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頁籤選單縮合
題 名 | 大黃及其有效成分(Emodin)對糖尿病腎病變治療效果之研究=Effects of Rhubarb and Its Active Consituent (Emodin,Rhatannin)on Diabetic Nephropathy in Streptozotocin-Diabetic Rats |
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作 者 | 顧進裕; | 書刊名 | 中醫藥年報 |
卷 期 | 17:3 1999.05[民88.05] |
頁 次 | 頁149-173 |
分類號 | 413.34、413.34 |
關鍵詞 | 糖尿病腎病變; 大白鼠; 大黃; 大黃素; 單寧類; Diabetic nephropathy; Rats; Rhubarb; Emodin; Captopril; Tannins; |
語 文 | 中文(Chinese) |
中文摘要 | 糖尿病腎病變是造成新進尿毒症洗腎病人的最重要原因,其致 病機轉可能與乙型轉型生長因子及腎臟肥大、腎臟纖維化 有關,最近我們更發現其與TGF-β受器有關。 大黃(rhubarb)最近被發現可能可以減少糖尿病腎病腎病變,也 可能可以延緩慢性腎衰謁病人變成尿毒症的時間,因此本計劃研究 大黃及其有效成份(emodin, rhatanning)糖尿病腎病變治療的效果,利 用Streptozotocin糖尿病大白鼠,分成控制組、胰島素、Captopril治 療組、大黃(或其有效成份(emodin, rhatannin)治療組等七組來研究其 第7天、第一、三月之血液及尿液中TGF-β1與腎臟大小、腎臟 TGF-β1及其第二型受器傳訊者核糖核酸及組織免疫染色,及其與蛋 白尿及腎臟組織病理之相關性。 結果發現糖尿病大白鼠的腎臟肥大在第7天、第一、三月圴有出 現,且胰島素治療可以逆轉此腎臟肥大,但Captopril、大黃、 emodin及rhatannin 治療則無法逆轉此腎臟肥大:至於糖尿病大白鼠 自第三月起才有蛋白尿,而胰島素、Captopril、大黃、emodin(但非 rhatannin)治療則能逆轉此現象:而各組大白鼠的血液及腎臟TGF- β1及其受器mRNA並無變化,但糖尿病大白鼠在各時期的腎臟 TGF-β1組織染色均有明顯的增加、Captopril、大黃、emodin(但非 rhatannin)治療則能逆轉此現象。 我們的結論是糖尿病可以增加腎臟的TGF-β1蛋白質表現,而雖 然TGF-β1mRNA用RT-PCR看不出有變化,但我們打算進一步用更 敏感的Competitive RT-PCR來看是否有變化,因此胰島素、 Captopril、大黃、emodin治療可能利用逆轉腎臟的TGF-β1蛋白質來 達到治療糖尿病腎病變的效果。 |
英文摘要 | Dabetic nephroparth (DN)is the leading cause of new dialysis patients. Whereas the pathogenesis of DN is unclear, it may be associated with transforming growth factor-β(TGF-β)and renal hypertrophy or renal fibrosis. Recently, we also found that it may also be related with TGF-β receptors. Rhubarb is a laxative in traditional Chinese herbs. It has recently being found to inbibit renal hypertrophy in dabetic animals in mainland China. One of Rhubarb's active constituents (emodin) have also being found to be antipproliferative to cultured renal cells. Nonetheless, its mechanism of action is still unknown. Therefore, we studied the effects of Rhubarb and its active constituent (emodin, rhatannin) on DN and its mechanisms of action as related to TGF-β and its type Ⅱ receptors. We studied normal streptozotocin-diabetic and insulin-treated rats. They will each be divided into control, captopril and Rhubarb, emodin and rhatannin-treated groups. Their plasma and urinary TGF-β1 and proteinuria, renal TGF-β1 and type ⅡTGF-β1 receptor mRNA (by RT- PCR) and immunohistochemistry were measured. Results:We found that diabetic rats (DM) had renal hypertrophy at 1 week, 1month and 3 months and insulin (but not Rhubarb, emodin and captopril) treatment reversed this phenomenon. Proteinuria occurred since 3 month in the DM rats. Insulin, Rhubarb, emodin and captopril(but not rhatannin) treatment reversed this phenomenon. RT-PCR revealed no changes in TGF-β1mRNA and type ⅡTGF-β1 receptors in all time perilds. Renal immuno-histochemistry revealed that DM rats had increased expressions TGF-β1 protein in all time periods. Insulin, Rhubarb, cmodin and captopril (but not rhatannin) treatment effectively reversed this phenomenon. We concluded that diabetic kidney had increased renal TGF-β1 (bu not TGF-β1 type Ⅱ receptor) protein expressions. Although RT-PCR showed no changes in TGF-β1 mRNA, we are planning to further check it by the more sensitive competitive RT-PCR. Therefore, we speculate that insulin, captopril, Rhubarb and emodin (but not rhatannin) were effective in treating diabetic nephropathy (reversing proteinuria) possibly by reversing renal TGF-β1 protein expression. |
本系統中英文摘要資訊取自各篇刊載內容。