Picroside Ⅱ Reduces Inflammation in Allergic Asthma Rats by Inhibiting NF-κB/MAPK Signaling Pathway
Objective:To investigate the effect of Picroside Ⅱ on inflammatory response and NF-κB/MAPK signaling pathway in rats with allergic asthma.Methods:The rat model of allergic asthma was established by ovalbumin sensitization and aerosol inhalation.The rats with successful modeling were randomly divided into model group,Picroside Ⅱ group and activator group(C16-PAF group),and the healthy rats without modeling were selected as control group,with 8 rats in each group.After the modeling,the rats in the Picroside Ⅱgroup(C16-PAF group)were given Picroside Ⅱ at an intragastric dose of 80 mg/kg daily,and the rats in the C16-PAF group were given a daily intragastric dose of 80 mg/kg Picroside Ⅱ and 50 μL of C16-PAF solution(MAPK activator)at a concentration of 4 μmol/L,and the drug was administered for 14 days for each group.The rats in the model group were given the same amount of normal saline by intra-gastric administration,while the rats in the control group were given the same amount of normal saline by intraperitoneal injection,atom-ization inhalation and intragastric administration at the same period of modeling and administration,respectively.The rat lung function index of FVC,PEF,FEV0.3 and FEV0.3/FVC were recorded by whole body plethysmography.The pathological changes of rat lung were detected by hematoxylin-eosin(HE)staining.The counts of leukocytes,lymphocytes,eosinophils and neutrophils in the bronchoalveolar lavage fluid(BALF)of rats were analyzed by Reye's staining.The levels of OVA-IgE and ET-1 in serum and the levels of inflammatory factors IL-4,IL-5,IL-13 and IFN-γ in BALF were detected by ELISA.The expression levels ofp-p38MAPK and p-NF-κBp65 in rat lung tissue were analyzed by immunohistochemical staining.The expression level of protein in NF-κB/MAPK signaling pathway were detected by Western blot.Results:In the control group,the basic structure and morphology of rat lung tissue were normal,and no inflammatory cell infiltration and tissue lesion were observed.In the model group,there was obvious inflammatory cell infiltration in rat lung tissue,and the wall of bronchial cavity was thickened,the lumen was shrunk,and the wall of alveolar cavity was thickened and severely dam-aged.The infiltration of lung inflammatory cells and the damage of alveolar and bronchial structures were significantly improved in the Picroside Ⅱ group.The injury of lung tissue in the C16-PAF group was similar to that in the model group,but the severity was slightly reduced.Compared with control group,the values of FVC,FEV0.3,FEV0.3/FVC and PEF in model group were decreased(P＜0.05),and the counts of lymphocytes,eosinophils,neutrophils,white blood cells,IL-4,IL-5 and IL-13 in BALF were increased(P＜0.05).The levels of IFN-y in BALF were decreased(P＜0.05),IgE and ET-1 levels in serum were increased(P＜0.05),and the expression levels of p-NF-KBp65 and p-p38MAPK protein in rat lung tissue were increased(P＜0.05).Compared with model group,the values of FVC,FEV0.3,FEV0.3/FVC and PEF in Picroside Ⅱ group were increased(P＜0.05),and the counts of lymphocytes,eosinophils,neutrophils,white blood cells,IL-4,IL-5 and IL-13 in BALF group were decreased(P＜0.05).The level of IFN-y in BALF was increased(P＜0.05),IgE and ET-1 levels in serum were decreased(P＜0.05),and the expression levels of p-NF-KBp65 and p-p38MAPK in rat lung tissue were decreased(P＜0.05).Compared with Picroside Ⅱ group,the values of FVC,FEV0.3,FEV0.3/FVC and PEF in C16-PAF group were decreased(P＜0.05),and the counts of lymphocytes,eosinophils,neutrophils,white blood cell,IL-4,IL-5 and IL-13 in BALF were increased(P＜0.05).The level of IFN-y in BALF was decreased(P＜0.05),IgE and ET-1 levels in serum were increased(P＜0.05),and the expression levels of p-NF-KBp65 and p-p38MAPK in rat lung tissue were increased(P＜0.05).Compared with the model group,there was no significant difference in all indexes in the C16-PAF group(P＞0.05).Conclusion:Picroside Ⅱ may reduce the inflammatory process of asthmatic rats by inhibiting NF-κB/MAPK signaling pathway.
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