China
Africa
Explore chapters and articles related to this topic
Marine Chondroitin Sulfate and Its Potential Applications
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Chondroitin sulfate appears to be a powerful mast cell inhibitor of both allergic and non-immune activation, with therapeutic consequences. Mast cells are responsible for the development of allergies and potential inflammatory responses and originate in the bone marrow. Chondroitin sulfate inhibited mast cell secretagogue compound 48/80 (48/80)–induced histamine production in rat peritoneal mast cells in a dose-dependent manner. Inhibition by chondroitin sulfate increased with pre-incubation time and remained after the medication was washed off, but cromolyn’s impact was restricted by rapid tachyphylaxis. Histamine production from rat connective tissue mast cells (CTMCs) was also suppressed immunologically. Ultrastructural autoradiography reveals that chondroitin sulfate is mostly linked with the plasma and perigranular membrane (Theoharides et al., 2000).
Role of Wild Plants in Curing and Healing the Skin Diseases
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Wild Plants, 2020
Mudassar Mehmood, Rao Zahid Abbas
The dose of aqueous extracts of C. intybus (CIAE) inhibited mast cell-immediate allergic reactions. These extracts dose-dependently prohibited the anaphylactic reactions induced by compound 48/80 in mice. At the dose rate of 1000 mg/kg it is also remarkably reduced local anaphylactic reactions that are initiated by anti-dinitrophenyl IgE. The watery concentrate of C. intybus denies shaft cell-intervened brisk sort of unfavorable susceptible responses in vivo and in vitro. It is found that C. intybus prohibits prostaglandin E (2) and cyclooxygenase (2), and besides diminishing immunotoxicity incited by ethanol, have moderating properties (Jippo et al. 2000). A cosmetic composition is additionally created that anticipates maturing of the skin in which the active fixing is an extract of the elevated pieces of C. intybus. Its effectiveness consists of its capacity to preclude radical reactions, in particular by the chelation of iron.
Cell Adhesion Molecules in Mast Cell Adhesion and Migration
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Harissios Vliagoftis, Dean D. Metcalfe
Local challenge of the rat mesentery with compound 48/80 increases the leukocyte rolling fraction, decreases rolling velocity, and induces firm leukocyte adhesion in postcapillary venules, as shown by intravital microscopy (68). In another study evaluating the effect of histamine in a similar system, it was reported that histamine has the same effects; in addition, it increased the clearance of albumin from blood to the superfusate (69). In the first study, the effects of compound 48/80 were inhibited by a monoclonal anti-P-selectin antibody, but not by combined treatment with and H2 histamine receptor antagonists. Moreover, the response to compound 48/80 was not duplicated by exogenous histamine or 5-hydroxytryptamine (serotonin). This was said to indicate that mediator(s) other than histamine and serotonin evoke P-selectin-dependent leukocyte rolling, and thereby promoted firm leukocyte adhesion in mast cell-dependent inflammation (68). However, in the second study the effect that was inhibited by antagonists appeared to be mediated by P-selectin. Antibodies against P-selectin and also soluble sialyl-Lewisx oligosaccharide inhibited all effects except those from increased extravasation (69). This mast cell-dependent leukocyte recruitment and micro vascular permeability was inhibited by the addition of nitric oxide (70).
Mast cells disrupt the duodenal mucosal integrity: Implications for the mechanisms of barrier dysfunction in functional dyspepsia
Published in Scandinavian Journal of Gastroenterology, 2023
Zhiming Wang, Menghao Hao, Liping Wu, Yumei He, Xiaobin Sun
Rabbit anti-occludin and rabbit anti-ZO-1 antibodies were purchased from Abcam (Cambridge, UK). Rabbit anti-claudin-8 antibody for immunofluorescence was purchased from Affinity Biosciences (Cincinnati, OH) and that used for western blotting was purchased from Abcam (Cambridge, UK). Mouse anti-GAPDH antibody was purchased from ProteinTech (Chicago, IL). Secondary antibodies were goat anti-rabbit or anti-mouse HRP‐linked antibodies and were purchased from Santa Cruz Biotechnology (Santa Cruz, CA). Alexa 488-conjugated anti-mouse IgG was purchased from Invitrogen (Carlsbad, CA). Cy3-conjugated goat anti-rabbit IgG was purchased from Servicebio (Wuhan, China). Compound 48/80 (C48/80, a stimulator of MC degranulation) was purchased from Sigma-Aldrich (St. Louis, MO). MK-4827 (a PAR-2 receptor antagonist) and SCH772984 (an ERK inhibitor) were purchased from Selleck Chemicals (Houston, TX). Recombinant human tryptase was purchased from Promega Biotech (Madison, WI).
