-6 mol/L）收縮血管后應(yīng)用乙酰膽堿（1×10-8、1×10-7、1×10-6、1×10-5 mol/L）舒張血管，檢測血管張力變化。結(jié)果 與對照組比較，漢黃芩素處理細(xì)胞后，各組細(xì)胞活力沒有顯著變化。與對照組比較，漢黃芩素（5、20 μmol/L）顯著促進(jìn)NO的產(chǎn)生（P<0.01），但亞硝基左旋精氨酸甲酯（L-NAME）可以抑制漢黃芩素的這種作用（P<0.01）。漢黃芩素（0.5、5、20μmol/L）可以濃度相關(guān)性地促進(jìn)心臟微血管內(nèi)皮細(xì)胞eNOS蛋白表達(dá)，與對照組比較，漢黃芩素產(chǎn)生的eNOS蛋白水平差異非常顯著（P<0.01）。乙酰膽堿（1×10-8、1×10-7、1×10-6、1×10-5 mol/L）能夠濃度相關(guān)性地舒張離體大鼠胸主動脈環(huán)。與對照組比較，漢黃芩素（20μmol/L）孵育血管24 h，能顯著增加乙酰膽堿對大鼠胸主動脈血管環(huán)的舒張程度，降低胸主動脈血管環(huán)的收縮率（P<0.01、0.05）。結(jié)論 漢黃芩素可能通過促進(jìn)血管內(nèi)皮細(xì)胞eNOS蛋白表達(dá)和NO產(chǎn)生這一途徑增強(qiáng)乙酰膽堿對血管的舒張作用。;Objective To study the effect of wogonin induced by acetylcholine on the vasodilation of rat thoracic aorta and explore its mechanism. Method The experiments were divided into control group and medication group. The medication group was treated with DMEM/F12 medium containing different concentrations of wogonin, while the control group was treated with DMEM/F12 medium containing the same volume of DMSO as the medication group. Rat cardiac microvascular endothelial cells were incubated with wogonin treated for 24 h. Cell viability was measured by MTT assay, NO content was measured by nitrate reductase assay, and eNOS protein expression was detected by ELISA method. The thoracic aortic rings of rats were incubated with wogonin treated for 24 h, NE (1×10-6 mol/L) was used to constrict blood vessels, and the acetylcholine (1×10-8, 1×10-7, 1×10-6, and 1×10-5 mol/L) was used to relax blood vessels to detect the changes of vascular tension. Results Compared with the control group, there was no significant changes of the cell viability in each group after treatment with wogonin. Compared with the control group, wogonin (5, 20μmol/L) significantly promoted NO production (P<0.01), but L-NAME could inhibit the effect of wogonin (P<0.01). Wogonin (0.5, 5, 20 μmol/L) could promote eNOS protein expression in cardiac microvascular endothelial cells in a concentration-dependent manner. Compared with the control group, the level of eNOS protein produced by wogonin was significantly different (P<0.01). Acetylcholine (1×10-8, 1×10-7, 1×10-6, and 1×10-5 mol/L) could dilate isolated rat thoracic aortic rings in a concentration-dependent manner. Compared with the control group, wogonin (20 μmol/L) incubated for 24 h significantly increased the relaxation of the thoracic aortic rings and decreased the contraction rate of the thoracic aortic rings in rats (P<0.01, 0.05). Conclusion Wogonin may enhance vasodilation of acetylcholine by promoting expression of eNOS protein and NO production in vascular endothelial cells."/>

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首頁 > 過刊瀏覽>2019年第34卷第1期 >2019,34(1):11-14. DOI:10.7501/j.issn.1674-5515.2019.01.003
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漢黃芩素增強(qiáng)乙酰膽堿對大鼠胸主動脈血管的舒張作用研究

Vasodilation of thoracic aorta in rats of wogonin by enhancement of acetylcholine

