Okra polysaccharide-2 plays a vital role on the activation of RAW264.7 cells by TLR2/4-mediated signal transduction pathways
Okra polysaccharide-2 plays a vital role on the activation of RAW264.7 cells by TLR2/4-mediated signal transduction pathways
复制标题
黄秋葵多糖-2通过TLR2/4介导的信号转导途径对RAW264.7细胞的激活起着至关重要的作用
DOI：
10.1016/j.intimp.2020.106708
复制
发表时间：
2020-09-01
影响因子：
5.6
通讯作者：
Chen, Huricha
中科院分区：
文献类型：
--
作者：
Chen, Yun;Zhou, Ruigang;Chen, Huricha
黄秋葵多糖是黄秋葵的主要活性成分。并能有效刺激巨噬细胞的激活。但其免疫调节机制尚不清楚。因此，本研究旨在通过研究黄秋葵多糖2（RPS 2）对小鼠巨噬细胞Toll样受体（TLR）2/4介导的信号转导通路的影响，揭示其可能的作用机制。为了证实RPS-2是否通过TLR 2或TLR 4刺激巨噬细胞活化，在RPS-2处理前用TLR 2/4抑制剂预处理RAW 264. 7小鼠巨噬细胞1 h，然后检测NO、IL-10、TNF-α水平。说明TLR 2和TLR 4是RPS-2免疫调节作用的关键。然后通过Western blot分析RPS-2对NF-κ B B和MAPK信号通路的影响。结果显示RPS-2可诱导p65、I κ B α、p38、ERK 1/2和JNK的磷酸化。同时，特异性抑制剂降低了这些磷酸化水平以及NO、IL-10和TNF-α的量。综上所述，RPS-2通过NF-κ B和MAPK信号转导途径激活巨噬细胞。
Polysaccharide is the main active component of okra (Abelmoschus esculentus L.) and it can effectively stimulate the activation of macrophages. However, the immune regulatory mechanism is still not clear. Therefore, the present study aimed to reveal the possible mechanism by investigating the effect of okra polysaccharide-2 (RPS2) on Toll-like receptor (TLR) 2/4-mediated signal transduction pathways in RAW264.7 murine macrophage cells. In order to confirm whether RPS-2 stimulated macrophages activation via TLR2 or TLR4, RAW264.7 murine macrophage cells were pretreated with TLR2/4 inhibitors for 1 h before RPS-2 treatment, and then the NO, IL-10, TNF-alpha levels were tested. The results indicated that both TLR2 and TLR4 were the keys of immune regulatory effect of RPS-2. Afterwards, the effect of RPS-2 on NF-kappa B and MAPKs signaling pathways were studied by western blot analysis. It showed RPS-2 induced the phosphorylation of p65, I kappa B alpha, p38, ERK1/2 and JNK. At the same time, the specific inhibitors reduced these phosphorylation levels as well as NO, IL-10 and TNF-alpha amounts. In a word, RPS-2 activated macrophages by NF-kappa B and MAPKs signal transduction pathways.