scholarly journals Inhibitory Effect of Crude-Drug Extracts on the Degranulation of Mast Cells (RBL-2H3)

2011 ◽  
Vol 58 (7) ◽  
pp. 330-334 ◽  
Author(s):  
Mariko Asano ◽  
Megumi Dohi ◽  
Kazunaga Yazawa ◽  
Takashi Kometani ◽  
Kyoko Takahashi
2018 ◽  
Vol 66 (3) ◽  
pp. 323-331 ◽  
Author(s):  
Pio Conti ◽  
Alessandro Caraffa ◽  
Gianpaolo Ronconi ◽  
Chiara M. Conti ◽  
Spiros K. Kritas ◽  
...  

2003 ◽  
Vol 16 (1) ◽  
pp. 43-47 ◽  
Author(s):  
M.G. Alexandrakis ◽  
D.S. Kyriakou ◽  
D. Seretakis ◽  
W. Boucher ◽  
R. Letourneau ◽  
...  

Mast cells play an important role in allergic inflammation by releasing histamine, tryptase and several inflammatory cytokines. Human leukemic mast cells (HMC-1) have been used to study mast cell mediators and their role in inflammatory mechanisms. HMC-1 contain and release several inflammatory mediators, of which the proteolytic enzyme tryptase is most characteristic. Retinoids, including retinoic acid, are naturally occurring and synthetic derivatives of vitamin A. All-trans-retinoic (ATRA) acid had been previously reported to inhibit cell proliferation, differentiation and apoptosis. In the present study, we investigated the effect of ATRA on the proliferation and secretion of tryptase in HMC-1. HMC-1 were treated with ATRA at 10-4M, 10-5M or 10-6M for 3,4 or 5 days in culture. Control HMC-1 were treated with equal amount of culture medium only. ATRA decreased the number of HMC-1 as compared to the control group. The same treatment for 3, 4 or 5 days also decreased intracellular tryptase levels. These results indicate that ATRA significantly inhibits both proliferation and growth as shown by the decreased intracellular tryptase levels in HMC-1. ATRA may be a useful agent in the treatment of mast cell proliferative disorders.


1979 ◽  
Vol 9 (1) ◽  
pp. 65-66 ◽  
Author(s):  
W. Kazimierczak ◽  
K. Bańkowska ◽  
B. Adamas ◽  
Cz. Maśliński

1998 ◽  
Vol 242 (3) ◽  
pp. 697-702 ◽  
Author(s):  
Hidefumi Suzuki ◽  
Masao Takei ◽  
Tatsutoshi Nakahata ◽  
Hiromi Fukamachi

1997 ◽  
Vol 100 (6) ◽  
pp. S25-S32 ◽  
Author(s):  
Motohiro Kurosawa ◽  
Hiroo Amano ◽  
Naotomo Kanbe ◽  
Sachiko Akimoto ◽  
Yuko Takeuchia ◽  
...  

2021 ◽  
Vol 19 ◽  
pp. 205873922110008
Author(s):  
ZhiYang Yu ◽  
Yang Liu ◽  
Mi Tian ◽  
LiDong Zhang ◽  
Hao Cheng ◽  
...  

Inhalation of anesthetic agents have been observed to confer neuroprotection for decades. The present study was intended to determine whether desflurane (DES) prohibits mast cells (MCs) from degranulation induced by lateral ventricular injection (LVC) with Compound 48/80 (C48/80) in C57BL/6. Total 100 mice were recruited to this study, but only 88 male mice (20–24 weeks) were survived from the procedure, and randomized and allocated into four groups: (A) the saline group; (B) the C48/80 group; (C) the sodium cromoglycate (CRO + C48/80) group; (D) 7.5% DES preconditioning for 2 h + C48/80 lateral ventricular injection (DES + C48/80) group. The slices of mice brain thalamus were performed for toluidine blue staining (MCs) and immunochemistry (fluorescence of Iba1 and GFAP, respectively), and brain tissues were extracted to probe IL-6, TNF-α, NF-κB (p65), and TLR4 against GAPDH by western blotting. Our results demonstrated that administration of C48/80 provoked degranulation of mast cells at thalamus, increasing the fluorescence intensities of Iba1 and GFAP, and over-expressing IL-6, TNF-α, NF-κB(p65), and TLR4. However, pre-conditioning inhalation of DES prohibited MCs from degranulation, diminishing the fluorescent intensities of Iba1 and GFAP, decreasing expressed levels of IL-6, TNF-α, NF-κB(p65), as well as TLR4. It suggests inhalation DES could inhibit the neuroinflammation and deactivate glial and astrocytes via direct prohibiting degranulation of MCs at thalamus in the central nervous system (CNS).


Blood ◽  
1999 ◽  
Vol 93 (4) ◽  
pp. 1189-1196 ◽  
Author(s):  
Akihiko Ito ◽  
Eiichi Morii ◽  
Dae-Ki Kim ◽  
Tatsuki R. Kataoka ◽  
Tomoko Jippo ◽  
...  

The mi locus of mice encodes a transcription factor of the basic-helix-loop-helix-leucine zipper protein family (MITF). The MITF encoded by the mutant mi allele (mi-MITF) deletes 1 of 4 consecutive arginines in the basic domain. The mice of mi/migenotype express mi-MITF, whereas the mice of tg/tggenotype have a transgene at the 5′ flanking region of themi gene and do not express any MITF. To investigate the function of mi-MITF in cultured mast cells (CMCs), we took two approaches. First, mRNA obtained from mi/mi CMCs ortg/tg CMCs was subtracted from complementary (c) DNA library of normal (+/+) CMCs, and the (+/+-mi/mi) and (+/+-tg/tg) subtraction libraries were obtained. When the number of clones that hybridized more efficiently with +/+ CMC cDNA probe than with mi/mi or tg/tg CMC cDNA probe was compared using Southern analysis, the number was larger in the (+/+-mi/mi) library than in the (+/+-tg/tg) library. Second, we compared mRNA expression of six genes betweenmi/mi and tg/tg CMCs by Northern analysis. The transcription of three genes encoding mouse mast cell proteases was impaired in both mi/mi and tg/tg CMCs. On the other hand, the transcription of three genes encoding c-kit receptor, tryptophan hydroxylase, and granzyme B was markedly reduced inmi/mi CMCs, but the reduction was significantly smaller intg/tg CMCs. These results indicated the inhibitory effect ofmi-MITF on the transactivation of particular genes in CMCs.


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