Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama, 930-0194, Japan.
Sekolah Tinggi Ilmu Farmasi Makassar, Perintis Kemerdekaan Street Km 13.7, Makassar, 90242, Indonesia.
BMC Complement Med Ther. 2021 Apr 9;21(1):115. doi: 10.1186/s12906-021-03291-5.
Morus alba L. bark has been widely used in traditional medicine for treating several inflammatory diseases, such as hypertension, diabetes mellitus and coughing; however, the molecular mechanisms underlying its anti-inflammatory effects are not well understood.
We examined the effects of an extract of Morus alba L. bark (MabE) on Toll-like receptor (TLR) ligand-induced activation of RAW264.7 macrophages using a luciferase reporter assay and immunoassays. For the in vivo experiment, we used an imiquimod-induced ear edema model to examine the anti-inflammatory effects of MabE.
MabE inhibited the TLR ligand-induced activation of NF-κB in RAW264.7 cells without affecting their viability. Consistent with the inhibition of NF-κB activation, MabE also inhibited the production of IL-6 and IL-1β from TLR ligand-treated RAW264.7 cells. In vivo MabE treatment inhibited the ear swelling of IMQ-treated mice, in addition to the mRNA expression of IL-17A, IL-1β and COX-2. The increases in splenic γδT cells in IMQ-treated mice and the production of IL-17A from splenocytes were significantly inhibited by MabE treatment.
Our study suggests that the anti-inflammatory effects of MabE on the activation of the macrophage cell line RAW246.7 by TLRs and IMQ-induced ear edema are through the inhibition of NF-κB activation and IL-17A-producing γδT cells, respectively.
桑白皮在传统医学中被广泛用于治疗高血压、糖尿病和咳嗽等多种炎症性疾病；然而，其抗炎作用的分子机制尚不清楚。
我们使用荧光素酶报告基因检测和免疫检测法，研究了桑白皮提取物（MabE）对 Toll 样受体（TLR）配体诱导 RAW264.7 巨噬细胞激活的影响。在体内实验中，我们使用咪喹莫特诱导的耳肿胀模型来研究 MabE 的抗炎作用。
MabE 抑制 TLR 配体诱导的 RAW264.7 细胞中 NF-κB 的激活，而不影响其活力。与 NF-κB 激活的抑制一致，MabE 还抑制了 TLR 配体处理的 RAW264.7 细胞中 IL-6 和 IL-1β 的产生。体内 MabE 处理抑制了 IMQ 处理小鼠的耳部肿胀，以及 IL-17A、IL-1β 和 COX-2 的 mRNA 表达。MabE 处理还显著抑制了 IMQ 处理小鼠脾脏 γδT 细胞的增加和脾细胞中 IL-17A 的产生。
我们的研究表明，MabE 对 TLR 诱导的 RAW246.7 巨噬细胞系激活和 IMQ 诱导的耳肿胀的抗炎作用分别是通过抑制 NF-κB 激活和产生 IL-17A 的 γδT 细胞。
