Dun Yaoyan, Liu Min, Chen Jing, Peng Danli, Zhao Haixia, Zhou Zhiyong, Wang Ting, Liu Chaoqi, Guo Yuhui, Zhang Changcheng, Yuan Ding
Medical College of China Three Gorges University, Yichang, China.
Renhe Hospital of China Three Gorges University, Yichang, China.
J Ginseng Res. 2018 Jan;42(1):50-56. doi: 10.1016/j.jgr.2016.12.011. Epub 2016 Dec 31.
Saponins from (SPJ) are the most abundant and main active components of , which replaces ginseng roots in treatment for many kinds of diseases in the minority ethnic group in China. Our previous studies have demonstrated that SPJ has the effects of anti-inflammation through the mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways. The present study was designed to investigate whether SPJ can modulate intestinal tight junction barrier in aging rats and further to explore the potential mechanism.
Aging rats had been treated with different doses (10 mg/kg, 30 mg/kg, and 60 mg/kg) of SPJ for 6 mo since they were 18 mo old. After the rats were euthanized, the colonic samples were harvested. Levels of tight junctions (claudin-1 and occludin) were determined by immunohistochemical staining. Levels of proinflammatory cytokines (interleukin-1β and tumor necrosis factor-α) were examined by Western blot. NF-κB and phosphorylation of MAPK signaling pathways were also determined by Western blot.
We found that SPJ increased the expression of the tight junction proteins claudin-1 and occludin in the colon of aging rats. Treatment with SPJ decreased the levels of interleukin-1β and tumor necrosis factor-α, reduced the phosphorylation of three MAPK isoforms, and inhibited the expression of NF-κB in the colon of aging rats.
The studies demonstrated that SPJ modulates the damage of intestinal epithelial tight junction in aging rats, inhibits inflammation, and downregulates the phosphorylation of the MAPK and NF-κB signaling pathways.
刺五加皂苷(SPJ)是刺五加中含量最为丰富且主要的活性成分,在中国少数民族中,刺五加已取代人参根用于多种疾病的治疗。我们之前的研究表明,SPJ可通过丝裂原活化蛋白激酶(MAPK)和核因子κB(NF-κB)信号通路发挥抗炎作用。本研究旨在探讨SPJ是否能调节衰老大鼠的肠道紧密连接屏障,并进一步探究其潜在机制。
18月龄的衰老大鼠自该月龄起接受不同剂量(10毫克/千克、30毫克/千克和60毫克/千克)的SPJ治疗,为期6个月。大鼠处死后,采集结肠样本。通过免疫组织化学染色测定紧密连接蛋白(claudin-1和occludin)的水平。通过蛋白质免疫印迹法检测促炎细胞因子(白细胞介素-1β和肿瘤坏死因子-α)的水平。同时,也通过蛋白质免疫印迹法测定NF-κB和MAPK信号通路的磷酸化水平。
我们发现,SPJ可增加衰老大鼠结肠中紧密连接蛋白claudin-1和occludin的表达。SPJ治疗可降低白细胞介素-1β和肿瘤坏死因子-α的水平,减少三种MAPK亚型的磷酸化,并抑制衰老大鼠结肠中NF-κB的表达。
这些研究表明,SPJ可调节衰老大鼠肠道上皮紧密连接的损伤,抑制炎症反应,并下调MAPK和NF-κB信号通路的磷酸化水平。