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  • 學位論文

水飛薊素及玉山薊發酵液對四氯化碳肝損傷大鼠之尿中甲基乙二醛、D-乳酸及丙二醛的影響

The Effect of Silymarin and Fermentation Liquid of Cirsium Kawakamii on Urinary Methylglyoxal, D-Lactate and Malondialdehyde Level in Carbon Tetrachloride-Induced Rat Liver Injury

指導教授 : 李仁愛

摘要


先前研究證實,大鼠給與四氯化碳後尿中D-乳酸含量增加,本研究管餵肝保護藥物-水飛薊素或民間常用肝保護草藥-玉山薊的發酵液給與四氯化碳誘導之肝損傷大鼠後,探討尿中D-乳酸及其前驅物-甲基乙二醛及脂質過氧化主要產物-丙二醛含量於肝損傷回復時之變化。四十隻七週齡SD大鼠,隨機均分成正常組、肝損傷組、水飛薊治療組、玉山薊治療組。實驗共給藥八週,之後靜置,於第一週、第六週及第十二週收集血液及尿液。結果顯示,玉山薊發酵液具有較水飛薊素為佳之肝保護效果及清除氫氧自由基能力。肝損傷組、水飛薊治療組及玉山薊治療組於第一週之尿中甲基乙二醛、D-乳酸及丙二醛含量與正常組皆具有顯著減少。第六週之尿中D-乳酸含量於水飛薊治療組與肝損傷組及玉山薊治療組相比皆顯著增加(分別為0.38 ± 0.12, 0.16 ± 0.06, 0.16 ± 0.08 mM/ μM creatinine),其含量與組織切片損傷程度相符。第十二週之尿中甲基乙二醛含量於水飛薊治療組與肝損傷組及玉山薊治療組相比皆顯著增加(分別為9.83 ± 1.25, 6.43 ± 1.59, 5.52 ± 1.72 μM/ mM creatinine),但其含量與組織切片損傷程度不具相關性;丙二醛含量則無顯著差異。尿中D-乳酸含量與肝損傷之相關性高於尿中甲基乙二醛及丙二醛含量。

並列摘要


In our previous study, CCl4 caused elevated urinary D-lactate level in rat. In this study, we investigated urinary D-lactate, it’s precursor- methylglyoxal and main product of lipid peroxidation- malondialdehyde level during hepatic regeneration by co-administration rat with CCl4 and hepatoprotective medicine- silymarin or fermentation liquid of Cirsium Kawakamii which has hepatoprotective capacity. Forty SD rats were randomly divided into 4 groups: normal, injury, silymarin and Cirsium kawakamii group. Blood and urine were collected at week 1, 6 and 12. The results show that (1) Cirsium kawakamii has more hepatoprotective and hydroxyl radical-scavenging power than silymarin, (2) CCl4 caused decreased urinary methylglyoxal, D-lactate and malondialdehyde level at week 1, (3) silymarin group has elevated urinary D-lactate level than injury and Cirsium Kawakamii groups at week 6 and this result was correlate with hepatic injury (urinary D-lactate levels in each groups were 0.38 ± 0.12, 0.16 ± 0.06, 0.16 ± 0.08 mM/ μM creatinine), (4) silymarin group has elevated urinary methylglyoxal level than injury and Cirsium Kawakamii groups at week 12 and this result wasn’t correlate with hepatic injury (urinary methylglyoxal levels in each groups were 9.83 ± 1.25, 6.43 ± 1.59, 5.52 ± 1.72 μM/ mM creatinine) and, (5) urinary malondialdehyde level in each groups have no differences. In conclusion, urinary D-lactate level has more correlative to hepatic injury than methylglyoxal and malondialdehyde level.

參考文獻


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