Cardioprotective Effects of Astragalin against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart

Qu, Daoxu; Han, Jichun; Ren, Huanhuan; Yang, Wenxiao; Zhang, Xinjie; Zheng, Qi; Wang, Dong

doi:10.1155/2016/8194690

Cited by 55 publications

(45 citation statements)

References 35 publications

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“…Measurement of heart hemodynamic parameters revealed that 10 µmol/l of each agent significantly improved functional recovery during early reperfusion (data not shown). This is consistent with the results of some studies indicating that this moderate dose may demonstrate protective effects (21,22). Therefore, 10 µmol/l was selected for the experiments performed in the current study.…”

Section: Chemicals Astragalin and Dihydromyricetin (Purity ≥98%)supporting

confidence: 89%

Astragalin and dihydromyricetin as adjuncts to histidine‑tryptophan‑ketoglutarate cardioplegia enhances protection during cardioplegic arrest

Wang

Zhang

et al. 2018

Mol Med Report

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The present study used an in vitro model of cold cardioplegia in isolated working rat hearts to evaluate the possible effects of two flavonoids, astragalin and dihydromyricetin, as adjuncts to histidine‑tryptophan‑ketoglutarate (HTK) cardioplegia. The following three groups of male Sprague Dawley rats were evaluated: The HTK group, treated with HTK alone; the HTK‑A group, treated with 10 µmol/l astragalin; and the HTK‑D group, treated with 10 µmol/l dihydromyricetin. Isolated rat hearts were perfused with Krebs‑Henseleit buffer for 30 min and incubated with the respective cardioplegic solution for 6 h at 4˚C. Subsequently, astragalin or dihydromyricetin was added to the cardioplegic solutions. Following 30 min of reperfusion, the left ventricular developed pressure (LVDP), maximum up/down rate of left ventricular pressure (±dp/dtmax) and heart rate were documented as indices of myocardial function using a physiological recorder. Myocardial infarct size (IS) was estimated using 2,3,5‑triphenyltetrazolium chloride staining. Lactate dehydrogenase (LDH) and creatine kinase (CK) levels were also determined to assess the degree of cardiac injury. Cardiomyocyte apoptosis analysis was performed using an in situ cell death detection kit. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), interleukin‑6 (IL‑6), tumor necrosis factor‑α (TNF‑α), C‑reactive protein (CRP) levels, as well as the glutathione/glutathione disulfide (GSH/GSSG) ratio were determined and analyzed using ELISA kits. The protein levels of caspase‑9 and B‑cell lymphoma‑2 (Bcl‑2) were determined using western blot analysis. The results demonstrated that exposure to astragalin or dihydromyricetin significantly improved the recovery of LVDP (P<0.05 and P<0.01, respectively), the +dP/dtmax (P<0.05 for dihydromyricetin only) and the ‑dP/dtmax (P<0.05 and P<0.01, respectively), increased SOD levels (P<0.05 and P<0.01, respectively) and GSH/GSSG ratios (P<0.05), reduced myocardial IS (P<0.05 and P<0.01, respectively), decreased CK, LDH, IL‑6 (all P<0.05 and P<0.01, respectively), MDA (P<0.05), CRP (P<0.05) and TNF‑α levels (P<0.05 and P<0.01, respectively), increased Bcl‑2 levels (P<0.01) and decreased caspase‑9 levels (P<0.01). The results indicated that the addition of either flavonoid (particularly dihydromyricetin) to HTK enhances protection during ischemia, decreases myocardial dysfunction by enhancing anti‑inflammatory activities, attenuates myocardial oxidative injury and prevents apoptosis during ischemia/reperfusion.

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Section: Chemicals Astragalin and Dihydromyricetin (Purity ≥98%)supporting

confidence: 89%

Astragalin and dihydromyricetin as adjuncts to histidine‑tryptophan‑ketoglutarate cardioplegia enhances protection during cardioplegic arrest

Wang

Zhang

et al. 2018

Mol Med Report

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“…GSH with glutathione peroxidase (GPx) metabolizes hydrogen peroxide and organic hydroperoxodes to hinder the peroxidation chain reaction and protect protein thiol groups from non-enzymatic oxidation [19]. There are lots of studies revealing that GSH level was significantly decreased in different IRI models [20,[40][41][42].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Vitamin C Supplementation on Kidney Function and Vascular Reactivity Following Renal Ischemic Injury in Mice

