[The effect of desloratadine on the TXB2 and leukotrienes levels in the nasal lavage fluid of allergic rhinitis animal model].

OBJECTIVE: To observe the thromboxane (TX)B2 and cysteinyl leukotrienes (LTs) levels in the nasal lavage fluid of allergic rhinitis model and to observe the effect of desloratadine on the mediators. METHOD: In the positive control group, 8-12 week old male or female guinea pigs were intranasal sensitized and challenged with ovalbumin solution. The antihistamine treatment group was treated with desloratadine and the negative control group was sham-sensitized and sham-challenged. The nasal lavage fluid of each group was collected 5 hours after challenge and the levels of TXB2 and LTs in the nasal lavage fluid were measured. RESULT: In the positive control group, the TXB2 and LTs levels were the highest of the three groups and the desloratadine treated group had lower level (P < 0.05 and P < 0.01). The negative control showed the lowest level. CONCLUSION: Our study demonstrated that in this model of allergic rhinitis, the levels of TXB2 and LTs in nasal lavage fluid increased dominantly after allergen challenge and desloratadine could inhibit the release of TXB2 and LTs, which implied that the therapeutic mechanism of desloratadine might contribute to the inhibitory effect on TXB2 and LTs production or release in allergic rhinitis subjects.

[The immunohistochemical observations of NOS in the nasal mucosa of allergic rhinitis animal model of guinea pigs].

OBJECTIVE: To study the immunoreactivity and distribution of both iNOS and eNOS isoforms, and observe the effect of desloratadine on them. METHOD: The guinea pigs were sensitized and challenged followed by harvest of their nasal tissue for immunohistochemical staining. The slides images were semiquantitatively analyzed and compared with the desloratadine treated group and negative control group. RESULT: Both iNOS and eNOS were positively stained in each group. The immunoreactivity of iNOS had no significant difference between groups (P > 0.05), but eNOS had stronger immunoreactivity in the model group and the desloratadine treated group when compared with the negative control group (P < 0.01 and P < 0.05). In addition to the distribution area of iNOS, eNOS was also positive stained in the goblet cells. Desloratadine had no influence on iNOS and eNOS immunoreactivity. CONCLUSION: eNOS might play a more important role than iNOS in regulating the NO level of the nasal tissue of the guinea pigs suffered from allergic rhinitis, and desloratadine had no involvement in regulating the expression of iNOS and eNOS.

[Effects of budesonide, desloratadine and dexamethasone on interleukine-4 release and expression from human mast cell line].

OBJECTIVE: Since human mast cell is an important source of cytokines, it is of importance to understand the effects of anti-allergic drugs on cytokines modulation in mast cells. In the present study, we aimed at observing whether IL-4 could be released from human mast cell line (HMC-1) after the stimulation of PMA + A23187, and the effects of systemic glucocorticosteroid, dexamethasone, topical glucocorticosteroid, budesonide and H1 antagonist, desloratadine on IL-4 release and mRNA expression. METHODS: HMC-1 was stimulated with 25 ng/ml phorbol 12-myristate 13-acetate (PMA) and 2.5 x 10(-7) mol/L ionomycin (A23187) and cultured for 6 hours, 12 hours and 24 hours respectively in the presence or absence of 10(-6)-10(-10) mol/L concentrations of test drugs. Culture supernatants were collected and the levels of IL-4 were assayed by enzyme-linked immunosorbent assays (ELISA). The mRNA expression of IL-4 was measured by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: HMC-1 expressed IL-4 mRNA and the resulting protein production of IL-4 released after being stimulated with PMA plus A23187. Dexamethasone, budesonide and desloratadine had potent inhibitory effect on IL-4 release at any concentrations and time points, with significant deference (P < 0.05) compared to the control cells. The inhibitory effect did not show time-dependent and concentration-dependent manner. Desloratadine and budesonide showed neither up-regulatory nor down-regulatory effects on IL-4 mRNA expression at the test concentrations, however, desloratadine could down-regulate IL-4 mRNA expression. CONCLUSIONS: HMC-1 could express and produce IL4 after stimulation. Dexamethasone, budesonide and desloratadine all had inhibitory effects on IL-4 release from HMC-1. In addition, desloratadine could also inhibit the IL-4 mRNA expression.