發(fā)布日期：2019-01-26
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    [關(guān)鍵詞]
    [摘要]
    目的 探討漢黃芩素增強(qiáng)乙酰膽堿對大鼠胸主動脈血管的舒張作用及其作用機(jī)制。方法 實(shí)驗(yàn)分為對照組和加藥組，加藥組使用含有不同濃度漢黃芩素的DMEM/F12培養(yǎng)基作用；對照組使用含有與加藥組相同體積二甲基亞砜（DMSO）的DMEM/F12培養(yǎng)基作用。漢黃芩素孵育大鼠心臟微血管內(nèi)皮細(xì)胞24 h，MTT法檢測細(xì)胞活力；硝酸還原酶法檢測細(xì)胞上清NO含量；ELISA法檢測細(xì)胞內(nèi)皮型一氧化氮合酶（eNOS）蛋白表達(dá)。漢黃芩素孵育大鼠胸主動脈環(huán)24 h，去甲腎上腺素（1×10-6 mol/L）收縮血管后應(yīng)用乙酰膽堿（1×10-8、1×10-7、1×10-6、1×10-5 mol/L）舒張血管，檢測血管張力變化。結(jié)果 與對照組比較，漢黃芩素處理細(xì)胞后，各組細(xì)胞活力沒有顯著變化。與對照組比較，漢黃芩素（5、20 μmol/L）顯著促進(jìn)NO的產(chǎn)生（P<0.01），但亞硝基左旋精氨酸甲酯（L-NAME）可以抑制漢黃芩素的這種作用（P<0.01）。漢黃芩素（0.5、5、20μmol/L）可以濃度相關(guān)性地促進(jìn)心臟微血管內(nèi)皮細(xì)胞eNOS蛋白表達(dá)，與對照組比較，漢黃芩素產(chǎn)生的eNOS蛋白水平差異非常顯著（P<0.01）。乙酰膽堿（1×10-8、1×10-7、1×10-6、1×10-5 mol/L）能夠濃度相關(guān)性地舒張離體大鼠胸主動脈環(huán)。與對照組比較，漢黃芩素（20μmol/L）孵育血管24 h，能顯著增加乙酰膽堿對大鼠胸主動脈血管環(huán)的舒張程度，降低胸主動脈血管環(huán)的收縮率（P<0.01、0.05）。結(jié)論 漢黃芩素可能通過促進(jìn)血管內(nèi)皮細(xì)胞eNOS蛋白表達(dá)和NO產(chǎn)生這一途徑增強(qiáng)乙酰膽堿對血管的舒張作用。
    [Key word]
    [Abstract]
    Objective To study the effect of wogonin induced by acetylcholine on the vasodilation of rat thoracic aorta and explore its mechanism. Method The experiments were divided into control group and medication group. The medication group was treated with DMEM/F12 medium containing different concentrations of wogonin, while the control group was treated with DMEM/F12 medium containing the same volume of DMSO as the medication group. Rat cardiac microvascular endothelial cells were incubated with wogonin treated for 24 h. Cell viability was measured by MTT assay, NO content was measured by nitrate reductase assay, and eNOS protein expression was detected by ELISA method. The thoracic aortic rings of rats were incubated with wogonin treated for 24 h, NE (1×10-6 mol/L) was used to constrict blood vessels, and the acetylcholine (1×10-8, 1×10-7, 1×10-6, and 1×10-5 mol/L) was used to relax blood vessels to detect the changes of vascular tension. Results Compared with the control group, there was no significant changes of the cell viability in each group after treatment with wogonin. Compared with the control group, wogonin (5, 20μmol/L) significantly promoted NO production (P<0.01), but L-NAME could inhibit the effect of wogonin (P<0.01). Wogonin (0.5, 5, 20 μmol/L) could promote eNOS protein expression in cardiac microvascular endothelial cells in a concentration-dependent manner. Compared with the control group, the level of eNOS protein produced by wogonin was significantly different (P<0.01). Acetylcholine (1×10-8, 1×10-7, 1×10-6, and 1×10-5 mol/L) could dilate isolated rat thoracic aortic rings in a concentration-dependent manner. Compared with the control group, wogonin (20 μmol/L) incubated for 24 h significantly increased the relaxation of the thoracic aortic rings and decreased the contraction rate of the thoracic aortic rings in rats (P<0.01, 0.05). Conclusion Wogonin may enhance vasodilation of acetylcholine by promoting expression of eNOS protein and NO production in vascular endothelial cells.
    [中圖分類號]
    [基金項(xiàng)目]
    國家自然科學(xué)基金資助項(xiàng)目（81603648，81803829）