Sun Jing, Wu Jinfeng, Xu Changqing, Luo Qingli, Li Bei, Dong Jingcheng
Department of Integrative Medicine, Huashan Hospital, Fudan University, 12 Middle Urumqi Road, Shanghai 200040, China.
Department of Dermatology, Huashan Hospital, Fudan University, 12 Middle Urumqi Road, Shanghai 200040, China.
Int Immunopharmacol. 2015 Jan;24(1):88-94. doi: 10.1016/j.intimp.2014.11.016. Epub 2014 Nov 26.
Paeoniflorin (PF), one of the major active ingredients of Chinese peony, has demonstrated anti-inflammatory and immunoregulatory effects. However, it has remained unclear whether PF treatment can inhibit allergic inflammation in asthma. In this study, we evaluated the effects of PF on pulmonary function and airway inflammation in asthmatic mice. The allergic asthma models were established in BALB/c mice. The mice were sensitized and challenged with ovalbumin. Airway hyperresponsiveness was detected by direct airway resistance analysis. Lung tissues were examined for inflammatory cell infiltration. IL-5, IL-13, IL-17, and eotaxin in bronchoalveolar lavage fluid (BALF) and their mRNA expression in lung tissue were examined by ELISA and realtime PCR, respectively. The total IgE level in serum was measured by ELISA. The protein expression of p-ERK and p-JNK was detected by western blot. Our data showed that PF oral administration significantly reduced airway hyperresponsiveness to aerosolized methacholine and decreased IL-5, IL-13, IL-17 and eotaxin levels in the BALF, and decreased IgE level in the serum. Histological studies showed that PF administration markedly decreased inflammatory infiltration. Similarly, treatment with PF significantly inhibited IL-5, IL-13, IL-17 and eotaxin mRNA expression in lung tissues. The protein expression levels of p-ERK and p-JNK were substantially decreased after oral administration of PF. In summary, PF displayed anti-inflammatory effects in the OVA-induced asthmatic model by decreasing the expression of IL-5, IL-13, IL-17 and eotaxin. These effects were mediated at least partially by inhibiting the activation of MAPK pathway.
芍药苷（PF）是中药芍药的主要活性成分之一，已显示出抗炎和免疫调节作用。然而，PF治疗是否能抑制哮喘中的过敏性炎症仍不清楚。在本研究中，我们评估了PF对哮喘小鼠肺功能和气道炎症的影响。在BALB/c小鼠中建立过敏性哮喘模型。用卵清蛋白对小鼠进行致敏和激发。通过直接气道阻力分析检测气道高反应性。检查肺组织中的炎性细胞浸润。分别通过ELISA和实时PCR检测支气管肺泡灌洗液（BALF）中的IL-5、IL-13、IL-17和嗜酸性粒细胞趋化因子及其在肺组织中的mRNA表达。通过ELISA测量血清中的总IgE水平。通过蛋白质印迹法检测p-ERK和p-JNK的蛋白表达。我们的数据表明，口服PF可显著降低对雾化乙酰甲胆碱的气道高反应性，并降低BALF中IL-5、IL-13、IL-17和嗜酸性粒细胞趋化因子水平，以及血清中的IgE水平。组织学研究表明，给予PF可显著减少炎性浸润。同样，PF治疗可显著抑制肺组织中IL-5、IL-13、IL-17和嗜酸性粒细胞趋化因子mRNA的表达。口服PF后，p-ERK和p-JNK的蛋白表达水平显著降低。总之，PF通过降低IL-5、IL-13、IL-17和嗜酸性粒细胞趋化因子的表达在OVA诱导的哮喘模型中显示出抗炎作用。这些作用至少部分是通过抑制MAPK途径的激活介导的。
