Beneficial effects of astringinin, a resveratrol analogue, on the ischemia and reperfusion damage in rat heart

Hung, Li-Man; Chen, Jan‐Kan; Lee, Ren-Shen; Liang, Hsiu-Chuan; Su, Ming‐Jai

doi:10.1016/s0891-5849(01)00474-9

Cited by 70 publications

(48 citation statements)

References 26 publications

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“…Several studies reported that myocardial injury in occlusion-reperfusion animal includes apoptosis and necrosis [21][22][23][24]. In our previous experiments, we verified that some natural compounds have cardioprotective effects on ischemia-reperfusion injury via releasing NO and increasing coronary flow [17,25,26]. However, in this study, the beneficial protection of myocardium by bunazosin was not associated with an increase of coronary flow.…”

Section: Discussionsupporting

confidence: 50%

Comparison of the cardiac effects between quinazoline-based α1-adrenoceptor antagonists on occlusion–reperfusion injury

Lee

2007

J Biomed Sci

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Quinazoline-based compounds such as prazosin and its congeners including doxazosin, bunazosin, and terazosin are widely used as antihypertensive agents. However, there were many clinical observations showing that using these agents may result in higher risk of cardiovascular accidents in recent years. In this study, we compared the effects of four alpha-adrenoceptor antagonists: prazosin, doxazosin, bunazosin, and terazosin on occlusion-reperfusion injury. Langendorff-perfused rat hearts were pretreated with these four antagonists, and then the left main coronary artery was occluded. After 30 min occlusion, the hearts were reperfused for 2 h and the infarct sizes were measured. Two of the compounds studied, prazosin and doxazosin, apparently increased infarct size, CK-MB, and LDH activities after 2 h reperfusion. In contrast, bunazosin decreased infarct size and those biochemical indicators of cellular damage compared to control hearts. Although infarct size after reperfusion was differently changed by these four alpha-adrenoceptor antagonists, TUNEL-positive nuclei and caspase-3 protein expressions of all the groups were not significantly different. We supposed that the different effects of these four agents on infarct size came from the difference in necrosis rather than apoptosis.

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Section: Discussionsupporting

confidence: 50%

Comparison of the cardiac effects between quinazoline-based α1-adrenoceptor antagonists on occlusion–reperfusion injury

Lee

2007

J Biomed Sci

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“…Therefore, novel bioengineered compounds should be tested as well as cocktails of classical antioxidants in order to reduce the reperfusion injury within the myocardium (Hung et al 2001), which may become efficient supportive treatments for myocardial recovery after AMI and successful convalescence of patients.…”

Section: Discussionmentioning

confidence: 99%

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

Nikolić-Heitzler

Rabuzin

Tatzber

et al. 2006

Tohoku J. Exp. Med.

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[247][248][249][250][251][252][253][254][255] Acute myocardial infarction causing cardiac ischemia is responsible for the majority of cardiac related deaths. Medical interventions that ensure rapid reperfusion, such as percutaneous coronary intervention, are aimed to allow myocardial re-oxygenation. However, this generates reactive oxygen species, resembling ischemiareperfusion type of injury based on oxidative stress. In the present study we monitored dynamic changes of total serum peroxides, total antioxidant capacity and soluble intercellular adhesion molecule-1 as well as the titer of antibodies against oxidized low-density lipoproteins in the blood during the convalescence period of 32 patients with acute myocardial infarction treated by percutaneous coronary intervention. Samples were taken at admittance and at two hours, four hours, three days and seven days following percutaneous coronary intervention. Total antioxidant capacity dropped to 82% ( p < 0.05). The titer of antibodies against oxidized low-density lipoproteins transiently decreased within the first three days, and increased afterwards. The values of serum peroxides and soluble intercellular adhesion molecule-1 increased continuously in respect to the initial levels reaching the maximum at the time of release from hospital. These findings indicate a persistent oxidative stress that might be associated with intravascular inflammation in patients during convalescence and release from hospital. myocardial infarction; percutaneous coronary intervention; inflammation; soluble intercellular adhesion molecule-1; lipid peroxidation © 2006 Tohoku University Medical Press While oxidative stress has been shown to be related with the age and living habits (Ozbay and Dulker 2002), it plays an important role in the development of vascular diseases that affect vital organs, in particular brain and heart (Zarkovic 2003;Zarkovic et al. 2004;Madamanchi et al.

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“…The potential of resveratrol as a cancer chemoprevention reagent has been extensively reviewed (Gusman et al, 2001;Bhat and Pezzuto, 2002;Savouret and Quesne, 2002;Aziz et al, 2003). The possible role of resveratrol, a phytoestrogen, in cardiovascular protection has also been discussed recently (Hung et al, 2001;Wu et al, 2001). Nevertheless, there are two concerns with regard to the use of resveratrol as chemoprevention agent.…”

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confidence: 99%

A methoxy derivative of resveratrol analogue selectively induced activation of the mitochondrial apoptotic pathway in transformed fibroblasts

Gosslau

Chen

et al. 2005

Br J Cancer

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Resveratrol (R-3), a trihydroxy trans-stilbene from grape, inhibits multistage carcinogenesis in animal models. A resveratrol derivative 3,4,5,4 0 -tetrahydroxystilbene (R-4) exhibits potent growth inhibitory effect against transformed human cells. Here we report that 3,4,5,4 0 -tetramethoxystilbene (MR-4), converted from R-4, was more potent against cancer cell lines (WI38VA, IMR-90SV, HeLa, LNCaP, HT-29, and HepG2), but had almost no inhibitory effect on the growth of normal cells (WI38, IMR-90, BJ-T) at the concentrations tested. The IC 50 value of MR-4 on the growth inhibition of transformed WI38VA human cells was 0.5 mM, as compared to the value of greater than 50 mM for the normal WI38 cells. Resveratrol, however, did not exhibit such clear differential effect and the IC 50 value of R-3 for WI38VA cells was about 50 mM. The growth inhibitory effect of MR-4 correlated with the induction of apoptosis in the transformed cells. When normal WI38 cells and transformed WI38VA cells were compared, MR-4 induced increases of the Bax/Bcl-2 mRNA ratio, p53 and Bax protein level, activation of caspases, and DNA fragmentation in transformed, but not in normal cells. Further analysis revealed that MR-4 caused a rapid appearance of perinuclear aggregation of mitochondria in WI38VA but not in WI38 cells, suggesting that the mitochondria could serve as an early target of MR-4. R-3 also induced apoptosis and mitochondrial clustering but only at a much higher concentration, close to 500 mM. Taken together, the specific activation of the mitochondria-mediated apoptotic pathway could be a major reason for the striking differential growth inhibitory effect of MR-4.

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Beneficial effects of astringinin, a resveratrol analogue, on the ischemia and reperfusion damage in rat heart

Cited by 70 publications

References 26 publications

Comparison of the cardiac effects between quinazoline-based α1-adrenoceptor antagonists on occlusion–reperfusion injury

Comparison of the cardiac effects between quinazoline-based α1-adrenoceptor antagonists on occlusion–reperfusion injury

Persistent Oxidative Stress after Myocardial Infarction Treated by Percutaneous Coronary Intervention

A methoxy derivative of resveratrol analogue selectively induced activation of the mitochondrial apoptotic pathway in transformed fibroblasts

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