Isorhamnetin inhibits ovalbumin-induced pulmonary inflammation in asthmatic mice |
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Authors: | ZHU Min ZHAO Li-min WANG Pei XIAO Ya-li |
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Institution: | [Department of Respiratory and Critical Care Medicine, Henan Provincial People's Hospital (People's Hospital of Zhengzhou University), Zhengzhou 450003, China] |
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Abstract: | AIM To investigate the effect of isorhamnetin on pulmonary inflammation in asthmatic mice and to analyze its primary mechanism. METHODS BALB/c mice were randomly divided into normal control group, asthma model group, isorhamnetin low-dose (50 mg/kg) treatment group and isorhamnetin high-dose (150 mg/kg) treatment group. Ovalbumin (OVA) was used to establish a mouse asthma model. HE staining and PAS staining were used to observe the pathological changes of lung tissue. The contents of cysteinyl leukotriene1 (CysLT1), cystelinyl leukotriene receptor 1 (CysLTR1), interleukin-4 (IL-4), IL-5, IL-13 and tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid (BALF) were measured by ELISA. The expression of nuclear factor of activated T cells 4(NFATc4) in lung tissue was detected by immunohistochemical staining. The protein expression of NFATc4, intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was determined by Western blot. RESULTS Isorhamnetin improved histopathological changes in OVA-induced asthma model mice, reduced the contents of CysLT1, CysLTR1, IL-4, IL-5, IL-13 and TNF-α in BALF, and reduced NFATc4, ICAM-1 and VCAM-1 expression in lung tissue (P<0.05). CONCLUSION Isorhamnetin inhibits the inflammatory response of lung tissue in asthmatic model mice, and the mechanism may be related to the inhibition of the calcineurin/NFATc4 signaling pathway. |
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Keywords: | Isorhamnetin Asthma Inflammatory response Calcineurin/NFATc4 signaling pathway |
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