Histological studies were carried out on the degranulation of mesenteric mast cells of white rats caused by injections of morphine hydrochbride and meperidine hydrochbride intravenously, intraperitoneally, and by local injection of the rat's mesentery and the following conclusions were obtained. 1. In the groups of intravenous, intraperitoneal, and local injections of morphine hydrochloride, fairly significant degranulation of the mesenteric mast cell was observed, which was probably associated with the concomitant liberation of tissue histamine derived from its source. 2. In the groups of intravenous and intraperitoneal injections of meperidine hydrochbride, the significant degranulation of the mesenteric mast ,cell was recognized. However, the local injections displayed no cytological change of the cell and no increased permeability of dermal capillaries was observed at the injecting site. 3. The degranulation of the mesenteric mast cell followed by an administration of meperidine hydrochloride was effectively inhibited after an adrenalectomy.
Animals ; Female ; Male ; Mast Cells/*drug effects ; Meperidine/*adverse effects ; Mesentery/drug effects/*pathology ; Morphine/*adverse effects ; Rats

The aim of this work was to study effects of ketotifen fumarate (KF) on prevention of tissue damage in testes of rats with experimental autoimmune orchitis (EAO) and on the contralateral testis in a model of prolonged testicular cord torsion (TCT). Rats with EAO or TCT were injected intraperitoneally once daily with KF or saline solution (vehicle group). Incidence and severity of testicular damage were evaluated by histopathology using an EAO score or a Johnsen score. Mast cells (MC) were identified by histochemistry and quantified. In EAO model, KF significantly reduced severity of histopathological testicular damage compared to rats in the vehicle group. KF also reduced the number of testicular MC compared to vehicle group. Similarly, in TCT model, multifocal damage of the contralateral testis was observed 30 days after testicular torsion characterized by sloughing of the germinal epithelium, seminiferous tubule atrophy, and interstitial edema. Focal signs of inflammation and fibrosis of seminiferous tubular walls were also observed. In contrast, sections of contralateral testis of rats injected with KF and killed 30 days after surgery showed normal histological features. A significant decrease in the number of MC was observed in rats treated with KF compared to untreated animals. In conclusion, we demonstrated that treatment with KF reduced testicular inflammatory process and MC infiltrates in both EAO and TCT models. The results suggest a promising treatment for infertile male patients with testicular pathologies associated with inflammation and germ cell loss.
Animals ; Autoimmune Diseases/pathology* ; Cell Count ; Epididymis/pathology* ; Epididymitis/pathology* ; Histamine H1 Antagonists/pharmacology* ; Hypersensitivity, Delayed ; Immunity, Cellular/drug effects* ; Ketotifen/pharmacology* ; Male ; Mast Cells/pathology* ; Orchitis/pathology* ; Rats ; Severity of Illness Index ; Spermatic Cord Torsion/pathology* ; Testis/pathology* ; Vaccination

OBJECTIVETo observe the effect of Tongxie Yaofang (TY) on the number of mast cells (MCs) and the expression of cytokines in rats with visceral hypersensitivity, and to explore roles of TY in treating visceral hypersensitivity and its possible mechanism.

METHODSTotally 30 male adult Sprague Dawley (SD) rats were randomly divided into the blank control group, the model group, and the TY treatment group, 10 in each group. The irritable bowel syndrome (IBS) rat model was established by combining colorectal distention with restraint stress in the TY treatment group and the model group. The visceral hypersensitivity was assessed by abdominal withdrawal reflex (AWR). From the 2nd day of successful modeling, rats in the treatment group were admiministered with TY at the daily dose of 4 g/kg for 4 successive weeks. Equal volume of normal saline was given to rats in the model group for 4 successive weeks. No treatment was given to rats in the blank control group. Four weeks later the number of MCs was counted by using toluidine blue staining. The expression of interleukin-4 (IL-4) and interleukin-9 (IL-9) both in colonic mucosa and serum were measured by enzyme linked immunosorbent assay (ELISA), and the expression of protease-activated receptor type 2 (PAR-2) was detected by Western blot.

