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首页> 外文期刊>Journal of Cellular Physiology >β‐asarone inhibited cell growth and promoted autophagy via P53/Bcl‐2/Bclin‐1 and P53/AMPK/mTOR pathways in Human Glioma U251 cells
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β‐asarone inhibited cell growth and promoted autophagy via P53/Bcl‐2/Bclin‐1 and P53/AMPK/mTOR pathways in Human Glioma U251 cells

机译：β的细辛脑抑制细胞生长和提升自噬通过P53 / Bcl 2 / Bclin还是1和P53 / AMPK / mTOR通路在人类神经胶质瘤U251细胞

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Glioma is the most common type of primary brain tumor and has an undesirable prognosis. Autophagy plays an important role in cancer therapy, but it is effect is still not definite. P53 is an important tumor suppressor gene and protein that is closely to autophagy. Our aim was to study the effect of β‐asarone on inhibiting cell proliferation in human glioma U251 cells and to detect the effect of the inhibition on autophagy through the P53 signal pathway. For cell growth, the cells were divided into four groups: the model, β‐asarone, temozolomide (TMZ), and co‐administration groups. For cell autoghapy and the P53 pathway, the cells were divided into six groups: the model, β‐asarone, 3MA, Rapa, Pifithrin‐μ, and NSC groups. The counting Kit‐8 assay and flow cytometry (FCM) were then used to measure the cell proliferation and cycle. Electron microscopy was used to observe autophagosome formation. Cell immunohistochemistry/‐immunofluorescence, FCM and Western blot (WB) were used to examine the expression of Beclin‐1 and P53. The levels of P53 and GAPDH mRNA were detected by RT‐PCR. Using WB, we determined autophagy‐related proteins Beclin‐1, LC3‐II/I, and P62 and those of the P53 pathway‐related proteins P53, Bcl‐2, mTOR, P‐mTOR, AMPK, P‐AMPK, and GAPDH. We got the results that β‐asarone changed the cellular morphology, inhibited cell proliferation, and enhanced the expression of P53, LC3‐II/I, Beclin‐1, AMPK, and pAMPK while inhibiting the expression of P62, Bcl‐2, mTOR, and pmTOR. All the data suggested that β‐asarone could reduce the cell proliferation and promote autophagy possible via the P53 pathway in U251 cells.
机译：神经胶质瘤是最常见的一种主要的大脑肿瘤,预后不良。在癌症治疗中发挥着重要作用,但它还不明确的是效果。重要的肿瘤抑制基因和蛋白质是自噬密切。β细辛醚应承担对抑制细胞的影响在人类神经胶质瘤U251细胞增殖检测自噬抑制的效果通过P53通路的信号。这些细胞被分为四组:模型中,β高细辛醚temozolomide (TMZ)公司管理组织。P53通路,细胞被分成六个集团:《模特,β‐asarone 3MA,爸爸地理Pifithrinμ,NSC组。分析和流式细胞术(FCM)被使用测量细胞增殖和周期。电子显微镜用于观察自噬体的形成。免疫组织化学和免疫荧光,应承担的FCM和免疫印迹(WB)被用来检查Beclin还是1和P53的表达。和GAPDH mRNA, RT PCR检测。我们决定自噬相关蛋白Beclin高1 LC3高II /我在P62和P53的通路检测相关蛋白质P53、Bcl 2,应承担mTOR,P量mTOR, AMPK, P量AMPK, GAPDH。结果β细辛脑改变了细胞形态学、抑制细胞增殖和增强的P53的表达,LC3高II /我在Beclin量1,AMPK, pAMPK而抑制P62, Bcl 2,应承担mTOR, pmTOR。数据表明,β细辛醚可以减少细胞增殖,促进自噬可能通过在U251细胞P53通路。

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