GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Olmesartan prevents cardiac rupture in mice with myocardial infarction by modulating growth differentiation factor 15 and p53
    Wiley ; 2014
    In:  British Journal of Pharmacology Vol. 171, No. 15 ( 2014-08), p. 3741-3753
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 171, No. 15 ( 2014-08), p. 3741-3753
    Abstract: Cardiac rupture is a catastrophic complication that occurs after acute myocardial infarction ( MI ) and, at present, there are no effective pharmacological strategies for preventing this condition. Here we investigated the effect of the angiotensin II receptor blocker olmesartan ( O lm) on post‐infarct cardiac rupture and its underlying mechanisms of action. Experimental Approach C 57 B l/6 mice with MI were treated with O lm, aldosterone ( A ldo) or vehicle. Cultured neonatal cardiomyocytes and fibroblasts were exposed to normoxia or anoxia and treated with angiotensin II ( A ng II ), RNH 6270 (active ingredient of O lm) or A ldo. Key Results The mortality rate and incidence of cardiac rupture in MI mice during the first week in the O lm‐treated group were significantly lower than in the vehicle‐treated group. O lm or RNH 6270 reduced myeloperoxidase staining in the infarcted myocardium, decreased apoptosis in cultured cardiomyocytes and fibroblasts, as assessed by H oechst staining and TUNEL assay, attenuated the accumulation of p53 and phosphorylated p53 and cleaved caspase 3 induced by MI or A ng II, as assessed by Western blotting, and up‐regulated growth differentiation factor‐15 ( GDF ‐15). In cultured cardiomyocytes and fibroblasts, treatment with A ng II, Aldo or anoxia significantly down‐regulated the expression of GDF ‐15. Conclusions and Implications O lm prevents cardiac rupture through inhibition of apoptosis and inflammation, which is attributable to the down‐regulation of p53 activity and up‐regulation of GDF ‐15. Our findings suggest that early administration of an AT 1 receptor anatagonist to patients with acute MI is a potential preventive approach for cardiac rupture.
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.2014.171.issue-15
    DOI: 10.1111/bph.12736
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 2029728-2
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Trimetazidine Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury by Promoting AMP-activated Protein Kinase–dependent Autophagic Flux
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of Cardiovascular Pharmacology Vol. 69, No. 6 ( 2017-06), p. 389-397
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 69, No. 6 ( 2017-06), p. 389-397
    Abstract: Trimetazidine (TMZ), a metabolic agent, may protect against myocardial ischemia/reperfusion injury. Because of the critical role of autophagy in cardioprotection, we aimed to evaluate whether autophagy was involved in TMZ-induced protection during hypoxia/reoxygenation (H/R). Neonatal rat cardiomyocytes were subjected to H/R injury, and they were divided into 7 groups: control, control+TMZ, control+chloroquine (Cq)/compound C (com C), H/R, H/R+TMZ, H/R+Cq/com C, and H/R+TMZ+Cq/com C. Autophagic flux was primarily assessed by Western blot and tandem fluorescent mRFP-GFP-LC3. Assays for MTS, terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling, and lactate dehydrogenase release were performed to assess cell injury. Our results showed that TMZ pretreatment had a cardioprotective effect against H/R injury. The H/R+TMZ group had an increased ratio of LC3-II to LC3-I and increased autophagic flux (degradation of p62 and increases in autophagosomes and autolysosomes). TMZ also reduced apoptosis and enhanced cell survival while inducing autophagy. Correspondingly, autophagy inhibition with Cq blocked this protective effect. Furthermore, TMZ-induced enhancement of autophagy could be related to increased AMP-activated protein kinase (AMPK) phosphorylation and decreased Mammalian target of rapamycin (mTOR) phosphorylation, which was abolished by an AMPK-specific inhibitor (com C). Our data provide evidence that TMZ pretreatment protects against H/R injury by promoting autophagic flux through the AMPK signaling pathway.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000000487
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...