RESULTSCompared with the blank control group, the visceral sensitivity was significantly elevated, the number of MCs in the ileocecal junction increased, and the expression of IL-4, IL-9, and PAR-2 in serum and the colonic mucosa significantly increased (P < 0.05). Compared with the model group, the visceral sensitivity significantly decreased, the number of MCs reduced, and the expression of PAR-2 in the colonic mucosa significantly reduced (all P < 0.05), and the expression of IL-4 in colonic mucosa and IL-9 in serum were obviously reduced in the TY treatment group (P < 0.05).

CONCLUSIONTY might improve the visceral hypersensitivity by acting on MCs related cytokines and reducing degranulation of MCs.

Animals ; Cytokines ; metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Intestines ; drug effects ; metabolism ; pathology ; Irritable Bowel Syndrome ; drug therapy ; metabolism ; pathology ; Male ; Mast Cells ; drug effects ; Rats ; Rats, Sprague-Dawley

BACKGROUNDStudy of the relationship between mast cells and atherosclerosis is mostly dependent on pathological observation and cytology experiments. To investigate the effects of mast cells degranulation on plaque and their possible mechanisms we used apolipoprotein E knockout mice which had been placed perivascular common carotid collar with mast cells degranulator compound 48-80.

METHODSForty apolipoprotein E knockout mice were fed a western-type diet and operated on with placement of perivascular right common carotid collar. Four weeks after surgery, the mice were intraperitoneally injected with compound 48-80 (0.5 mg/kg) or D-Hanks every other day for 4 times. The serum lipids and activity of tryptase were measured. Tissue sections were stained with hematoxylin and eosin. Corresponding sections were stained with toluidine blue and immunohistochemically with antibodies against macrophage-specific antigen, alpha-smooth muscle actin, interleukin-1beta and von Willebrand factor. Simultaneously, basic fibroblast growth factor was detected by in situ hybridization and immunofluorescence.

RESULTSNo pathological change was observed in common carotid non-collar placement but atherogenesis in common carotid collar placement of both groups. There was a significant increase in plaque area ((5.85+/-0.75) x 10(4) vs (0.86+/-0.28) x 10(4) microm(2), P<0.05), the degree of lumen stenosis ((81+/-15)% vs (41+/-12)%, P<0.05), the activity of tryptase in serum ((0.57+/-0.13) U/L vs (0.36+/-0.10) U/L, P<0.05), and the percentage of degranulated mast cells ((80.6+/-17.8)% vs (13.5+/-4.1)%, P<0.05). The expressions of macrophage-specific antigen, alpha-smooth muscle actin, interleukin-1beta, basic fibroblast growth factor and the density of neovessel in plaque were more in the compound 48-80 group than in the control group.

CONCLUSIONSPerivascular common carotid collar placement can promote atherosclerotic plaque formation in apolipoprotein E knockout mice. Compound 48-80 increases plaque area and the degree of lumen stenosis by the mechanism that compound 48-80 promotes proliferation of smooth muscle cells and aggregation of macrophages. Compound 48-80 promotes angiogenesis in plaque. The mechanism is potentially that compound 48-80 increases the expressions of basic fibroblast growth factor mRNA and protein in plaque. Compound 48-80 enhances the expression of interleukin-1beta in plaque.

Animals ; Apolipoproteins E ; genetics ; Atherosclerosis ; chemically induced ; genetics ; metabolism ; pathology ; Carotid Arteries ; drug effects ; pathology ; Fluorescent Antibody Technique ; Immunohistochemistry ; In Situ Hybridization ; In Vitro Techniques ; Male ; Mast Cells ; drug effects ; metabolism ; Mice ; Mice, Knockout ; p-Methoxy-N-methylphenethylamine ; pharmacology

OBJECTIVETo investigate the mechanism of how curcumin improves pulmonary vascular remodeling associated with chronic pulmonary arterial hypertension.

