Xie Yunjie, Zhang Haitao, Zhang Yang, Wang Chong, Duan Deyi, Wang Zheng
Cell Physiol Biochem. 2018;49(4):1380-1388. doi: 10.1159/000493415. Epub 2018 Sep 11.
BACKGROUND/AIMS: Chinese angelica polysaccharide (CAP) is the main effective ingredient of angelica sinensis and exerts anti-inflammatory and anti-apoptotic effects on many diseases. This study aimed to explore the pharmacological potential of CAP on spinal cord injury (SCI).
PC12 cells were pretreated by CAP and were subjected to LPS. Transfection was performed to alter the expression of COX-1. Cell viability and apoptotic cell rate were measured by CCK-8 and flow cytometry respectively. qRT-PCR and western blot analysis were performed to assess the expression changes of pro-inflammatory cytokines, apoptosis-related factor and core kinases in PI3K/AKT pathway.
LPS stimulation induced significant cell damage in PC12 cells as cell viability was repressed, apoptosis was induced and the expression levels of IL-1β, IL-6, IL-8, and TNF-α were increased. CAP pretreatment protected PC12 cells against LPS-induced cell damage. Meanwhile CAP treatment reduced the expression of COX-1 even in LPS-stimulated PC12 cells. More importantly, COX-1 overexpression abolished the protective effects of CAP on LPS-injured PC12 cells. Finally, Western blot analytical results showed that CAP activated PI3K/AKT pathway also in a COX-1-dependent manner.
CAP exerted anti-apoptotic and anti-inflammatory effects on LPS-injured PC12 cells via down-regulation of COX-1.
背景/目的：当归多糖（CAP）是当归的主要有效成分，对多种疾病具有抗炎和抗凋亡作用。本研究旨在探讨CAP对脊髓损伤（SCI）的药理潜力。
用CAP预处理PC12细胞，然后给予脂多糖（LPS）。进行转染以改变COX-1的表达。分别用CCK-8和流式细胞术检测细胞活力和凋亡细胞率。采用qRT-PCR和蛋白质印迹分析评估PI3K/AKT途径中促炎细胞因子、凋亡相关因子和核心激酶的表达变化。
LPS刺激导致PC12细胞明显的细胞损伤，表现为细胞活力受到抑制、诱导凋亡以及IL-1β、IL-6、IL-8和TNF-α的表达水平升高。CAP预处理可保护PC12细胞免受LPS诱导的细胞损伤。同时，CAP处理即使在LPS刺激的PC12细胞中也能降低COX-1的表达。更重要的是，COX-1过表达消除了CAP对LPS损伤的PC12细胞的保护作用。最后，蛋白质印迹分析结果表明，CAP还以COX-1依赖的方式激活PI3K/AKT途径。
CAP通过下调COX-1对LPS损伤的PC12细胞发挥抗凋亡和抗炎作用。
