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Intervention effects of lotus leaf flavonoids on gastric mucosal lesions in mice infected with Helicobacter pylori

机译:莲花黄酮类化合物对幽门螺杆菌胃粘膜病变胃粘膜病变的干预作用

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Helicobacter pylori ( H. pylori ) is one of the main factors that cause gastric lesions. The lotus leaf is an edible plant used in traditional Eastern medicine. This study evaluates the intervention effects of lotus leaf flavonoids (LLF) on gastric mucosal lesions in mice infected with H. pylori and explores their mechanism of action. High-performance liquid chromatography analysis reveals that LLF contain kaempferitrin (kaempferol-3,7-dirhamnoside), hypericin, astragalin (kaempferol-3-glucoside), phlorizin, and quercetin. LLF can reduce the number of gastric mucosal lesions and tissue lesions in mice with H. pylori -induced gastric lesions. LLF can increase the levels of somatostatin and vasoactive intestinal peptide in the serum of mice with gastric lesions and decrease the levels of substance P and endothelin-1 to inhibit gastric lesions. LLF can also reduce the levels of interleukin (IL)-6, IL-12, tumor necrosis factor (TNF)-α, and interferon-gamma cytokines in the serum of mice with gastric lesions. Using a quantitative polymerase chain reaction assay it can be seen that LLF can downregulate mRNA expressions of TNF-α, IL-1β, myeloperoxidase, keratin (KRT) 16, KRT6b, and transglutaminase 3 epidermal in the gastric tissues of mice with gastric lesions. Western blot analysis indicates that LLF can downregulate the protein expressions of caspase-1, Nod-like receptor protein 3, IL-1β, TNF-α, and Toll-like receptor 4 in the gastric tissues of mice with gastric lesions. LLF have beneficial effects on gastric lesions induced by H. pylori . Meanwhile LLF is more active in competition with ranitidine. LLF represent an active substance that can inhibit H. pylori -induced gastric lesions. The flavones of LLF may enhance the inhibition of gastric mucosal lesions by promoting the interaction between the compounds.
机译:幽门螺杆菌(H.Pylori)是导致胃病变的主要因素之一。莲花是一种用于传统东部医学的可食用植物。本研究评估了莲花叶类黄酮(LLF)对幽门螺杆菌胃粘膜病变的干预作用,并探讨了它们的作用机制。高效液相色谱分析显示,LLF含有Kaempferitrin(Kaempferol-3,7-Dirhamnoside),金刚素,黄芪(Kaempferolol-3-葡糖苷),甘醇素和槲皮素。 LLF可以减少与H.幽门螺杆菌诱导的胃病变小鼠胃粘膜病变和组织病变的数量。 LLF可以通过胃病变增加小鼠血清中生长抑素和血管活性肠肽的水平,降低物质P和内皮蛋白-1的水平抑制胃病变。 LLF还可以减少白细胞介素(IL)-6,IL-12,肿瘤坏死因子(TNF)-α和干扰素 - γ细胞因子在小鼠血清中的胃病变。使用定量聚合酶链式反应测定可以看出,LLF可以在用胃病变的小鼠的胃组织中下调TNF-α,IL-1β,髓过氧化物酶,角蛋白(KRT)16,KRT6B和转谷氨酰胺酶3表皮的MRNA表达。 Western印迹分析表明,LLF可以在用胃病变的小鼠的胃组织中下调Caspase-1,Nod样受体蛋白3,IL-1β,TNF-α和Toll样受体4的蛋白质表达。 LLF对H. Pylori诱导的胃病变具有有益作用。同时LLF在与雷尼丁的竞争中更活跃。 LLF代表一种可抑制幽门螺杆菌诱导的胃病变的活性物质。 LLF的黄酮可以通过促进化合物之间的相互作用来增强胃粘膜病变的抑制。

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