These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Morphine alleviates myocardial ischemia/reperfusion injury in rats by inhibiting TLR4/NF-κB signaling pathway.
    Author: Wang Y, Wang L, Li JH, Zhao HW, Zhang FZ.
    Journal: Eur Rev Med Pharmacol Sci; 2019 Oct; 23(19):8616-8624. PubMed ID: 31646595.
    Abstract:
    OBJECTIVE: The aim of this study was to investigate the effect of morphine on myocardial ischemia/reperfusion (I/R) injury in rats and its underlying mechanism, thereby providing a reference for the prevention and treatment of myocardial I/R injury in clinical practice. MATERIALS AND METHODS: A total of 60 male Sprague-Dawley (SD) rats were randomly divided into 3 groups, including: Sham group (n=20), I/R group (n=20) and I/R + morphine group (n=20) using a random number table. The left anterior descending coronary artery (LAD) of rat was ligated and re-canalized, and the I/R model was established in rats. Rats in I/R + sevoflurane (SEV) group were pretreated with 2.5% SEV. Infarction area of heart in each group was detected using triphenyltetrazolium chloride (TTC) test. Ejection fraction % (EF%) and fraction shortening % (FS%) were determined by echocardiography. Hematoxylin-eosin (HE) staining assay was performed to detect the morphological changes of cardiac myocardial cells in each group. Meanwhile, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) staining was adopted to detect the apoptosis of myocardial cells and fibroblasts. In addition, the expression levels of toll-like receptor 4 (TLR4) and p65 in heart samples of rats in each group were measured via immuno-histochemical staining. Finally, the influence of morphine on TLR4/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway was detected using Western blotting. RESULTS: Morphine significantly alleviated I/R-induced cardiac dysfunction in rats, whereas significantly increased EF% and FS% (p<0.05). In addition, morphine evidently inhibited myocardial infarction caused by I/R injury. Meanwhile, it reduced the infarction area from [(59.61±3.41) %] to [(26.67±3.62) %] (p<0.05). The results of HE staining showed that compared with I/R group, I/R + morphine group exhibited remarkably tidier cardiac myofilament, less degradation and necrosis, as well as significantly relieved cellular edema. Immuno-histochemical staining results revealed that morphine overtly reversed decreased expressions of TLR4 and p65 induced by I/R in rats (p<0.05). Furthermore, Western blotting found that morphine significantly inhibited the protein expressions of TLR4 and phosphorylated p65. CONCLUSIONS: Morphine clearly alleviates I/R-induced myocardial injury in rats. The possible mechanism may be associated with the inhibition on TLR4/NF-κB signaling pathway.
    [Abstract] [Full Text] [Related] [New Search]