell activation accompanies the C5a response, 2) inhibition of mast cell degranulation inhibits the response, and 3) histamine release plays a role in the C5a-induced myocardial ischemia. The left anterior descending coronary artery (LAD) of open-chest pigs (n = 13) was perfused with arterial blood at constant pressure (95 mmHg). Coronary blood flow (CBF) was measured (in-line flowmeter) and regional function [percent segment shortening (%SS)] determined with sonomicrometry. A coronary vein was cannulated for measurement of plasma TxB2 and histamine (a marker of mast cell degranulation). Intracoronary C5a (500 ng) decreased coronary blood flow (45% of preinfusion levels) and LAD %SS (65% of preinfusion) and was accompanied by increases in coronary venous TxB2 (delta 63.3 ng/ml) and histamine (delta 200 nM). Mast cell inhibition with lodoxamide (2 mg/kg iv, n = 8) attenuated the C5a-induced fall in CBF (14 vs. 53% decrease, P < 0.01) and %SS (10 vs. 38% decrease, P < 0.01) and also reduced the C5a-induced increase in both coronary venous histamine (delta 26 vs. 278 nM, P < 0.05) and TxB2 (delta 0.34 vs. 63.3 ng/ml, P < 0.01). However, histamine H1 (pyrilamine) and H2 (ranitidine) receptor blockade had no effect on the C5a-induced fall in CBF or LAD %SS.(ABSTRACT TRUNCATED AT 250 WORDS)

MAST CELL DEGRANULATION DURING ISCHEMIA REPERFUSION INJURY OF THE SMALL INTESTINE.

Shock ◽  
1994 ◽  
Vol 2 (Supplement) ◽  
pp. 33
Author(s):  
Mihály Boros ◽  
George FJ Newlands ◽  
Kaoru Hatanaka
Keyword(s):  
Mast Cell ◽  
Small Intestine ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mast Cell Degranulation

The effect of ulinastation on the small intestine injury and mast cell degranulation in a rat model of sepsis induced by CLP

2009 ◽  
Vol 61 (5) ◽  
pp. 481-490 ◽  
Author(s):  
Yi-Jing Zhang ◽  
Ming Li ◽  
Mei Meng ◽  
Mei Feng ◽  
Cheng-Yong Qin
Keyword(s):  
Mast Cell ◽  
Small Intestine ◽  
Rat Model ◽  
Mast Cell Degranulation

Endothelin-1 induces mucosal mast cell degranulation in the rat small intestine

Life Sciences ◽  
2000 ◽  
Vol 67 (16) ◽  
pp. 1947-1958 ◽  
Author(s):  
László Szalay ◽  
József Kaszaki ◽  
Sándor Nagy ◽  
Mihály Boros
Keyword(s):  
Mast Cell ◽  
Small Intestine ◽  
Mast Cell Degranulation ◽  
Mucosal Mast Cell ◽  
Rat Small Intestine ◽  
Endothelin 1

scholarly journals Mast cell degranulation and de novo histamine formation contribute to sustained postexercise vasodilation in humans

2017 ◽  
Vol 122 (3) ◽  
pp. 603-610 ◽  
Author(s):  
Steven A. Romero ◽  
Jennifer L. McCord ◽  
Matthew R. Ely ◽  
Dylan C. Sieck ◽  
Tahisha M. Buck ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Mast Cell ◽  
Aerobic Exercise ◽  
Histidine Decarboxylase ◽  
De Novo ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Mast Cell Degranulation ◽  
Local Blood Flow

In humans, acute aerobic exercise elicits a sustained postexercise vasodilation within previously active skeletal muscle. This response is dependent on activation of histamine H1and H2receptors, but the source of intramuscular histamine remains unclear. We tested the hypothesis that interstitial histamine in skeletal muscle would be increased with exercise and would be dependent on de novo formation via the inducible enzyme histidine decarboxylase and/or mast cell degranulation. Subjects performed 1 h of unilateral dynamic knee-extension exercise or sham (seated rest). We measured the interstitial histamine concentration and local blood flow (ethanol washout) via skeletal muscle microdialysis of the vastus lateralis. In some probes, we infused either α-fluoromethylhistidine hydrochloride (α-FMH), a potent inhibitor of histidine decarboxylase, or histamine H1/H2-receptor blockers. We also measured interstitial tryptase concentrations, a biomarker of mast cell degranulation. Compared with preexercise, histamine was increased after exercise by a change (Δ) of 4.2 ± 1.8 ng/ml ( P < 0.05), but not when α-FMH was administered (Δ−0.3 ± 1.3 ng/ml, P = 0.9). Likewise, local blood flow after exercise was reduced to preexercise levels by both α-FMH and H1/H2blockade. In addition, tryptase was elevated during exercise by Δ6.8 ± 1.1 ng/ml ( P < 0.05). Taken together, these data suggest that interstitial histamine in skeletal muscle increases with exercise and results from both de novo formation and mast cell degranulation. This suggests that exercise produces an anaphylactoid signal, which affects recovery, and may influence skeletal muscle blood flow during exercise.NEW & NOTEWORTHY Blood flow to previously active skeletal muscle remains elevated following an acute bout of aerobic exercise and is dependent on activation of histamine H1and H2receptors. The intramuscular source of histamine that drives this response to exercise has not been identified. Using intramuscular microdialysis in exercising humans, we show both mast cell degranulation and formation of histamine by histidine decarboxylase contributes to the histamine-mediated vasodilation that occurs following a bout of aerobic exercise.

Anaphylaxis-induced mesenteric vascular permeability, granulocyte adhesion, and platelet aggregates in rat

1998 ◽  
Vol 275 (1) ◽  
pp. H274-H284 ◽  
Author(s):  
Geoffrey D. Withers ◽  
Paul Kubes ◽  
Geoffrey Ibbotson ◽  
R. Brent Scott
Keyword(s):  
Mast Cell ◽  
Platelet Aggregation ◽  
Vascular Permeability ◽  
Cell Activation ◽  
Leukocyte Adhesion ◽  
Mast Cell Degranulation ◽  
Mast Cell Activation ◽  
Induce Platelet Aggregation ◽  
Platelet Aggregate ◽  
Platelet Aggregates

This study investigates the response of small venules to IgE-dependent, antigen-mediated mast cell activation. Intravital microscopy was utilized to visualize 25- to 40-μm mesenteric venules, mast cell degranulation (on-line detection), vascular permeability changes (albumin leakage), leukocyte adhesion, and the formation of platelet aggregates in rats sensitized with 10 μg of intraperitoneal egg albumin (EA) in saline- or sham-sensitized (saline alone) rats. Sensitized rats challenged with EA (1 mg/ml superfusing mesentery), but not sensitized rats challenged with BSA or sham-sensitized rats challenged with EA, exhibited mast cell degranulation with significant time-dependent increases in vascular permeability (inhibited by diphenhydramine, salbutamol, and indomethacin), leukocyte adhesion (inhibited by Web-2086), and the formation of cellular aggregates (platelet), which were associated with intermittent obstruction of venular flow. Anti-platelet antibody, but not anti-neutrophil antibody or fucoidin (selectin antagonist), prevented platelet aggregate formation. Compound 48/80-induced mast cell degranulation caused similar changes in permeability (via different mediators) and leukocyte adhesion but did not induce platelet aggregation. EA-induced platelet aggregation was not inhibited by any of the mediators tested, and platelets isolated from sensitized rats failed to aggregate in response to direct EA challenge, suggesting release of an unidentified inflammatory mediator as the factor initiating platelet aggregation.

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