Tanshinone IIA alleviates ovalbumin-induced allergic rhinitis symptoms by inhibiting Th2 cytokine production and mast cell histamine release in mice
Published in Pharmaceutical Biology, 2022
Qing Chen, Liping Shao, Yong Li, Mian Dai, He Liu, Nan Xiang, Hui Chen
The concentration of histamine release from mast cells was determined by histamine test kit. Compound 48/80 (C48/80; C2313, Sigma-Aldrich, St. Louis, MO) can be used to facilitate histamine release (Won Jung et al. 2012). The collected human mast cell line HMC-1 in logarithmic growth phase was divided into four groups: (1) control group, (2) C48/80 group, (3) C48/80 + 5 μmol/L TIIA (TIIA-5) group and (4) C48/80 + 10 μmol/L TIIA (TIIA-10) group. Cells in each group (except for control group) were pre-treated using 0.5 μg/mL C48/80 at 37 °C for 1 h. Then, the cells in C48/80 + 5 μmol/L TIIA (TIIA-5) and C48/80 + 10 μmol/L TIIA (TIIA-10) groups, were treated with C48/80 and TIIA at different concentrations at 37 °C for 30 min, respectively. Finally, the culture supernatant was collected after centrifugation at 400×g for 5 min at 4 °C. Same as the above experimental procedures, mast cell histamine release was detected by histamine ELISA kit. The OD value of each well was measured with a microplate reader at a wavelength of 450 nm. Histamine release was calculated as the percent of total (cellular + extracellular) histamine.
In vitro prediction of in vivo pseudo-allergenic response via MRGPRX2
Published in Journal of Immunotoxicology, 2021
Linu M. John, Charlotte M. Dalsgaard, Claus B. Jeppesen, Kilian W. Conde-Frieboes, Katrine Baumann, Niels P. H. Knudsen, Per S. Skov, Birgitte S. Wulff
To determine if the potencies of the compounds tested in the cell-based MRGPRX2 assay correlated in a translationally-relevant setting, histamine release was assessed in freshly-acquired abdominal human skin specimens from patients undergoing cosmetic surgery. Exposure of skin specimens to sermorelin, cetrorelix and Substance P (tested on MRGPRX2 potency) and Compound 48/80 (widely-used in animal and tissue models as a mast cell activator [Rothschild 1970; Kumar et al. 2020]) induced histamine release with peak values occurring at 10 min post-administration of compound (Figure 2(A)). Based on technical replicates for each compound, all compounds induced a greater excursion in histamine release at 10 min compared to the vehicle (19.0 [± 2.8] ng/mL), with Substance P (714.3 [± 25.7] ng/mL) and cetrorelix (115.3 [± 2.1] ng/mL) causing the largest peak values, followed by sermorelin (62.0 [± 5.3] ng/mL) and Compound 48/80 (55.7 [± 0.6] ng/mL). AUC values over the 60-min measurement period reflected the rank order of histamine release observed at peak histamine release (Figure 2(B)). Note: the extent of histamine release induced by Substance P (Figure 2) was not mirrored in the rank ordering on in vitro response to MRGPRX2 (Figure 1), possibly due to additional activation of the neurokinin-1 receptor (NK1R) or other receptors on mast cells by this compound (Erin et al. 2004; Subramanian et al. 2016; Green et al. 2019; Zhan et al. 2019).