發明
中華民國
103121754
I 531373
將胜肽用於製備預防或治療心臟相關疾病之醫藥組合物之用途及含有該胜肽之營養補充品
東海大學
2016/05/01
High Fat Diet??VHVV acts against High Fat Dietinduced cardiac hypertrophy, apoptosis, and fibrosis. ?? The proposed mechanisms by which VHVV acts against High Fat Dietinduced cardiac hypertrophy, apoptosis, and fibrosis. The up arrow , parallel line, and down arrow represent up-regulation, and down-regulation by High Fat Diet, respectively. The stop symbol represents the inhibition by VHVV treatment. Cardiac hypertrophy pathway appears to be increased due to increases in IL-6, MEK5, ERK5, calcineurin, NFATc3, ANP, BNP, p-P38 and p-JNK1/2. Cardiac apoptosis pathway appears to be increased due to a decrease in anti-apoptotic Bcl-2 expression and increases in pro-apoptotic cytochrome C and cleaved caspases-3 levels. Cardiac fibrosis pathway appears to be increased due to increases in FGF2, p-ERK1/2, uPA, MMP-9 and -2. Our data demonstrated that VHVV attenuates the High Fat Diet induced cardiac hypertrophy, apoptosis, and fibrosis, which may be due to the inhibition of the IL-6 related MEK5-ERK5 pathway, MAPK activation, and FGF-2-ERK-uPA fibrosis pathway, as well as the increase in anti-apoptotic Bcl-2. 高脂飲食VHVV對抗高脂飲食引起的心臟肥大,細胞凋亡和纖維化。 VHVV對抗高脂飲食誘發的心臟肥大,細胞凋亡和纖維化的機制。向上箭頭,平行線和向下箭頭分別代表高脂飲食的上調和下調。停止符號表示通過VHVV處理的抑制。高脂產生IL-6,MEK5,ERK5,鈣調神經磷酸酶,NFATc3,ANP,BNP,p-P38和p-JNK1 / 2的分子表現顯著增加,心臟肥大途徑分子表現也顯著增加。心肌細胞凋亡途徑由於抗凋亡Bcl-2表達的減少,而促凋亡細胞cytochrome c的表達增加和caspases-3分子表現增加。心臟纖維化途徑於FGF2,p-ERK1 / 2,uPA,MMP-9和-2的分子表現也增。因此我們的數據發現,VHVV減輕了上述高脂飲食誘導的心肌肥大,細胞凋亡和纖維化的機轉,這可能是由於抑制了與IL-6相關的MEK5-ERK5途徑,MAPK活化和FGF-2-ERK-uPA纖維化路徑所致。
研發處
04-23594711
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