PEDF improves cardiac function in rats subjected to myocardial ischemia/reperfusion injury by inhibiting ROS generation via PEDF‑R

Although miR-327 had a protective effect on cardiomyocytes as described previously, the potential mechanism still needs further exploration. The aim of this study was to investigate the role and mechanism of miR-327 on oxidative stress in myocardial ischemia/reperfusion injury (MI/RI) process. Oxidative stress and cardiomyocytes injury were detected in rat model of MI/RI, hypoxia/reoxygenation (H/R), and tert-butyl hydroperoxide (TBHP) model of H9c2 cells. In vitro, downregulation of miR-327 inhibited both H/R- and TBHP-induced oxidative stress, and suppressed apoptosis. Meanwhile, fibroblast growth factor 10(FGF10) was enhanced by miR-327 knocked down, followed by the activation of p-PI3K and p-Akt, and the translocation of Nrf2. However, miR-327 overexpression performed with opposite effects. Consistent with the results in vitro, downregulation of miR-327 attenuated reactive oxygen species (ROS) generation as well as intrinsic apoptosis, and alleviated I/R injury. In conclusion, inhibition of miR-327 improved antioxidative ability and myocardial cell survival via regulating the FGF10/Akt/Nrf2 pathway.

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P515Phosphorylcholine antibodies preserve cardiac function and reduce infarct size by attenuation of the inflammatory response following myocardial ischemia-reperfusion injury

Cardiovascular Research ◽

10.1093/cvr/cvy060.372 ◽

2018 ◽

Vol 114 (suppl_1) ◽

pp. S125-S126

Author(s):

N J Pluijmert ◽

RCM De Jong ◽

M R De Vries ◽

K Pettersson ◽

J W Jukema ◽

...

Keyword(s):

Myocardial Ischemia ◽

Inflammatory Response ◽

Cardiac Function ◽

Infarct Size ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Reduce Infarct Size ◽

Myocardial Ischemia Reperfusion Injury ◽

Myocardial Ischemia Reperfusion

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Annexin A5 reduces infarct size and improves cardiac function after myocardial ischemia-reperfusion injury by suppression of the cardiac inflammatory response

Scientific Reports ◽

10.1038/s41598-018-25143-y ◽

2018 ◽

Vol 8 (1) ◽

Cited By ~ 10

Author(s):

Rob C. M. de Jong ◽

Niek J. Pluijmert ◽

Margreet R. de Vries ◽

Knut Pettersson ◽

Douwe E. Atsma ◽

...

Keyword(s):

Myocardial Ischemia ◽

Inflammatory Response ◽

Cardiac Function ◽

Infarct Size ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Annexin A5 ◽

Myocardial Ischemia Reperfusion Injury ◽

Myocardial Ischemia Reperfusion

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Cardioprotective Effect of Betulinic Acid on Myocardial Ischemia Reperfusion Injury in Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2014/573745 ◽

2014 ◽

Vol 2014 ◽

pp. 1-10 ◽

Cited By ~ 14

Author(s):

Anzhou Xia ◽

Zhi Xue ◽

Yong Li ◽

Wei Wang ◽

Jieyun Xia ◽

...

Keyword(s):

Myocardial Ischemia ◽

Cardiac Function ◽

Reperfusion Injury ◽

Betulinic Acid ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Tunel Assay ◽

Sham Operation ◽

Myocardial Ischemia Reperfusion Injury ◽

Myocardial Ischemia Reperfusion

Objectives. This study aims to investigate the effect of betulinic acid (BA) on myocardial ischemia reperfusion/injury in an open-chest anesthetized rat model.Methods. The model was induced by 30 minutes left anterior descending occlusion followed by 2 hours reperfusion. There are six groups in our present study: sham operation group, ischemia/reperfusion group, low-dosage BA group, medium-dosage BA group, high-dosage BA group, and fosinopril sodium group. Rats in the latter four groups were administrated with BA (50, 100, and 200 mg/kg, i.g.) or fosinopril sodium (10 mg/kg, i.g.) once a day for 7 days before operation, respectively. Rats in the former two groups were given the same volume of vehicle (0.5% CMC-Na, i.g.). During the operation, cardiac function was continuously monitored. Serum LDH and CK were measured with colorimetric assays. The expression of Bcl-2 and Bax and the apoptosis of cardiomyocytes were investigated with western blot and TUNEL assay, respectively.Results. Pretreatment with BA improved cardiac function and attenuated LDH and CK activities compared with IR group. Further investigation demonstrated that the expression of Bcl-2 and Bax and TUNEL assay was in line with the above results.Conclusion. BA may reduce the release of LDH and CK, prevent cardiomyocytes apoptosis, and eventually alleviate the extent of the myocardial ischemia/reperfusion injury.

