Kee Ji-Ye, Inujima Akiko, Andoh Tsugunobu, Tanaka Ken, Li Feng, Kuraishi Yasushi, Sakurai Hiroaki, Shibahara Naotoshi, Saiki Ikuo, Koizumi Keiichi
Division of Pathogenic Biochemistry, Graduate School Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, 930-0194, Japan.
J Nat Med. 2015 Apr;69(2):209-17. doi: 10.1007/s11418-014-0880-6. Epub 2014 Dec 17.
Moutan Cortex and its major compounds have been shown to possess various biological activities, including anti-inflammatory properties. However, the effects of Moutan Cortex aqueous fraction (MCA) and its molecular mechanisms have yet to be elucidated. In this study, we attempted to evaluate the effects of MCA on mast cell-mediated allergy inflammation in vitro and in vivo compared with major Moutan Cortex compounds. Thus, we examined the anti-inflammatory effects of a water extract of Moutan Cortex by comparing the inhibition of β-hexosaminadase and tumor necrosis factor-α (TNF-α) release in an aqueous fraction with other major compounds of Moutan Cortex. The inhibitory mechanism of MCA was investigated by western blotting in IgE-mediated DNP-BSA-stimulated RBL-2H3 cells. We confirmed the pharmacological effects of MCA on compound 48/80-induced allergic reactions in a mouse model by assessing scratching behavior and passive cutaneous anaphylaxis (PCA)-like reaction. Consequently, MCA inhibited IgE-mediated DNP-BSA-induced β-hexosaminadase and TNF-α release via inactivation of p38, ERK, Akt, and NF-κB in RBL-2H3 cells. MCA reduced compound 48/80-induced PCA reaction and scratching behavior in mice. This inhibitory effect of MCA is more potent than major compounds of Moutan Cortex. In conclusion, our results suggest that MCA has more potential in the treatment of allergic inflammatory diseases compared to other major compounds of Moutan Cortex.
牡丹皮及其主要化合物已被证明具有多种生物活性,包括抗炎特性。然而,牡丹皮水提物(MCA)的作用及其分子机制尚未阐明。在本研究中,我们试图在体外和体内评估MCA与牡丹皮主要化合物相比对肥大细胞介导的过敏性炎症的影响。因此,我们通过比较水提物中β-己糖胺酶和肿瘤坏死因子-α(TNF-α)释放的抑制情况与牡丹皮其他主要化合物,来研究牡丹皮水提取物的抗炎作用。通过蛋白质印迹法在IgE介导的DNP-BSA刺激的RBL-2H3细胞中研究MCA的抑制机制。我们通过评估抓挠行为和被动皮肤过敏反应(PCA)样反应,在小鼠模型中证实了MCA对化合物48/80诱导的过敏反应的药理作用。结果,MCA通过使RBL-2H3细胞中的p38、ERK、Akt和NF-κB失活,抑制了IgE介导的DNP-BSA诱导的β-己糖胺酶和TNF-α释放。MCA减少了化合物48/80诱导的小鼠PCA反应和抓挠行为。MCA的这种抑制作用比牡丹皮的主要化合物更强。总之,我们的结果表明,与牡丹皮的其他主要化合物相比,MCA在治疗过敏性炎症疾病方面具有更大的潜力。