METHODSThe model of chromic hypoxia hypercapniapulmoary remodeling was made. Twenty-four male rats were randomly divided into 4 groups (n = 6): group I (normoxia control group), group II (hypxia and hypercapnia model group), group II (disodium cromoglycate control group), group IV (curcumin treated group). The last 3 group rats were put in a hypoxia cabin where the concentrate of O2 was 8% - 11% and the concentrate of CO2 was 3% - 5%, for 8 h a day and lasting 4 w in total. Group III rats were intraperitoneally injected with disodium cromoglycate (20 mg/kg) and group IV rats were administrated with curcumin by gavage (150 mg/kg). The morphological changes of pulmonary vessel walls and the ultrastructure of mast cells were observed by the optics microscope and the transmission electron microscope. Mast cells and its degranulation state were measured by toluidine blue staining and immunohistochemistry. Data were expressed as means ± SD (standard deviation) and analyzed with SPSS17.0 software.

RESULTS(1) By optics microscopy observation, the value of WA/TA was significantly higher in II group than other groups (P < 0.05). (2) Electron microscope showed that the endothelial cells of pulmonary arterioles in III and IV group were near to I group and the proliferation of pulmonary arterial media smooth cell layer and collagen fibers in adventitia was much lighter than those in II group. The membrane of mast cells was more intact in I, III, IV group than II group. (3) The number of mast cells, the degranulation rate of master cells and the number of positive tryptase stained cells in II group were significantly more than those in other groups. (P < 0.05).

CONCLUSIONCurcumin may inhibit the remodeling of pulmonary vessel induced by chronic hypoxia hypercapnia by mast cell regulation.

Animals ; Cell Degranulation ; Curcumin ; pharmacology ; Hypercapnia ; physiopathology ; Hypertension, Pulmonary ; drug therapy ; Hypoxia ; physiopathology ; Lung ; pathology ; Male ; Mast Cells ; physiology ; ultrastructure ; Pulmonary Artery ; drug effects ; Rats ; Rats, Sprague-Dawley ; Vascular Remodeling ; drug effects

OBJECTIVECheongseoikki-tang (CIT, Korean), also called Qingshu Yiqi decoction () and Seisho-ekki-to (Japanese), is well known as an effective traditional combination of herbs for treating cardiovascular diseases. This study was to research its effects on bone marrow-derived mast cell (BMMC)-mediated allergy and inflammation mechanisms.

METHODSIn this study, the biological effect of Cheongseoikki-tang ethanol extract (CITE) was evaluated, focusing on its effects on the production of allergic mediators by phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187 (A23187)-stimulated BMMCs. These allergic mediators included interleukin-6 (IL-6), prostaglandin D2 (PGD2), leukotriene C4 (LTC4), and β-hexosaminidase (β-hex).

RESULTSOur data revealed that CITE inhibited the production of IL-6, PGD2, LTC4, and β-hex induced by PMA plus A23187 (P<0.05).

CONCLUSIONThese findings indicate that CITE has the potential for use in the treatment of allergy.

Animals ; Anti-Inflammatory Agents ; pharmacology ; therapeutic use ; Bone Marrow Cells ; pathology ; Calcimycin ; pharmacology ; Cell Degranulation ; drug effects ; Cell Survival ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Hypersensitivity ; drug therapy ; pathology ; Interleukin-6 ; secretion ; Leukotriene C4 ; pharmacology ; Male ; Mast Cells ; drug effects ; pathology ; physiology ; Mice ; Mice, Inbred BALB C ; Prostaglandin D2 ; biosynthesis ; Tetradecanoylphorbol Acetate ; pharmacology ; beta-N-Acetylhexosaminidases ; metabolism

OBJECTIVETo investigate the effect of sodium cromoglycate on experimental endometriosis in rats.

