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Studies on the therapeutic effect of propolis in streptozotocin-induced diabetic mice

机译:蜂胶在链脲佐菌素诱导的糖尿病小鼠中的治疗疗效研究

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Propolis oral administration in diabetic mice can increase the expression of TLR-3 and ameliorate homeostatic imbalance. The TLR-3 expression increased in both B cells and T cells. In this study, we also found that propolis may improve insulin expression in pancreatic beta cells. Administering propolis at a dose of 100-200 mg/mL may significantly increase insulin synthesis. Propolis might protect healthy cells from apoptosis in cisplatin exposure. Cisplatin can induce spleen cells to remain in the G0/G1 phase or to reach the apoptosis stage in the absence of propolis. In contrast, cisplatin, when administered together with propolis to a culture of spleen cells, cannot force the cells to undergo apoptosis. In a culture of spleen cells in the presence of propolis, the cells did not show any responses. This suggests that propolis does not disrupt normal cell physiology and supports cell health when cells are exposed to cisplatin. Furthermore, propolis can suppress the production of the pro-inflammatory cytokine interferon-gamma (IFN-γ).
机译:蜂鸣器小鼠蜂胶口服给药可以增加TLR-3的表达和改善稳态不平衡。 B细胞和T细胞中的TLR-3表达增加。在这项研究中,我们还发现蜂胶可以改善胰腺β细胞中的胰岛素表达。在100-200mg / ml的剂量下给予蜂胶可以显着增加胰岛素合成。蜂胶可能保护顺铂暴露中的细胞凋亡的健康细胞。顺铂可以诱导脾细胞保留在G0 / G1相中或在没有蜂胶的情况下达到凋亡阶段。相反,当与蜂胶到脾细胞培养物一起施用时,顺铂不能强迫细胞进行细胞凋亡。在蜂窝细胞存在下在蜂胶的培养中,细胞没有显示任何反应。这表明蜂胶不会破坏正常的细胞生理学并在细胞暴露于顺铂时支持细胞健康。此外,蜂胶可以抑制促炎细胞因子干扰素-γ-γ(IFN-γ)的产生。

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