Objective:To evaluate the effect of myricetin on ovalbumin(OVA)-induced allergic rhinitis in mice.Methods:Mice were sensitized and challenged using OVA(5%,500 mL)intraperitoneally and intranasally,respectively,on an a...Objective:To evaluate the effect of myricetin on ovalbumin(OVA)-induced allergic rhinitis in mice.Methods:Mice were sensitized and challenged using OVA(5%,500 mL)intraperitoneally and intranasally,respectively,on an alternative day for 14 days,followed by administration of myricetin(50,100,and 200 mg/kg)till day 21.Nasal symptoms,biochemical parameters,protein expressions,and histopathology were observed.Results:OVA-induced increased nasal symptoms including rubbing,sneezing,and discharge were significantly reduced by myricetin(100and 200 mg/kg)(P<0.05).Myricetin also protected against histamine challenge and attenuated elevated serum immunoglobulin E(IgE;total and OVA-specific),total IgG1,andβ-hexosaminidase levels,as well as leukotriene C4 and interleukins levels in nasal lavage fluid(P<0.05).Western blot analysis showed that myricetin significantly upregulated the protein expression of T-box expressed in T cells,while downregulating the protein expression of GATA binding protein 3,NF-κB,and IκB-α(P<0.05).Additionally,OVA-induced histopathological abberations in the nasal mucosa was markedly ameliorated by myricetin treatment(P<0.05).Conclusions:Myricetin exerts anti-allergic effects against OVAinduced allergic rhinitis via regulating Th1/Th2 balance.展开更多
Objective:To evaluate the therapeutic effect of Glycyrrhetinic Acid on cough variant asthma(CVA)mice and to investigate the possible mechanism in reducing lung inflammation.Methods:48 young female Balb/c mice were div...Objective:To evaluate the therapeutic effect of Glycyrrhetinic Acid on cough variant asthma(CVA)mice and to investigate the possible mechanism in reducing lung inflammation.Methods:48 young female Balb/c mice were divided into Control,CVA,Prednisone Acetate,Glycyrrhetinic Acid high-dose,Glycyrrhetinic Acid middle-dose and Glycyrrhetinic Acid lowdose groups randomly,with 8 mice in each group.The CVA mice model was established by ovalbumin(OVA)sensitization and OVA challenge,the animal asthma behavior was observed after drug administration,and the index of the lung of mice were recorded.The level of OVAsIgE in the bronchoalveolar lavage fluid(BALF)was tested by ELISA.The pathological changes of the lung tissue were observed by Hematoxylin and Eosin(H&E)staining.The protein expressions of T-bet,IFN-γ,Gata3,IL-4 and IL-13 in the lung tissue were determined by Western blot.Results:Compared with the CVA group,the index of lung of mice,the OVA-sIgE level in BALF and expression levels of Th2-related factor in the lung tissue of mice in Prednisone Acetate and Glycyrrhetinic Acid groups were significantly decreased(P<0.05 or P<0.01),the infiltration of inflammatory cells in the lung tissue was reduced,while expressions of Th1-related factor in the lung tissue was significantly increased(P<0.05 or P<0.01).Conclusion:Glycyrrhetinic acid has therapeutic effect on CVA mice,the underlying mechanism of Glycyrrhetinic acid alleviating lung impairment and airway inflammation may be associated with mediating the Th1/Th2 imbalance in the lung tissue.展开更多
文摘Objective:To evaluate the effect of myricetin on ovalbumin(OVA)-induced allergic rhinitis in mice.Methods:Mice were sensitized and challenged using OVA(5%,500 mL)intraperitoneally and intranasally,respectively,on an alternative day for 14 days,followed by administration of myricetin(50,100,and 200 mg/kg)till day 21.Nasal symptoms,biochemical parameters,protein expressions,and histopathology were observed.Results:OVA-induced increased nasal symptoms including rubbing,sneezing,and discharge were significantly reduced by myricetin(100and 200 mg/kg)(P<0.05).Myricetin also protected against histamine challenge and attenuated elevated serum immunoglobulin E(IgE;total and OVA-specific),total IgG1,andβ-hexosaminidase levels,as well as leukotriene C4 and interleukins levels in nasal lavage fluid(P<0.05).Western blot analysis showed that myricetin significantly upregulated the protein expression of T-box expressed in T cells,while downregulating the protein expression of GATA binding protein 3,NF-κB,and IκB-α(P<0.05).Additionally,OVA-induced histopathological abberations in the nasal mucosa was markedly ameliorated by myricetin treatment(P<0.05).Conclusions:Myricetin exerts anti-allergic effects against OVAinduced allergic rhinitis via regulating Th1/Th2 balance.
基金National Natural Science Foundation of China (No.81960887)Innovation Project of Guangxi Graduate Education (No.YCXJ2021119)。
文摘Objective:To evaluate the therapeutic effect of Glycyrrhetinic Acid on cough variant asthma(CVA)mice and to investigate the possible mechanism in reducing lung inflammation.Methods:48 young female Balb/c mice were divided into Control,CVA,Prednisone Acetate,Glycyrrhetinic Acid high-dose,Glycyrrhetinic Acid middle-dose and Glycyrrhetinic Acid lowdose groups randomly,with 8 mice in each group.The CVA mice model was established by ovalbumin(OVA)sensitization and OVA challenge,the animal asthma behavior was observed after drug administration,and the index of the lung of mice were recorded.The level of OVAsIgE in the bronchoalveolar lavage fluid(BALF)was tested by ELISA.The pathological changes of the lung tissue were observed by Hematoxylin and Eosin(H&E)staining.The protein expressions of T-bet,IFN-γ,Gata3,IL-4 and IL-13 in the lung tissue were determined by Western blot.Results:Compared with the CVA group,the index of lung of mice,the OVA-sIgE level in BALF and expression levels of Th2-related factor in the lung tissue of mice in Prednisone Acetate and Glycyrrhetinic Acid groups were significantly decreased(P<0.05 or P<0.01),the infiltration of inflammatory cells in the lung tissue was reduced,while expressions of Th1-related factor in the lung tissue was significantly increased(P<0.05 or P<0.01).Conclusion:Glycyrrhetinic acid has therapeutic effect on CVA mice,the underlying mechanism of Glycyrrhetinic acid alleviating lung impairment and airway inflammation may be associated with mediating the Th1/Th2 imbalance in the lung tissue.