METHODSEndometriosis model was established in 36 unpregnant female SD rats by transplanting autologous fragments of endometrium to the inner surface of the abdominal wall. The endometriotic lesions were measured by a second laparotomy 2 weeks after surgery. Then the rats were randomly divided into four groups (n=8 in each group) to receive intraperitoneal injection of different doses of sodium cromoglycate for 2 weeks: high-dose group (20 mg·kg⁻¹·d⁻¹); low-dose group (10 mg·kg⁻¹·d⁻¹); the negative control group and the blank control group. The animals were sacrificed and the size of the lesions were measured. The endometriosis model of SD rats was identified by HE staining and immunohistochemical staining of keratin and vimentin. The total number of mast cells and their degranulation were measured by Toluidine blue staining; the concentrations of TNF-α in serum were measured by enzyme linked immunosorbent assay; the concentrations of estradiol in serum were measured by enzyme immunoassay; the expression of tryptase and nerve growth factor (NGF) were measured by immunohistochemical staining.

RESULTSThe number of activated mast cells (MC) by Toluidine blue staining in high-dose group was significantly lower than that in negative control group (P<0.05), and its ratio of degranulation/total number of MC was significantly lower than that in negative control group or blank control group (P<0.05). The serum TNF-α levels and tryptase expression in tissues in high-dose group were significantly lower than those in negative control group or blank control group (P<0.05). However, no significant difference in the size of endometriotic lesions and expression of NGF was found among groups (P>0.05).

CONCLUSIONSodium cromoglycate can stabilize mast cells from degranulation, which may relieve the clinical symptoms of endometriosis by reducing TNF-α and tryptase levels.

Animals ; Cromolyn Sodium ; pharmacology ; Disease Models, Animal ; Endometriosis ; drug therapy ; Endometrium ; pathology ; Female ; Mast Cells ; drug effects ; Nerve Growth Factor ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tryptases ; metabolism ; Tumor Necrosis Factor-alpha ; blood

AIMTo investigate the role of fexofenadine, a mast cell blocker, on semen quality in the treatment of infertile men.

METHODSThe study included 16 Turkish idiopathic infertile men with azoospermia or oligozoospermia who underwent testicular biopsy to examine mast cells containing tryptase. In all patients, a complete medical history, clinical examination, semen analysis and serum hormone assay were carried out. The biopsy specimens were immunohistochemically stained with antihuman tryptase for mast cells. The number of total mast cells per seminiferous tubule was calculated and recorded as mast cell index. The patients were divided into two groups according to their mast cell index: the higher (> or =1, n=9) and the lower (<1, n=7) index groups. Fexofenadine was administered orally at a dose of 180 mg/day for 4 to 9 months. Pre- and post-treatment semen parameters, including total motile sperm counts (TMC) were recorded and compared. Spontaneous pregnancies after the treatment were registered.

RESULTSThere was no statistically significant difference in TMC between the pre-treatment and post-treatment values in patients with higher and lower mast cell index (P> or =0.05). In both groups, nobody had a significant response to the treatment and there was no spontaneous pregnancy after the treatment.

CONCLUSIONAlthough testicular dysfunction is closely associated with increased number of testicular mast cells, fexofenadine, a mast cell blocker, appears not having any benefit in the treatment of Turkish infertile men with a significant increase in testicular mast cells.

Adult ; Biopsy, Needle ; Follicle Stimulating Hormone ; blood ; Histamine H1 Antagonists ; therapeutic use ; Humans ; Infertility, Male ; drug therapy ; pathology ; Male ; Mast Cells ; drug effects ; enzymology ; pathology ; Middle Aged ; Semen ; drug effects ; physiology ; Serine Endopeptidases ; metabolism ; Sperm Count ; Sperm Motility ; drug effects ; Terfenadine ; analogs & derivatives ; therapeutic use ; Testis ; anatomy & histology ; pathology ; Tryptases ; Turkey

