The purpose of this research is to evaluate the effect of Mahaenggamseok-tang-gagambang (MGTG) on airway hyper- responsiveness (AHR), immune cells, cytokines and lung tissue in OVA-induced asthmatic mice. C57BL/6 mice were injected, inhaled and sprayed with OVA for 12 weeks (3times a week) for asthma sensitization and challenge. Two experimental groups were treated with different concentrations of MGTG (400 ㎎/㎏ and 200 ㎎/㎏) extract and cyclosporin A (10 ㎎/㎏) for the later 8 weeks. Enhanced pause (Penh) levels were measured by whole body plethysmography. Immune cells were analyzed by flow cytometer in peripheral blood monocyte cell (PBMC) and lung cells. The IL-1b, IL-12, IFN-γ, OVA-IgE, IL-4, IL-5, TNF-α were analyzed by ELISA kit in serum and splenocyte+a-cCD3/a-CD28. Enhanced pause (Penh) levels of the MGTG groups (400 ㎎/㎏ and 200 ㎎/㎏) were decreased significantly compared with that of control group. The numbers of MGTG groups (400 ㎎/㎏ and 200 ㎎/㎏) on lung total cells were decreased significantly compared with that of control group. The numbers of MGTG groups (400 ㎎/㎏ and 200 ㎎/㎏) on CD3+/CD69+, B220+/CD22+, B220+/CD23+, B220+/IgE+, CCR3+ cells were decreased significantly compared with that of control group. The number of MGTG group (400 ㎎/㎏) on CD3+/CD49b+ cells was decreased significantly compared with that of control group. The level of MGTG groups (400 ㎎/㎏ and 200 ㎎/㎏) on IL-4, IL-5, IL-12, TNF-α, OVA-IgE were decreased significantly compared with that of control group. The level of MGTG group (400 ㎎/㎏) on IL-1b, IL-13, OVA-IgE were decreased significantly compared with that of control group. These results demonstrate that MGTG could be a desirable alternative therapy for allergic asthma by inhibiting the expression of immune cells, the activation of inflammatory mediator.
The purpose of this research is to evaluate the effect of Mahaenggamseok-tang-gagambang (MGTG) on airway hyper- responsiveness (AHR), immune cells, cytokines and lung tissue in OVA-induced asthmatic mice. C57BL/6 mice were injected, inhaled and sprayed with OVA for 12 weeks (3times a week) for asthma sensitization and challenge. Two experimental groups were treated with different concentrations of MGTG (400 ㎎/㎏ and 200 ㎎/㎏) extract and cyclosporin A (10 ㎎/㎏) for the later 8 weeks. Enhanced pause (Penh) levels were measured by whole body plethysmography. Immune cells were analyzed by flow cytometer in peripheral blood monocyte cell (PBMC) and lung cells. The IL-1b, IL-12, IFN-γ, OVA-IgE, IL-4, IL-5, TNF-α were analyzed by ELISA kit in serum and splenocyte+a-cCD3/a-CD28. Enhanced pause (Penh) levels of the MGTG groups (400 ㎎/㎏ and 200 ㎎/㎏) were decreased significantly compared with that of control group. The numbers of MGTG groups (400 ㎎/㎏ and 200 ㎎/㎏) on lung total cells were decreased significantly compared with that of control group. The numbers of MGTG groups (400 ㎎/㎏ and 200 ㎎/㎏) on CD3+/CD69+, B220+/CD22+, B220+/CD23+, B220+/IgE+, CCR3+ cells were decreased significantly compared with that of control group. The number of MGTG group (400 ㎎/㎏) on CD3+/CD49b+ cells was decreased significantly compared with that of control group. The level of MGTG groups (400 ㎎/㎏ and 200 ㎎/㎏) on IL-4, IL-5, IL-12, TNF-α, OVA-IgE were decreased significantly compared with that of control group. The level of MGTG group (400 ㎎/㎏) on IL-1b, IL-13, OVA-IgE were decreased significantly compared with that of control group. These results demonstrate that MGTG could be a desirable alternative therapy for allergic asthma by inhibiting the expression of immune cells, the activation of inflammatory mediator.
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