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Visnagin ameliorates myocardial ischemia/reperfusion injury through the promotion of autophagy and the inhibition of apoptosis

European Journal of Histochemistry ◽

10.4081/ejh.2020.3131 ◽

2020 ◽

Vol 64 (s2) ◽

Author(s):

Hai-rong Fu ◽

Xiao-shan Li ◽

Yong-hui Zhang ◽

Bin-bin Feng ◽

Lian-hong Pan

Keyword(s):

Myocardial Ischemia ◽

Cardiac Function ◽

Protective Effect ◽

Reperfusion Injury ◽

Sham Group ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Tunel Staining ◽

Myocardial Ischemia Reperfusion Injury ◽

Myocardial Ischemia Reperfusion

Visnagin is a furanochromone and one of the main compounds of Ammi visnaga L. that had been used to treat nephrolithiasis in Ancient Egypt. Nowadays, visnagin was widely used to treat angina pectoris, urolithiasis and hypertriglyceridemia. The potential mechanisms of visnagin involved in inflammation and cardiovascular disease were also identified. But the protective effect of visnagin on myocardial ischemia/reperfusion injury has not been confirmed. Our aim was, for the first time, to investigate the potential protective effect of visnagin on cardiac function after myocardial ischemia-reperfusion injury in a rat model, and to identify its underlying mechanism involving the inhibition of apoptosis and induction of autophagy. Thirty SD rats were randomly divided into sham group, ischemia/reperfusion group (IR), ischemia/reperfusion with visnagin (IR + visnagin) group. Myocardial ischemia/Reperfusion injury model was established. Hemodynamic measurements and echocardiography were used to analyze cardiac function, TUNEL staining and caspase activity, LC3 dots were detected with immunofluorescence staining, LC3 expression was evaluated by western blot analysis, transmission electron microscopy (TEM) was used to detect autophagosomes. Compared with the sham group and visnagin group, the cardiac dysfunction, LC3II, autophagy flow in the IR+ visnagin group increased significantly (P<0.01), but the activity of caspase-3 and caspase-9 and the apoptotic in the IR + visnagin group decreased significantly (P<0.01). In conclusion, visnagin may play a protective role in ischemia/reperfusion injury by inducing autophagy and reducing apoptosis.

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Endoxin-mediated myocardial ischemia reperfusion injury in rats in vitro

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y04-041 ◽

2004 ◽

Vol 82 (6) ◽

pp. 402-408 ◽

Cited By ~ 2

Author(s):

Yong-Sheng Ke ◽

He-Gui Wang ◽

De-Guo Wang ◽

Gen-Bao Zhang

Keyword(s):

Myocardial Ischemia ◽

Cardiac Function ◽

Atpase Activity ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Rat Hearts ◽

Myocardial Ischemia Reperfusion Injury ◽

Myocardial Ischemia Reperfusion ◽

Isolated Rat

Myocardial ischemia reperfusion results in an increase in intracellular sodium concentration, which secondarily increases intracellular calcium via Na+-Ca2+ exchange, resulting in cellular injury. Endoxin is an endogenous medium of digitalis receptor and can remarkably inhibit Na+/K+-ATPase activity. Although the level of plasma endoxin is significantly higher during myocardial ischemia, its practical significance is unclear. This research is to investigate whether endoxin is one of important factors involved in myocardial ischemia reperfusion injury. Ischemia reperfusion injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts. Heart rate (HR), left ventricular developed pressure (LVDP), and its first derivative (±dp/dtmax) were recorded. The endoxin contents, intramitochondrial Ca2+ contents, and the Na+/K+-ATPase activity in myocardial tissues were measured. Myocardial damages were evaluated by electron microscopy. The endoxin and intramitochondrial Ca2+ contents in myocardial tissues were remarkably higher, myocardial membrane ATPase activity was remarkably lower, the cardiac function was significantly deteriorated, and myocardial morphological damages were severe in myocardial ischemia reperfusion group vs. control. Anti-digoxin antiserum (10, 30 mg/kg) caused a significant improvement in cardiac function (LVDP and ±dp/dtmax), Na+/K+-ATPase activity, and myocardial morphology, and caused a reduction of endoxin and intramitochondrial Ca2+ contents in myocardial tissues. In the present study, the endoxin antagonist, anti-digoxin antiserum, protected the myocardium against the damages induced by ischemia reperfusion in isolated rat hearts. The results suggest that endoxin might be one of main factors mediating myocardial ischemia reperfusion injury.Key words: endoxin, anti-digoxin antiserum, myocardial reperfusion injury, morphological evaluation, Na+/K+-exchanging ATPase.

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