首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Screening and Identification of Molecular Targets Involved in Preventing Gastric Precancerous Lesions in Chronic Atrophic Gastritis by Qilianshupi Decoction
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Screening and Identification of Molecular Targets Involved in Preventing Gastric Precancerous Lesions in Chronic Atrophic Gastritis by Qilianshupi Decoction

机译:祁连山汤中慢性萎缩性胃炎中胃癌患者患者筛选和鉴定

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Chronic atrophic gastritis (CAG) is a common and possibly precancerous digestive tract disease. Development of drugs with effect of preventing precancerous lesions draws the eyes of global researchers. Qilianshupi decoction (QLSP) is a Traditional Chinese Medicine (TCM) that is commonly used to treat CAG, but few studies have explored the mechanism of QLSP on treating CAG. This study investigated the molecular targets of the component herbs of QLSP in preventing precancerous lesions based on network pharmacology. Network pharmacology analysis revealed that the 6 herbs regulated multiple CAG-related genes, among which the most important were cancer-related pathway (apoptosis, p53, and VEGF) and epithelial cell signaling in Helicobacter pylori infection. Further animal experiments showed that the expression of survivin and p53 in precancerous lesions of CAG rats was significantly increased which was suppressed by QLSP. Moreover, telomerase activity was inhibited in precancerous lesions of CAG rats, and telomere length of gastric mucosa was increased, which was reversed by QLSP. Our results suggest that the components of QLSP prevents gastric precancerous lesions through decreasing the expression of survivin and p53 and regulating telomerase activity and telomere length in CAG.
机译:慢性萎缩性胃炎(CAG)是一种常见的和可能的癌症消化道疾病。患有预防癌前病变的药物的发展吸引了全球研究人员的眼睛。祁连山汤(QLSP)是一种常用于治疗CAG的中药(TCM),但很少有研究探索了QLSP治疗CAG的机制。本研究研究了基于网络药理学预防QLSP的组分草药的分子靶标。网络药理学分析显示,6草药调节多个CAG相关基因,其中最重要的是癌症相关途径(凋亡,P53和VEGF)和幽门螺杆菌感染中的上皮细胞信号传导。进一步的动物实验表明,Survivin和P53在CAG大鼠的癌前病变中的表达显着增加,QLSP抑制了。此外,端粒酶活性在CAG大鼠的癌前病变中抑制,并且胃粘膜的端粒长度升高,QLSP反转。我们的研究结果表明,QLSP的组分通过降低Survivin和P53的表达来阻止胃癌癌前病变,并在CAG中调节端粒酶活性和端粒长度。

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