Si Shen Wan Regulates Phospholipase Cγ-1 and PI3K/Akt Signal in Colonic Mucosa from Rats with Colitis.
Si Shen Wan Regulates Phospholipase Cγ-1 and PI3K/Akt Signal in Colonic Mucosa from Rats with Colitis.
复制标题
DOI：
10.1155/2015/392405
复制
发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Zhao HM
中科院分区：
文献类型：
--
作者：
Liu DY;Xu R;Huang MF;Huang HY;Wang X;Zou Y;Yue HY;Zhao HM
本研究通过观察结肠炎大鼠结肠黏膜磷脂酶C-γ-1(PLC-γ-1)和PI3K/Akt信号的激活情况，探讨四神丸抑制肠上皮细胞凋亡的可能途径。用2，4，6-三硝基苯磺酸(TNBS)诱导SD大鼠实验性结肠炎。免疫印迹结果显示，三七总皂甙致大鼠结肠损伤后，肠粘膜组织中PI3K、p-Akt、IL-23水平升高，PLC-γ-1、HSP70水平降低。同时，酶联免疫吸附试验结果显示，肿瘤坏死因子刺激后，IL-2、IL-6和IL-17浓度升高，转化生长因子-β水平下降。治疗7d后，PI3K、p-Akt的表达和IL-2、IL-6、IL-17、IL-23的分泌显著减少，而PLC-γ-1、HSP70和转化生长因子-β的活性显著增强。我们以前的研究已经证明，SSW通过抑制肠上皮细胞的凋亡来修复结肠粘膜溃疡。本研究表明，四逆汤抑制内皮细胞凋亡的作用可能是通过激活PLC-γ1，抑制PI3K/Akt信号通路实现的。
The present study explored the feasible pathway of Si Shen Wan (SSW) in inhibiting apoptosis of intestinal epithelial cells (IECs) by observing activation of phospholipase Cγ-1 (PLC-γ1) and PI3K/Akt signal in colonic mucosa from rats with colitis. Experimental colitis was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) in the Sprague-Dawley rats. After SSW was administrated for 7 days after TNBS infusion, western blot showed an increment in levels of PI3K, p-Akt, and IL-23 and a decrement in levels of PLC-γ1 and HSP70 in colonic mucosal injury induced by TNBS. Meanwhile, assessments by ELISA revealed an increment in concentrations of IL-2, IL-6, and IL-17 and a reduction in level of TGF-β after TNBS challenge. Impressively, treatment with SSW for 7 days significantly attenuated the expressions of PI3K and p-Akt and the secretion of IL-2, IL-6, IL-17, and IL-23 and promoted the activation of PLC-γ1, HSP70, and TGF-β. Our previous studies had demonstrated that SSW restored colonic mucosal ulcers by inhibiting apoptosis of IECs. The present study demonstrated that the effect of SSW on inhibiting apoptosis of IECs was realized probably by activation of PLC-γ1 and suppression of PI3K/Akt signal pathway.