METHODS: The mechanisms of anti-inflammatory and autophagy-promoting activities of KRG-WE were evaluated in kidney, lung, liver, stomach, and colon of aged mice using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR), quantitative RT-PCR (qRT-PCR), and western blot analysis.
RESULTS: KRG-WE significantly suppressed the mRNA expression levels of inflammation-related genes such as interleukin (IL)-1β, IL-8, tumor necrosis factor (TNF)-α, monocyte chemoattractant protein-1 (MCP-1), and IL-6 in kidney, lung, liver, stomach, and colon of the aged mice. Furthermore, KRG-WE downregulated the expression of transcription factors and their protein levels associated with inflammation in lung and kidney of aged mice. KRG-WE also increased the expression of autophagy-related genes and their protein levels in colon, liver, and stomach.
CONCLUSIONS: The results suggest that KRG can suppress inflammatory responses and recover autophagy activity in aged mice.
方法:在肾脏中评估KRG-WE的抗炎和促进自噬活性的机制,肺,肝脏,胃,使用半定量逆转录聚合酶链反应(RT-PCR),定量RT-PCR(qRT-PCR),和蛋白质印迹分析。
结果:KRG-WE显著抑制炎症相关基因如白细胞介素(IL)-1β的mRNA表达,IL-8,肿瘤坏死因子(TNF)-α,单核细胞趋化蛋白-1(MCP-1),和肾脏中的IL-6,肺,肝脏,胃,和老年小鼠的结肠。此外,KRG-WE下调老年小鼠肺和肾脏炎症相关转录因子及其蛋白水平的表达.KRG-WE还增加了结肠中自噬相关基因的表达及其蛋白水平,肝脏,和胃。
结论:结果表明,KRG可以抑制老年小鼠的炎症反应并恢复自噬活性。