Zhu¹,

Zhang²,

Zhang³

et al. 2016

Kidney Blood Press Res

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Background/Aims: Renal ischemia/reperfusion injury (IRI) is a very common clinical event and usually leads to ischemic acute renal failure (ARF). In the present study, we investigated the protective role of vitamin C in renal function and renal arterial relaxation following ischemic injury. Methods: IRI model in mice was used. Various biochemical parameters including nitric oxide (NO), reduced glutathione (GSH), total reactive oxygen species (ROS) level and superoxide dismutase (SOD) were examined. Doppler was used to investigate renal arterial resistance. The isolated renal arterial rings served for hypoxia/reoxygenation analysis. Acetylcholine (ACh) and sodium nitroprusside (SNP)-induced relaxations of isolated renal arterial rings were exerted. Results: Vitamin C supplementation preserved kidney morphology and renal function following IRI. It was shown that pretreatment with vitamin C for mice subjected to IRI significantly elevated renal NO and GSH levels after reperfusion. Meanwhile, vitamin C administration decreased resistance index of renal artery and ameliorated oxidative stress secondary to IRI. The total ROS level in renal artery was decreased whereas the renal arterial SOD expression was increased by vitamin C supplementation following IRI. Pretreatment with vitamin C significantly potentiated the ACh and SNP-induced relaxations in both control and hypoxic renal arterial rings. Conclusion: Vitamin C protects kidney function and renal arterial reactivity against IRI. The protective role of vitamin C is linked to ROS, SOD, GSH and NO levels in renal ischemic injury.

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“…To evaluate the size of I/R-related myocardial infarct in rat hearts, we used TTC staining to measure the myocardial infarct size. The experiments were performed as described previously [ 14 , 22 – 24 ].…”

Section: Methodsmentioning

confidence: 99%

“…Flavonoids possess unique antioxidant properties and other pharmacological activities that may be relevant in protecting the heart from I/R injury; studies have also found that many flavonoids can protect against myocardial I/R injury [ 14 , 15 ]. Kaempferide (3,5,7-trihydroxy-4′-methoxyflavone, Kae) is a naturally occurring flavonoid that is isolated from the roots of Alpinia officinarum (lesser galangal) [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Kaempferide Protects against Myocardial Ischemia/Reperfusion Injury through Activation of the PI3K/Akt/GSK-3β Pathway

Wang

Zhang

et al. 2017

Mediators of Inflammation

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The aim of this study is to investigate both the efficacy and mechanism of action of kaempferide (Kae) as a therapy for the treatment of cardiovascular disease. A rat model of myocardial ischemia/reperfusion (I/R) injury was established by ligation of the left anterior descending coronary artery for 30 min followed by a 2 h perfusion. In our study, we show that Kae remarkably improved cardiac function, alleviated myocardial injury via a decrease in myocardial enzyme levels, and attenuated myocardial infarct size in a dose-dependent manner. In addition, preconditioning treatment with Kae was found to significantly decrease serum TNF-α, IL-6, C-reactive protein (CRP), MDA, and ROS levels, while it was found to increase serum levels of SOD. Nuclear factor erythroid 2-related factor 2 (Nrf2) and cleaved caspase-3 expression levels were observed to be downregulated, while phospho-Akt (p-Akt) and phospho-glycogen synthase kinase-3β (p-GSK-3β) expression levels were upregulated. However, cotreatment with LY294002 (a PI3K inhibitor) or TDZD-8 (a GSK-3β inhibitor) was found to abolish the above cardioprotective effects observed with the Kae treatment. The data presented in this study provides evidence that Kae attenuates I/R-induced myocardial injury through inhibition of the Nrf2 and cleaved caspase-3 signaling pathways via a PI3K/Akt/GSK 3β-dependent mechanism.

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Cardioprotective Effects of Astragalin against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart

Cited by 55 publications

References 35 publications

Astragalin and dihydromyricetin as adjuncts to histidine‑tryptophan‑ketoglutarate cardioplegia enhances protection during cardioplegic arrest

Astragalin and dihydromyricetin as adjuncts to histidine‑tryptophan‑ketoglutarate cardioplegia enhances protection during cardioplegic arrest

Evaluation of Vitamin C Supplementation on Kidney Function and Vascular Reactivity Following Renal Ischemic Injury in Mice

Kaempferide Protects against Myocardial Ischemia/Reperfusion Injury through Activation of the PI3K/Akt/GSK-3β Pathway

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