TRPV1 Contributes to Modulate the Nitric Oxide Pathway and Oxidative Stress in the Isolated and Perfused Rat Heart during Ischemia and Reperfusion.
TRPV1 Contributes to Modulate the Nitric Oxide Pathway and Oxidative Stress in the Isolated and Perfused Rat Heart during Ischemia and Reperfusion.
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DOI：
10.3390/molecules27031031
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发表时间：
2022-02-03
期刊：
影响因子：
--
通讯作者：
Torres-Narváez JC
中科院分区：
文献类型：
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作者：
Castrejón-Téllez V;Del Valle-Mondragón L;Pérez-Torres I;Guarner-Lans V;Pastelín-Hernández G;Ruiz-Ramírez A;Díaz-Juárez JA;Varela-López E;Oidor-Chan VH;Vargas-González A;Martínez-Memije R;Flores-Chávez P;León-Ruíz B;Arriaga-Carrillo S;Torres-Narváez JC
瞬时香草样受体1型(TRPV1)调节一氧化氮(NO)和降钙素基因相关肽(CGRP)介导的神经元和血管功能。在此，我们研究了TRPV1在心肌缺血再灌注损伤的调节和NO、四氢生物蝶呤(BH4)、cGMP途径、CGRP、总抗氧化能力(TAC)、丙二醛(MDA)和磷酸二酯酶-3(PDE-3)等方面的作用。采用大鼠离体心灌流技术，观察TRPV1激动剂辣椒素(CS)、拮抗剂辣椒碱(CZ)及其合用对心脏功能的影响。心脏分为三种状态：(1)对照组，(2)缺血和(3)缺血-再灌注。测定给予CS、CZ和CZ+CS后心脏机械活动及心肌组织中NO、cGMP、BH4、CGRP、TAC、MDA和PDE-3的含量。免疫印迹法检测内皮型一氧化氮合酶、诱导型一氧化氮合酶和磷酸化一氧化氮合酶(PNOS)的表达。通过组织学评价确定组织结构的变化。CS通过改善心脏机械活动，升高NO、cGMP、BH4、TAC和CGRP水平，预防缺血再灌注损伤。在缺血条件下，TRPV1和iNOS表达增加，eNOS和pNOS表达没有改变。结论：TRPV1的激活可能通过CGRP调节NO通路，从而对抗脑缺血再灌注损伤。
The transient vanilloid receptor potential type 1 (TRPV1) regulates neuronal and vascular functions mediated by nitric oxide (NO) and by the calcitonin gene-related peptide (CGRP). Here, we study the participation of TRPV1 in the regulation of myocardial injury caused by ischemia-reperfusion and in the control of NO, tetrahydrobiopterin (BH4), the cGMP pathway, CGRP, total antioxidant capacity (TAC), malondialdehyde (MDA) and phosphodiesterase-3 (PDE-3). Isolated hearts of Wistar rats perfused according to the Langendorff technique were used to study the effects of an agonist of TRPV1, capsaicin (CS), an antagonist, capsazepine (CZ), and their combination CZ+CS. The hearts were subjected to three conditions: (1) control, (2) ischemia and (3) ischemia-reperfusion. We determined cardiac mechanical activity and the levels of NO, cGMP, BH4, CGRP, TAC, MDA and PDE-3 in ventricular tissue after administration of CS, CZ and CZ+CS. Western blots were used to study the expressions of eNOS, iNOS and phosphorylated NOS (pNOS). Structural changes were determined by histological evaluation. CS prevented damage caused by ischemia-reperfusion by improving cardiac mechanical activity and elevating the levels of NO, cGMP, BH4, TAC and CGRP. TRPV1 and iNOS expression were increased under ischemic conditions, while eNOS and pNOS were not modified. We conclude that the activation of TRPV1 constitutes a therapeutic possibility to counteract the damage caused by ischemia and reperfusion by regulating the NO pathway through CGRP.
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DOI：
10.1016/j.jconrel.2014.09.027
发表时间：
2014-12-28
期刊：
Journal of controlled release : official journal of the Controlled Release Society
影响因子：
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作者：
Rollyson WD;Stover CA;Brown KC;Perry HE;Stevenson CD;McNees CA;Ball JG;Valentovic MA;Dasgupta P
通讯作者：
Dasgupta P
影响因子：
3.9
作者：
Geoffroy, V;Fouque, F;Benelli, C
通讯作者：
Benelli, C
瞬时受体电位香草酸1介导的内皮细胞源性降钙素基因相关肽的表达和分泌
影响因子：
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作者：
Luo, Dan;Zhang, Yi-Wei;Li, Yuan-Jian
通讯作者：
Li, Yuan-Jian
影响因子：
--
作者：
Bosnjak ZJ;Ge ZD
通讯作者：
Ge ZD
DOI：
10.3390/ijerph16193576
发表时间：
2019-10-01
影响因子：
--
作者：
Carlos Torres-Narvaez, Juan;Perez-Torres, Israel;del Valle-Mondragon, Leonardo
通讯作者：
del Valle-Mondragon, Leonardo