PURPOSE: The purpose of this study was to evaluate the effects of essential oil on oxidative stress, immunity, and skin condition in atopic dermatitis (AD) induced mice. METHODS: This study was a 3x3 factorial design. Factors were oil type (Lavender, Thyme, and 2:1 mixture of lavender and thyme oil [blending oil]) and treatment period (0 day, 7 days, and 21 days). The samples were 45 mice with AD and randomly assigned to nine groups of five mice per group. The dependent variables such as superoxide radical, IgE, degranulated mast cells, and epidermal thickness were measured. Data were collected from February to April in 2014. Descriptive statistics, One-way ANOVA, Two-way ANOVA, and Tukey's HSD test were performed using the SPSS WIN 20.0 program. RESULTS: Dependent variables were not statistically significantly different by the three oil types (p >.05). Essential oils such as lavender, thyme, and blending oil were all effective in reducing AD symptoms and especially 2:1 blending oil were most effective. There were statistically significant differences by the three treatment periods in all dependent variables (p <.001). There were statistically significant interactions between oil types and treatment periods in all dependent variables (p <.01). For decreasing superoxide radical, degranulated mast cells, and epidermal thickness, 2:1 mixed oil should be applied for at least 21 days. Otherwise to reduce IgE, 2:1 mixed oil should be used for at least 7 days. CONCLUSION: These findings provide bases for developing effective interventions for AD patients to manage their AD symptoms.
Animals ; Dermatitis, Atopic/chemically induced/*drug therapy/pathology ; Disease Models, Animal ; *Immunity/drug effects ; Immunoglobulin E/blood ; Lavandula/*chemistry/metabolism ; Mast Cells/cytology/metabolism ; Mice ; Oils, Volatile/chemistry/pharmacology/therapeutic use ; *Oxidative Stress/drug effects ; Picryl Chloride/toxicity ; Plant Oils/chemistry/pharmacology/*therapeutic use ; Singlet Oxygen/metabolism ; Skin/drug effects/pathology ; Thymus Plant/*chemistry/metabolism

OBJECTIVETo study the role of tranilast in the pathogenesis of myocardiac fibrosis in viral myocarditis.

METHODSSeventy-two BALB/C mice were randomly divided into control, model and intervention groups (n=24 each). Mice in the model and intervention groups were infected with Coxsackievirus B3 to induce viral myocarditis. The intervention group was given with tranilast (200 mg/kg) by gavage until sacrifice for sampling, while the other two groups were administered with the same volume of normal saline. Cardiac tissues were obtained from 8 mice on 7, 14 and 28 days after modeling. The mast cell number was observed by toluidine blue staining and thionine staining. The cardiac tissues were stained with hematoxylin and eosin as well as masson trichrome to observe the pathological changes in cardiac tissues. The mRNA and protein expression of osteopontin and transforming growth factor-β1 was measured by RT-PCR and immunohistochemistry respectively.

RESULTSIn the model group, the mRNA and protein expression of osteopontin reached the highest level on the 7th day, decreasing from the 14th day, and became to the least on the 28th day; while the expression of TGF-β1 increased from the 7th day, reaching a peak on the 14th day, and decreased slightly on the 28th day. The mRNA and protein expression of TGF-β1 and OPN was lower in the intervention group than the model group (P<0.05), but higher than the control group (P<0.05). The expression of OPN mRNA was positively correlated to the number of mast cells.

CONCLUSIONSTranilast can reduce myocardial fibrosis by decreasing the number of mast cells, inhibiting the expression of TGF-β1 and OPN.

Animals ; Fibrosis ; Male ; Mast Cells ; drug effects ; Mice ; Mice, Inbred BALB C ; Myocarditis ; complications ; Myocardium ; pathology ; Osteopontin ; analysis ; genetics ; Transforming Growth Factor beta1 ; analysis ; genetics ; ortho-Aminobenzoates ; pharmacology ; therapeutic use