北冬蟲夏草體內與體外生物活性：護肝與抗血管氧化傷害之研究(新制多年期第1年)

CNU IR > Pharmacy and Science > Dept. of Food Science & Technology > MOST Project > Item 310902800/2592

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/2592

Title:	北冬蟲夏草體內與體外生物活性：護肝與抗血管氧化傷害之研究(新制多年期第1年) Biological Activity of Cordyceps militaris in vivo and in vitro---Investigation of Hepatoprotection and Antivascular Oxidative Damage
Authors:	杜平悳王柏森
Contributors:	食品科技系
Date:	2007
Issue Date:	2008-07-31 16:51:23 (UTC+8)
Publisher:	台南縣：嘉南藥理科技大學食品科技系
Abstract:	本研究為探討北冬蟲夏草(蛹蟲草)體內與體外生物活性，分三年完成。第一年計畫為比較北冬蟲夏草水萃物(water extracts of Cordyceps militaris; CME)，冬蟲夏草水萃物(water extracts of Cordyceps sinensis; CSE)，市售冬蟲夏草水萃物(water extracts of commercial Cordyceps sinensis; CCSE)對細胞模式之護肝機能性表現。結果顯示CME、CSE與CCSE單獨處理對人類肝細胞株HepG2並無明顯毒性。CME，CSE與CCSE可以有效抑制tert-Butylhydroperoxide (t-BHP) 誘發細胞毒性，而CME與CSE二者的效果在統計上並無差異(P>0.05)。同時， CME，CSE與CCSE可以有效抑制t-BHP誘發細胞內氧化壓力的產生，且CSE之效用仍略高於CME，但統計上無差異(P>0.05)。另一方面，CME，CSE與CCSE也可以有效抑制t-BHP誘發細胞內Caspase 3 活性。以西方墨點分析法分析顯示CME，CSE與CCSE也可以有效抑制t-BHP誘發細胞內Caspase3蛋白之表現。綜合上述結果可知CME，CSE與CCSE對氧化壓力所引發之細胞凋亡具有氧化保護之機能作用，而其機轉可能與其降低胞內活性氧產生及抑制Caspase3活性有關。雖然， CME在本試驗模式效果略低於CSE，但是統計上並無差異(P>0.05)，顯示北冬蟲夏草水萃物對細胞模式具有顯著護肝機能性之表現。 In this three-year project, the major purpose is to investigate of the bioactivities of Cordyceps militaris in vivo and in vitro. The major goal of the first year is to compare hepatoprotective activities of CME, CSE, and CCSE, respectively, in cellular model. According to the data, CME, CSE, and CCSE did not exhibit obvious cytotoxicity toward HepG2 cells. On the other hand, the oxidative toxicity of t-BHP was decreased in the presence of CME, CSE, and CCSE respectively. No significant difference (p>0.05) was found between CME and CSE in protective effects of oxidative toxicity of t-BHP. Meanwhile, the intracellular oxidative stress induced by t-BHP in HepG2 cells was inhibited in the presence of CME, CSE, and CCSE, respectively. Further, the activity of intracellular caspase 3 induced by t-BHP was decreased in the presence of CME, CSE, and CCSE, respectively. By immunoblot, the protein levels of caspase 3 increased by t- BHP was inhibited in the presence of CME. According to the data mentioned above, the apoptosis progression induced by oxidative stress was inhibited by CSE, CME, and CCSE, respectively. The mechanism for the hepatoprotection in vitro may be attributed to decrease of oxidative stress and caspase 3 activity. This study indicated that CME displayed marked hepatoprotection in vitro.
Relation:	計畫編號：NSC96-2313-B041-001-MY3 計畫年度：96 計畫年度：96；起迄日期：2007-08-01-2008-07-31
Appears in Collections:	[Dept. of Food Science & Technology] MOST Project

Files in This Item:

File	Description	Size	Format
962313B041001MY3（第1年）.PDF		339Kb	Adobe PDF	892	View/Open
index.html		0Kb	HTML	1863	View/Open

Loading...