寡糖干預急性腎病變的機制研究-探討寡醣對CD44的干擾對腎小管發炎訊號路徑的影響

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题名:	寡糖干預急性腎病變的機制研究-探討寡醣對CD44的干擾對腎小管發炎訊號路徑的影響 Study on the mechanism of oligosaccharide intervention in acute kidney disease - focus on the influence of oligosaccharide-CD44 interfering on inflammation of renal tubules
作者:	黃乃仁 HUANG, NAI-JEN
贡献者:	臨床醫學研究所碩士班邱惠雯
关键词:	急性腎損傷 AKI
日期:	2021-06-08
上传时间:	2022-03-05 23:14:23 (UTC+8)
摘要:	急性腎損傷(Acute kidney injury, AKI)學理上為暫時性的腎功能下降，其中包含了結構性的受損以及功能性的下降。臨床上以血液肌酐酸(creatinine)濃度做為死亡風險的依據。AKI的致病原因相當複雜，以缺血性(ischaemia) AKI的最為常見。缺血性造成生理的改變包含了氧氣運送和代謝能力的下降，進而導致細胞受傷，也會引起發炎反應，造成腎臟的傷害加劇。目前沒有有效的方式可以減緩AKI發炎所造成的傷害。在細胞實驗中，我們透過MGC AnaeroPack®造成腎小管細胞缺氧，在缺氧之前我們會分別加入三種常見的寡糖，褐藻寡糖(fucoidan)、果寡糖(frucoto-oligosaccharide)及半乳寡糖(galacto-oligosacharide)，結果顯示這三種寡糖可減少缺氧造成的細胞死亡、ROS、CD44以及下游的pJNK訊息傳遞鏈，也可減少缺氧細胞培養液中促發炎因子(MCP-1、IL1-β、TNF-α )釋放。缺氧的腎小管細胞培養液會造成免疫細胞(RAW264.7)的激活，腎小管缺氧前加入寡糖的組別，細胞的增生則有減緩。動物實驗中，我們使用缺血/再灌注損傷(ischaemia-reperfusion injury, IRI)造成小鼠的AKI動物模式，我們於缺血/再灌注損傷前一天開始分別餵食三種寡糖，寡糖會餵食直到犧牲當天。結果顯示，從血液生化值中得知寡糖可以減少IRI造成的腎臟損傷，可以減緩血液中發炎因子(MCP-1、IL1-β、TNF-α)，在免疫組織染色中，寡糖也可以減少AKI誘發的CD44，在生理學上我們也看到寡糖可減緩腎小管的損傷。 Acute kidney injury (AKI) is defined by a temporary decline in renal function, including structural damage and decreased function. Clinically, serum creatinine level is used as the basis for diagnosis of severity. There is no effective way to reduce the inflammation-associated renal injury in AKI. The causes of AKI are complex, and ischemia is the most common. The physiological changes caused by ischemia include decreased oxygen transport and metabolic capacity, which cause cell injury and inflammatory responses to increase kidney injury. Many studies show that oligosaccharides such as fucoidan, galactooligosaccharides and fucotooligosaccharides have many biological benefits. For example, changing the intestinal microbiota and affecting physiological phenomena, including lipid metabolism, Alzheimer's disease, bile acid metabolism. In our previous studies, we found that oligo-fucoidan can directly decrease renal fibrosis in vitro and in vivo. Recent studies have indicated that immune cells expressed by CD44 can trigger apoptosis through JNK. Another study pointed out that excessive activation of JNK can cause a cytokine storm, which in turn leads to tissue damage and multiple organ failure. We confirmed that oligosaccharides reduced the release of pro-inflammatory factors caused by hypoxia through CD44 in cell experiments. oligosaccharides also reduce the proliferation of immune cells. In the AKI experiment, on the seventh day of AKI, the kidney damage caused by AKI still exists. The kidney damage of AKI mice fed with oligosaccharides was significantly reduced.
描述:	碩士指導教授：邱惠雯委員：鄭朝文委員：廖家德
数据类型:	thesis
显示于类别:	[臨床醫學研究所] 博碩士論文

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