短期高糖合併發炎微環境前處理促使間葉幹細胞活化並強化糖尿病性肝損傷的治療
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2020
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['研究背景:\n肝功能障礙是糖尿病相關的併發症之一。除了針對糖尿病進行藥物治療,幹細胞移植在治療糖尿病性肝病方面顯示出潛力,這是因為幹細胞具有組織再生的特點。儘管幹細胞有能力恢復肝功能在糖尿病、高葡萄糖環境引發的糖尿病減少幹細胞功能在幹細胞移植到糖尿病患者因為高葡萄糖環境引起的氧化壓力在幹細胞啟動凋亡信號,導致減少細胞生存能力和減少組織再生幹細胞的特徵。\n\n研究目的:\n本研究推測,幹細胞經短期高血糖合併發炎微環境前處理後,再移植到糖尿病環境中可提高幹細胞的特性和細胞存活率,並強化對糖尿病性肝損傷的治療。\n\n研究結果\n體外研究結果表明,短期(3小時)將間葉幹細胞暴露於高血糖結合炎症微環境(稱為高血糖前處理幹細胞)可通過表達受體酪氨酸激酶Receptor tyrosine kinase (c-Kit)提高幹細胞的生存能力和幹細胞特性。另外,高血糖前處理的幹細胞能抑制糖尿病肝臟活性氧物質和發炎因子的產生,對糖尿病肝的再生效果優於未經高血糖預處理的幹細胞,提示高血糖幹細胞與炎症微環境的結合啟動了幹細胞在治療糖尿病性肝病中的功能。\n']
['Research Background:\nLiver dysfunction is one of the complications associated with diabetes. In addition to drug therapy for diabetes, stem cell transplantation has shown potential in the treatment of diabetic liver disease because of the regenerative properties of stem cells. Although stem cells have the ability to restore liver function in diabetic, hyperglucose-induced diabetes reduces stem cell function in transplanted patients with diabetes due to oxidative stress caused by hyperglucose-induced oxidative stress in the stem cells initiating apoptosis signals, leading to reduced cell viability and reduced tissue regenerative stem cell characteristics.\nResearch Purpose:\nThis study hypothesized that the transplantation of stem cells into diabetic environment after short-term hyperglycemia combined with inflammatory microenvironment pretreatment could improve the characteristics and cell viability of stem cells and enhance the treatment of diabetic liver injury.\nThe results of the study:\nIn vitro studies showed that short-term (3 hours) exposure of mesenchymal stem cells to hyperglycemia coupled inflammatory microenvironment (known as hyperglycemia pretreatment stem cells) could improve the survival ability and stem cell characteristics of stem cells by expressing Receptor tyrosine kinase (C-kit). In addition, stem cells treated with hyperglycemia can inhibit the production of reactive oxygen species and inflammatory factors in diabetic liver, and the regenerative effect on diabetic liver is better than that of stem cells not pretreated with hyperglycemia, suggesting that the combination of hyperglycemia stem cells and inflammatory microenvironment activates the function of stem cells in the treatment of diabetic liver disease.\n']
['Research Background:\nLiver dysfunction is one of the complications associated with diabetes. In addition to drug therapy for diabetes, stem cell transplantation has shown potential in the treatment of diabetic liver disease because of the regenerative properties of stem cells. Although stem cells have the ability to restore liver function in diabetic, hyperglucose-induced diabetes reduces stem cell function in transplanted patients with diabetes due to oxidative stress caused by hyperglucose-induced oxidative stress in the stem cells initiating apoptosis signals, leading to reduced cell viability and reduced tissue regenerative stem cell characteristics.\nResearch Purpose:\nThis study hypothesized that the transplantation of stem cells into diabetic environment after short-term hyperglycemia combined with inflammatory microenvironment pretreatment could improve the characteristics and cell viability of stem cells and enhance the treatment of diabetic liver injury.\nThe results of the study:\nIn vitro studies showed that short-term (3 hours) exposure of mesenchymal stem cells to hyperglycemia coupled inflammatory microenvironment (known as hyperglycemia pretreatment stem cells) could improve the survival ability and stem cell characteristics of stem cells by expressing Receptor tyrosine kinase (C-kit). In addition, stem cells treated with hyperglycemia can inhibit the production of reactive oxygen species and inflammatory factors in diabetic liver, and the regenerative effect on diabetic liver is better than that of stem cells not pretreated with hyperglycemia, suggesting that the combination of hyperglycemia stem cells and inflammatory microenvironment activates the function of stem cells in the treatment of diabetic liver disease.\n']
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糖尿病, 肝損傷, 間葉幹細胞, 發炎微環境, diabetes mellitus, liver injury, mesenchymal stem cells, inflammatory microenvironment