ABSTRACT
OBJECTIVE To study the intervention effects and mechanism of Compound yu ’e nasal drops on ovalbumin induced allergic rhinitis in rats . METHODS The allergic rhinitis model of rat was induced with ovalbumin . Model rats were randomly divided into model group ,triamcinolone acetonide group (positive control ,0.026 mg/kg),Compound yu ’e nasal drops high-dose,medium-dose and low -dose groups (134.4、67.2、33.6 mg/kg),12 rats in each group . Another blank control group was set. Except for blank control group ,the corresponding drugs were given by nasal drip twice a day for 14 days. One hour after last administration,the nasal symptom scores of rats were recorded ;the levels of serum immunoglobulin E (IgE),interleukin-2(IL- 2),IL-13 and tumor necrosis factor -α(TNF-α)were measured by enzyme -linked immunosorbent assay . The changes of nasal mucosa in rat were observed by HE staining . The expressions of TNF -α,IL-2 and IL -13 in nasal mucosa were detected by Western blot. RESULTS Compared with blank control group ,nasal symptom score and the levels of serum IgE ,IL-2,IL-13,TNF-α in model group were increased significantly (P<0.01);obvious pathological injury was found in nasal mucosa ,and the expressions of TNF -α,IL-2 and IL -13 protein were increased significantly (P<0.01). Compared with model group ,Compound yu ’e nasal drops significantly reduced the nasal symptom score ,the levels of serum IgE ,IL-2,IL-13,TNF-α to different extents ,improved pathological injury of nasal mucosa and significantly inhibited the expressions of TNF -α,IL-2 and IL -13 protein(P<0.05 or P< 0.01). CONCLUSIONS Compound yu ’e nasal drops play significant effects against allergic rhinitis in rats by regulating the balance of t ype 1 helper T cells/type 2 helper T cells ,balancing and inhibiting the secretion of inflammatory cytokines .
ABSTRACT
PURPOSE: Activated leukocyte cell adhesion molecule (ALCAM), a member of the immunoglobulin superfamily, is highly expressed on dendritic cells. ALCAM and its receptor CD6 are co-stimulatory molecules in the immunological synapse; their interaction is required for T cell activation. While atopic dermatitis (AD) is recognized as a T helper 2 (Th2)-mediated allergic disease, the role of ALCAM in its pathogenesis is unclear. METHODS: ALCAM levels were measured in the serum of AD patients and AD-induced murine model by ovalbumin treatment. We next investigated transepidermal water loss, clinical score, Th2-immune responses, skin barrier gene expression and T-cell activation using wild-type (WT) and ALCAM deficiency mice. An oxazolone-induced AD-like model was also established and analyzed using WT- and ALCAM-deficient mice. RESULTS: We found that serum ALCAM levels were elevated in pediatric AD patients as well as WT AD mice, whereas Th2-type cytokine production and AD symptoms were suppressed in ALCAM-deficient mice. In addition, CD4+ effector T-cell counts in murine skin and skin-draining lymph nodes were lower in ALCAM-deficient mice than in their WT counterparts. ALCAM deficiency was also linked to higher expression of skin barrier genes and number of lamellar bodies. CONCLUSIONS: These findings indicate that ALCAM may contribute to AD pathogenesis by meditating a Th2-dominant immune response and disrupting the barrier function of the skin.