Regular dipyridamole therapy produces sustained protection against cardiac ischemia–reperfusion injury: Is it time to revisit PARIS?

Figueredo, Vincent M.; Okusa, Chika; Kaneda, Kazuhiro; Inamura, Yoshitaka; Miyamae, Masami

doi:10.1016/j.ijcard.2014.08.013

Cited by 6 publications

(7 citation statements)

References 23 publications

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“…The major source of cardiac NO generated by eNOS can exert a potent anti-inflammatory and antiapoptotic effect in MI/RI. 32 Our data demonstrated that pretreatment with BCF significantly upregulated phosphorylated eNOS and p-Akt protein expression, increased the NO content, and decreased the MPTP level. These findings suggested that the inhibition of MPTP opening in the myocardium might be at least partially involved in the antiapoptosis mechanisms of BCF in MI/RI.…”

Section: Discussionmentioning

confidence: 49%

Bauhinia championii flavone inhibits apoptosis and autophagy via the PI3K/Akt pathway in myocardial ischemia/reperfusion injury in rats

Jian¹,

Xuan²,

F³

et al. 2015

DDDT

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This study aimed to determine the effects of Bauhinia championii flavone (BCF) on myocardial ischemia/reperfusion injury (MI/RI) in rats and to explore potential mechanisms. The MI/RI model in rats was established by ligating the left anterior descending coronary artery for 30 minutes, then reperfusing for 3 hours. BCF at 20 mg/kg was given 20 minutes prior to ischemia via sublingual intravenous injection, with 24 μg/kg phosphoinositide 3-kinase inhibitor (PI3K; wortmannin) as a control. The creatine kinase-MB and nitric oxide content were assessed by colorimetry. The levels of mitochondrial permeability transition pores and tumor necrosis factor alpha were determined by an enzyme-linked immunosorbent assay. Cardiomyocyte apoptosis was detected by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Additionally, the expression of PI3K, endothelial nitric oxide synthase, caspase-3, and Beclin1 was analyzed by fluorescence quantitative polymerase chain reaction and Western blotting, respectively. Akt and microtubule-associated protein 1 light chain 3-II protein levels were also evaluated. Pretreatment with BCF significantly decreased the levels of creatine kinase-MB, tumor necrosis factor alpha, and mitochondrial permeability transition pores, but increased the nitric oxide content. Furthermore, BCF inhibited apoptosis, downregulated caspase-3, Beclin1, and microtubule-associated protein 1 light chain 3-II, upregulated PI3K, and increased the protein levels of phosphorylated Akt and endothelial nitric oxide synthase. However, all of the previously mentioned effects of BCF were blocked when BCF was coadministered with wortmannin. In conclusion, these observations indicated that BCF has cardioprotective effects against MI/RI by reducing cell apoptosis and excessive autophagy, which might be related to the activation of the PI3K/Akt signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 49%

Bauhinia championii flavone inhibits apoptosis and autophagy via the PI3K/Akt pathway in myocardial ischemia/reperfusion injury in rats

Jian¹,

Xuan²,

F³

et al. 2015

DDDT

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“…The similarity in the effects of the NBMPR and adenosine pre-treatment on the maximum contraction generated by phenylephrine in the aortas from wild-type mice suggests that NBMPR was enhancing extracellular adenosine levels and thereby mediating an adenosine-induced preconditioning-like effect. Others have also shown that treatment of tissues with adenosine [ 3 ], or with the adenosine uptake inhibitor dipyridamole [ 62 ], can protect those tissues from subsequent ischemia-reperfusion induced injury. Given that aortas from the Slc29a1 -null mice have been chronically exposed to elevated adenosine, they may already be preconditioned and consequently further exposure to adenosine or NBMPR has no effect.…”

Section: Discussionmentioning

confidence: 99%

Changes in aortic reactivity associated with the loss of equilibrative nucleoside transporter 1 (ENT1) in mice

Best¹,

Bone²,

Vilas³

et al. 2018

PLoS ONE

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Slc29a1 encodes for equilibrative nucleoside transporter subtype 1 (ENT1), the primary mechanism of adenosine transfer across cell membranes. Previous studies showed that tissues isolated from Slc29a1-null mice are relatively resistant to injury caused by vascular ischemia-reperfusion. To determine if there are similar changes in the microvasculature, and investigate underlying mechanism, we examined aortas isolated from wildtype and Slc29a1-null mice. Aorta macrostructure and gene expression were examined histologically and by qPCR, respectively. Wire myography was used to assess the contractile properties of isolated thoracic aortic rings and their response to adenosine under both normoxic and hypoxic conditions. In vivo haemodynamic parameters were assessed using the tail-cuff method. Slc29a1-null mice had significantly (P<0.05) increased plasma adenosine (2.75-fold) and lower blood pressure (~15% ↓) than wild-type mice. Aortas from Slc29a1-null mice were stiffer with a smaller circumference (11% ↓), and had an enhanced contractile response to KCl and receptor-mediated stimuli. Blockade of ENT1 with nitrobenzylthioinosine significantly enhanced (by ~3.5-fold) the response of aorta from wild-type mice to phenylephrine, but had minimal effect on aortas from Slc29a1-null mice. Adenosine enhanced phenylephrine-mediated constriction in the wild-type tissue under both normoxic (11.7-fold) and hypoxic (3.6-fold) conditions, but had no effect on the Slc29a1-null aortic aorta. In conclusion, aortas from Slc29a1-null mice respond to hypoxic insult in a manner comparable to wild-type tissues that have been pharmacologically preconditioned with adenosine. These data also support a role for ENT1 in the regulation of the protective effects of adenosine on contractile function in elastic conduit arteries such as thoracic aorta.

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“…The effective components of ginkgo-diyidamolum include extracts of traditional Chinese medicine, folium ginkgo, and western medicine, dipyridamole. The former one can be specifically against the platelet activating factor [15][16][17], while the latter one can inhibit adenosine diphosphate and thromboxane [18]. TRAIL is also included in tumor necrosis factor receptor which can induce apoptosis through two cascade amplifier channels, nuclear factor-kappa B and caspase [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

Effect of adjuvant therapy with ginkgo-damole on apoptosis, nerve injury and platelet aggregation of patients with acute cerebral infarction

2017

JAD

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Regular dipyridamole therapy produces sustained protection against cardiac ischemia–reperfusion injury: Is it time to revisit PARIS?

Cited by 6 publications

References 23 publications

Bauhinia championii flavone inhibits apoptosis and autophagy via the PI3K/Akt pathway in myocardial ischemia/reperfusion injury in rats

Bauhinia championii flavone inhibits apoptosis and autophagy via the PI3K/Akt pathway in myocardial ischemia/reperfusion injury in rats

Changes in aortic reactivity associated with the loss of equilibrative nucleoside transporter 1 (ENT1) in mice

Effect of adjuvant therapy with ginkgo-damole on apoptosis, nerve injury and platelet aggregation of patients with acute cerebral infarction

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