Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Abstract

Summary Introduction Myocardial ischemia/reperfusion injury (myocardial I/R injury) has a high disability rate and mortality. Novel treatments for myocardial I/R injury are necessary. Aim In order to explore the protective effect of hydromorphine on myocardial I/R injury, we illuminate the underlying mechanism of the protective effect. Results Hydromorphine significantly reduced myocardial infarct size (IFN/AAR), CKMB (Creatine Kinase MB) and TN‐T (Troponin T) release, and improved cardiac function compared with I/R group. However, these advantageous effects were partly suppressed in the presence of hydromorphine. Myocardial I/R injury significantly decreased the phosphorylation of Akt and eNOS, and down‐regulated total nitric oxide and nitrotyrosine content, while these inhibitory effects were partly abolished by hydromorphine. Conversely, the activated effects of hydromorphine on the phosphorylation of Akt and eNOS, and NO release were totally reversed by LY294002, which, used individually, show the same influence on reperfusion injury. Conclusions These findings suggest that hydromorphine postconditioning may protect isolated rat heart against reperfusion injury via activating P13K/Akt/eNOS signaling.

Effect of miR-134 against myocardial hypoxia/reoxygenation injury by directly targeting NOS3 and regulating PI3K/Akt pathway

“…It is known to all that the PI3K/Akt pathway is an important signaling pathway diametrically correlated with cellular behaviors and diverse molecular mechanisms 29 . Moreover, in accordance with the previous reports, the myocardial I/R injury moderation has a close interaction with the PI3K/Akt/eNOS signaling pathway 30 , which is consistent with our results that higher expression of NOS3 was beneficial to myocardial I/R injury. A large set of significant clusters has also raised the credibility of the correlation between the PI3K/Akt pathway and myocardial I/R injury through diverse target substances, such as total paeony glycoside, hesperidin, shikonin, 6-Gingerol and so forth 31 - 34 .…”

Efficacy of Alkaloids in Alleviating Myocardial Ischemia-Reperfusion Injury in Rats: A Meta-Analysis of Animal Studies

“…After screening titles and abstracts, 40 studies were considered potentially eligible for inclusion. After estimating full-text publications, 14 studies were excluded due to intervention or outcome data were unqualified [28][29][30][31][32][33][34][35][36][37][38][39][40][41], and four studies were excluded because pure alkaloids were not assessed [42][43][44][45]. Finally, 22 studies were included in the present meta-analysis [13-14, 19-27, 46-56] (Figure 1).…”

Estandarización del modelo langendorff de corazón aislado para evaluar los daños inducidos por isquemia-reperfusión

“…En contraste, la viabilidad del tejido se mantiene cuando se perfunde a 10,5 mL/min (79,06 a 82,36 mmHg control y 120 minutos, respectivamente). Autores como Liu y col. (2018) reportan valores de PDVI similares a los obtenidos en nuestro estudio [8]. Al valorar el impacto que sobre este parámetro poseen las intervenciones para generar I/R, observamos que la DO redujo la PDVI.…”

“…Evaluando este parámetro, volvemos a observar como el estrés inducido por una elevada velocidad de perfusión genera una reducción del trabajo cardiaco en el tiempo, enmascarando el efecto de la inducción de la isquemia por DO (Fig 2). Autores como Liu y col (2018) reportan valores de DP parecidos a los nuestros [8].…”