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首页> 外文期刊>Cellular Physiology and Biochemistry >Chinese Angelica Polysaccharide (CAP) Alleviates LPS-Induced Inflammation and Apoptosis by Down-Regulating COX-1 in PC12 Cells
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Chinese Angelica Polysaccharide (CAP) Alleviates LPS-Induced Inflammation and Apoptosis by Down-Regulating COX-1 in PC12 Cells

机译：当归多糖（CAP）通过下调PC12细胞中的COX-1减轻LPS诱导的炎症和细胞凋亡

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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). Methods 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. Results 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. Conclusion CAP exerted anti-apoptotic and anti-inflammatory effects on LPS-injured PC12 cells via down-regulation of COX-1.
机译：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。这项研究旨在探讨CAP对脊髓损伤（SCI）的药理潜力。方法采用CAP预处理PC12细胞并进行LPS处理。进行转染以改变COX-1的表达。细胞活力和凋亡率分别通过CCK-8和流式细胞仪测定。进行qRT-PCR和western blot分析，以评估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。结果LPS刺激可抑制PC12细胞的活力，诱导其凋亡，并诱导IL-1β，IL-6，IL-8和TNF-α的表达水平升高，从而引起PC12细胞的明显损伤。 CAP预处理可保护PC12细胞免受LPS诱导的细胞损伤。同时，CAP处理甚至可以降低LPS刺激的PC12细胞中COX-1的表达。更重要的是，COX-1的过表达消除了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也以COX-1依赖性方式激活PI3K / AKT途径。结论CAP通过下调COX-1的表达对LPS损伤的PC12细胞具有抗凋亡和抗炎作用。

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