内源性甲醛对血管的舒张作用及其机制初探
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- 英文论文题名：The Vasorelaxing Effect of Endogenous Formaldehyde and Its Underlying Mechanisms
- 论文作者：赵云 ; 李潇潇 ; 郭晴 ; 杨旭 ; 李睿
- 英文论文作者：Zhao Yun ; Li Xiaoxiao ; Guo Qing ; Yang Xu ; Li Rui ; Department of Biology ; Central China Normal University
- 年：2016
- 作者机构：华中师范大学生命科学学院;
- 论文关键词：内源性甲醛 ; 胸主动脉 ; 血管舒张 ; 机制
- 英文论文关键词：Endogenous Formaldehyde ; Thoracic Aorta ; Vasorelaxation ; Mechanism
- 会议召开时间：2016-07-01
- 会议录名称：中国化学会第30届学术年会摘要集-第二十六分会：环境化学
- 语种：中文
- 分类号：R114
- 学会代码：ZGHY
- 会议名称：中国化学会第30届学术年会-第二十六分会 ; 环境化学
- 会议地点：中国辽宁大连
- 主办单位：中国化学会
- 学会名称：中国化学会
- 页数：1
- 文件大小：141k
- 原文格式：D
- 会议级别：全国
摘要
为探究内源性甲醛对血管张力的影响及其内在机制,本文采用离体灌流方法,探究其对大鼠胸主动脉血管环的舒张作用及机制。结果显示:与生理盐水组相比,0.04、0.08 m M甲醛有一定的收缩血管效应,差异不显著(P>0.05);6min时,0.32、0.64、1.28、2.56m M能够引起血管舒张,差异极显著(P<0.01);10min时,0.16、0.32、0.64、1.28、2.56m M甲醛能够引起血管舒张,差异极显著(P<0.01)。与对照组相比,0.64、1.28、2.56m M作用血管6min以上,可溶性鸟苷酸环化酶(s GC)抑制剂亚甲蓝和K+通道抑制剂TEA能够部分抑制其舒张作用,差异显著(P<0.05)。10min时,L-Ca~(2+)通道抑制剂硝苯地平可以对0.64m M甲醛引起的血管舒张产生部分抑制,差异显著(P<0.01)。由此可得,0.04、0.08 m M甲醛不能引起大鼠胸主动脉血管环舒张,0.32、0.64、1.28、2.56m M甲醛可以对该血管环产生舒张作用;0.64、1.28、2.56m M甲醛对血管环的舒张作用可能与NO信号通路、K+通道以及L-Ca~(2+)通道部分相关。
To explore effects of endogenous formaldehyde(FA) on blood vessel and its underlying mechanism,this paper focus on the function of FA on rat thoracic aorta.Results showed that compared with saline group,0.04,0.08 m M FA had little contraction effect on vascular(P>0.05).0.32,0.64,1.28,2.56 m M FA caused significantly vasodilation in 6 minutes(P<0.01).The vasorelaxing effects of 0.16,0.32,0.64,0.32,0.64 m M FA were extremely significant in 10 minutes(P<0.01).When compared with saline,the vasodilation of 0.64,1.28,2.56 m M FA was suppressed by methylene blue and TEA,inhibitors of soluble guanylate cyclase acid and K+ channel respectively(P<0.05).And the vasodilation of 0.64 m M FA was inhibited partly by nifedipine(P<0.01),an inhibitor of L-Ca~(2+)channel.Thus,the vasodilation mechanisms on rat thoracic aorta of endogenous formaldehyde is related to NO signaling pathway,K+ channel and L-Ca~(2+) channel somehow.
To explore effects of endogenous formaldehyde(FA) on blood vessel and its underlying mechanism,this paper focus on the function of FA on rat thoracic aorta.Results showed that compared with saline group,0.04,0.08 m M FA had little contraction effect on vascular(P>0.05).0.32,0.64,1.28,2.56 m M FA caused significantly vasodilation in 6 minutes(P<0.01).The vasorelaxing effects of 0.16,0.32,0.64,0.32,0.64 m M FA were extremely significant in 10 minutes(P<0.01).When compared with saline,the vasodilation of 0.64,1.28,2.56 m M FA was suppressed by methylene blue and TEA,inhibitors of soluble guanylate cyclase acid and K+ channel respectively(P<0.05).And the vasodilation of 0.64 m M FA was inhibited partly by nifedipine(P<0.01),an inhibitor of L-Ca~(2+)channel.Thus,the vasodilation mechanisms on rat thoracic aorta of endogenous formaldehyde is related to NO signaling pathway,K+ channel and L-Ca~(2+) channel somehow.
引文
[1]Min,S;Lei,Z;Ruixin,W;Shuqiang,Y.Vascular.Pharmacology.2013,58:6470.
[2]孟紫强,李君灵,张全喜,杨振华.生物物理学报,2009(S1):220-221.
[3]Meng,Z;Yang,Z;Li,J;Zhang,Q.Vascular.Chemosphere.2012,89:57984.
[2]孟紫强,李君灵,张全喜,杨振华.生物物理学报,2009(S1):220-221.
[3]Meng,Z;Yang,Z;Li,J;Zhang,Q.Vascular.Chemosphere.2012,89:57984.