Pterostilbene protects against myocardial ischemia/reperfusion injury via suppressing oxidative/nitrative stress and inflammatory response

Yu, Zhaoxia; Wang, Shaohua; Zhang, Xiangyang; Liu, Ying; Zhao, Qiang; Liu, Tao

doi:10.1016/j.intimp.2016.11.018

Cited by 52 publications

(35 citation statements)

References 46 publications

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“…Pterostilbene display beneficial effects in lowering plasma lipoproteins and cholesterol, avoiding vascular endothelial cell apoptosis caused by oxidized low‐density lipoprotein (oxoLDL), and promoting cytoprotective macroautophagy in vitro or in vivo . Recent findings from animal model of Ischemia/Reperfusion Injury demonstrate that pterostilbene has therapeutic potential by modulating inflammatory response, oxidative stress, and apoptosis and up‐regulating gene expression . Similar result was also found in hypoxia‐reoxygenation injury experiments, suggesting the protective effect of ptersostilbene on cardiomyocytes is related to activating SIRT1 function .…”

Section: The Effect Of Resveratrol and Pterostilbene On Lifespan And mentioning

confidence: 56%

Effect of resveratrol and pterostilbene on aging and longevity

2017

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Over the past years, several studies have found that foods rich in polyphenols protect against age-related disease, such as atherosclerosis, cardiovascular disease, cancer, arthritis, cataracts, osteoporosis, type 2 diabetes (T2D), hypertension and Alzheimer's disease. Resveratrol and pterostilbene, the polyphenol found in grape and blueberries, have beneficial effects as antiaging compounds through modulating the hallmarks of aging, including oxidative damage, inflammation, telomere attrition and cell senescence. In this review, we discuss the relationship between resveratrol and pterostilbene and possible aging biomarker, including oxidative stress, inflammation, and highcalorie diets. Moreover, we also discuss the positive effect of Abbreviations: ABTS, 2,2 0 -Azino-bis (3-ethylbenzothiazoline-6-sulfonic acid; Akt, v-akt murine thymoma viral oncogene; AMPK, AMP-activated kinase; ARE, antioxidant response element; C. elegans, Caenorhabditis elegans; cAMP, cyclic adenosine monophosphate; CCL3, C-C motif chemokine ligand 3; CNS, central nervous system; CREB, cAMP response element binding protein; CRP, c-reactive protein; DPPH, 2,2-diphenyl-1-picryl-hydrazyl; eNOS, endothelial nitric oxide synthase; ERK, extracellular-signal-regulated kinase; ER-a, estrogen receptor alpha; FOXO1, forkhead box protein O1; FOXO3, forkhead box O3A protein; GSH, glutathione; GSH-Px, glutathione peroxidase; GSK3b, glycogen synthase kinase 3 b; hTERT, human telomerase reverse transcriptase; HtrA2, HtrA serine peptidase 2; IDH2, dehydrogenase 2; IFN-c, interferon gamma; IL-18, interleukin-18; IL-1b, interleukin 1 b; IL-6, interleukin-6; LDL, low-density lipoprotein; LPS, lipopolysaccharides; MAPK, mitogen-activated protein kinase; MLC, myosin light chain; MMP-1, matrix metalloproteinase-1; MMP-2, matrix metalloproteinase-2; MMP-9, matrix metalloproteinase-9; MnSOD, manganese superoxide dismutase; mRNA, messenger RNA; mtROS, mitochondrial reactive oxygen species; NADPH, nicotinamide adenine dinucleotide phosphate; NALP-3, NACHT 5 LRR and PYD domainscontaining protein 3; NAMPT, nicotinamide phosphoribosyltransferase; NFAT, nuclear factor of activated T-cells; NF-rB, nuclear factor-jB; NO, nitric oxide; Nrf2, nuclear factor erythroid 2-related factor 2; NS, Nutritional Supplement; OA, osteoarthritis; oxoLDL, oxidized low-density lipoprotein; PARK7, Parkinson disease protein 7; PARKIN, parkinson juvenile disease protein; PGC-1a, peroxisome proliferator-activated receptor gamma coactivator 1-a; PINK1, PTEN-induced putative kinase 1; PKB, protein kinase B; RhoA, Ras homolog gene family 5 member A; ROCK2, Rho-associated 5 coiled-coil containing protein kinase 2; ROS, reactive oxygen species; SAMP8, senescence accelerated mouse-prone 8; SCID, severe combined immunodeficiency; SHR, spontaneously hypertensive rat; SIRT1, sirtuin 1; SIRT4, sirtuin 4; SOD, superoxide peroxidase; STZ, streptozotocin; T2D, type 2 diabetes; TIMP-1, TIMP metallopeptidase inhibitor 1; TLR5, toll-like receptor 5; TNF-a, tumor necrosis factor alpha; UVB, ultraviol...

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Section: The Effect Of Resveratrol and Pterostilbene On Lifespan And mentioning

confidence: 56%

Effect of resveratrol and pterostilbene on aging and longevity

2017

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“…However, the cardio‐protective effects of PTS are not limited to its antioxidant action. Consistently, studies have shown that PTS has anti‐inflammatory properties (in addition to its antioxidant effects) in the heart mediated through various mechanisms, such as inhibition of COX2 and inducible NOS activities of NF‐κB signalling, decreasing myeloperoxidase activity, inhibition of angiotensin‐converting enzyme, elevation of endothelial NOS and a reduction in the levels of TNF‐α and IL‐1 (Lv et al ., ; Yu et al ., ). Therefore, the PTS‐induced cardio‐protective action may depend on several of these effects.…”

Section: Discussionmentioning

confidence: 97%

Pterostilbene reduces oxidative stress, prevents hypertrophy and preserves systolic function of right ventricle in cor pulmonale model

Lacerda

Türck

Seolin

et al. 2017

British J Pharmacology

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“…It is noteworthy that PT (10 mg/kg, administered intraperitoneally, once a day for five consecutive days) significantly attenuated myocardial IR-induced-inflammation, oxidative stress, and myocardial apoptosis via up-regulating Gas6/Axl pathway in non-diabetic rats [52]. Furthermore, PT administration (10 minutes before reperfusion) markedly reduced myocardial caspase-3 activity, via lowering nitrative/ oxidative stress by attenuating peroxynitrite production, ROS generation and inflammatory response following myocardial IR injury [53]. Previous studies also lend the support for an anti-apoptotic role of PT in non-cardiac tissues such as brain [54] and skeletal muscle [55] following IR injury.…”

Section: Discussionmentioning

confidence: 99%

AMPK Contributes to Cardioprotective Effects of Pterostilbene Against Myocardial Ischemia- Reperfusion Injury in Diabetic Rats by Suppressing Cardiac Oxidative Stress and Apoptosis

Kosuru

Cai

Kandula³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Pterostilbene (PT) exerts antidiabetic effects by decreasing blood glucose and modulating lipid metabolism and has been shown to attenuate myocardial ischemia-reperfusion (IR) injury in non-diabetic subjects. However, whether PT can protect against myocardial IR injury in diabetes is unknown. AMPK stimulation is indispensable in offering cardioprotection against myocardial IR injury in diabetes by limiting cardiac apoptosis. Thus, we hypothesized that PT may confer protection against myocardial IR injury in diabetes via AMPK activation. Methods: Sprague-Dawley rats at eight weeks of diabetes induction (induced by an intravenous dose of 65 mg/kg streptozotocin) were administered with vehicle or PT (20 and 40 mg/kg/day, p.o.) for four weeks (starting from week 9 to 12). At the end of week 12, myocardial IR injury was induced by subjecting the diabetic rats to 30 minutes of coronary artery ligation and followed by 2 hours of reperfusion. In in vitro studies, rat primary cardiomyocytes were incubated with low glucose (LG, 5.5 mM) or high glucose (HG, 30 mM) and exposed to 45 minutes hypoxia and 2 hours reoxygenation in the presence or absence of PT (0.5 µM) or the AMPK inhibitor compound C (CC, 5 µM). Results: PT significantly reduced post-ischemic cardiac infarct size, oxidative stress, plasma lactate dehydrogenase (LDH), creatine kinase-MB levels and apoptosis in diabetic rats. In cardiomyocytes, PT decreased hypoxia/ reoxygenation-induced oxidative stress, attenuated LDH and cleaved caspase3/caspase3 ratio and increased Bcl-2/Bax ratio and AMPK phosphorylation. However, CC administration blunted the cardioprotective effects of PT both in vivo and in vitro. Conclusion: Suppressing cardiac oxidative stress and apoptosis via AMPK stimulation may represent a primary mechanism whereby pterostilbene attenuates diabetic myocardial IR injury.

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Pterostilbene protects against myocardial ischemia/reperfusion injury via suppressing oxidative/nitrative stress and inflammatory response

Cited by 52 publications

References 46 publications

Effect of resveratrol and pterostilbene on aging and longevity

Effect of resveratrol and pterostilbene on aging and longevity

Pterostilbene reduces oxidative stress, prevents hypertrophy and preserves systolic function of right ventricle in cor pulmonale model

AMPK Contributes to Cardioprotective Effects of Pterostilbene Against Myocardial Ischemia- Reperfusion Injury in Diabetic Rats by Suppressing Cardiac Oxidative Stress and Apoptosis

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