Caffeic acid attenuates rat liver reperfusion injury through sirtuin 3-dependent regulation of mitochondrial respiratory chain

Mu, Hongna; Li, Quan; Pan, Chun‐Shui; Liu, Yuying; Li, Yan; Hu, Bai‐He; Sun, Kai; Chang, Xin; Zhao, Xiaojie; Fan, Jing‐Yu; Han, Jing‐Yan

doi:10.1016/j.freeradbiomed.2015.04.033

Cited by 35 publications

(17 citation statements)

References 50 publications

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“…This suggests that mice treated with CA maintained the ability to form a thrombus, but that thrombus formation was reduced and occurred at a reduced rate. Additionally, our early studies showed that CA could inhibit acute hyperhomocysteinemia-induced endothelia-leucocyte adhesion in mouse cerebral venules 24 and attenuate rat liver microcirculatory disturbance and oxidative injury through regulation of Sirt3 and mitochondrial respiratory chain 30 . The findings coupled with the present study support the concept that CA modulates thrombotic events through a multitude of pathways.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of caffeic acid on ADP-induced thrombus formation and platelet activation involves mitogen-activated protein kinases

Liu

et al. 2015

Sci Rep

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Caffeic acid (CA), one of the active constituents of Radix Salvia miltiorrhizae, exhibits antioxidant and anti-inflammatory activities. However, few studies have assessed the ability of CA to inhibit platelet mediated thrombus generation in vivo. In this study, we investigated the antithrombotic effect of CA in mouse cerebral arterioles and venules using intravital microscopy. The antiplatelet activity of CA in ADP stimulated mouse platelets in vitro was also examined in attempt to explore the underlying mechanism. Our results demonstrated that CA (1.25-5 mg/kg) significantly inhibited thrombus formation in vivo. In vitro, CA (25-100 μM) inhibited ADP-induced platelet aggregation, P-selectin expression, ATP release, Ca 2+ mobilization, and integrin αIIbβ3 activation. Additionally, CA attenuated p38, ERK, and JNK activation, and enhanced cAMP levels. Taken together, these data provide evidence for the inhibition of CA on platelet-mediated thrombosis in vivo, which is, at least partly, mediated by interference in phosphorylation of ERK, p38, and JNK leading to elevation of cAMP and down-regulation of P-selectin expression and αIIbβ3 activation. These results suggest that CA may have potential for the treatment of aberrant platelet activation-related diseases.In normal hemostasis, platelets prevent hemorrhage after injury and thereby preserve vascular integrity. But, aberrant platelet activation triggered by pathophysiological factors can lead to the development and progression of cardiovascular or cerebrovascular disorders such as hypertension, atherosclerosis, thrombosis and ischemic stroke [1][2][3][4] .At the injured vascular site, the exposed subendothelial collagen and von Willebrand factor (vWF) initiate platelet activation marked by the secretion of prothrombotic factors like adenosine diphosphate (ADP) and thrombin 5 . Platelet activation is further amplified by ADP and adenosine triphosphate (ATP) released from dense granules and adhesive molecules fibrinogen and P-selectin secreted by α -granules 6 . ADP activates G-protein-coupled receptor signaling mediated by two metabotropic purinergic receptors in platelets. The Gq-coupled P2Y1 receptor is responsible for intracellular calcium mobilization, shape change, and initiation of aggregation; the Gi-coupled P2Y12 receptor inhibits adenylyl cyclase and is responsible for the completion of the aggregation by ADP 7 . In addition, ADP-stimulated Gi-coupled P2Y12 receptor activates mitogen-activated protein kinases (MAPKs) [extracellular signal regulated kinases (ERKs), p38, and c-Jun NH 2 -terminal kinases (JNKs)] and PI-3k/Akt signaling leading to similar scenario of platelet activation and aggregation 8 .

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Section: Discussionmentioning

confidence: 99%

Inhibitory effect of caffeic acid on ADP-induced thrombus formation and platelet activation involves mitogen-activated protein kinases

Liu

et al. 2015

Sci Rep

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“…Thus, under stress conditions, increased expression of SIRT3 protects cardiomyocytes, in part by hindering the translocation of Bax to mitochondria (Sundaresan et al, 2008 ). Antioxidant caffeic acid can attenuate liver ischemia and reperfusion injury through regulating SIRT3, along with increased MnSOD expression and Bcl-2/Bax rate, and reduced cleaved caspase-3/9 protein expression (Mu et al, 2015 ). Rhamnetin protects H9c2 cardiomyoblasts against H 2 O 2 -induced apoptosis, its mechanisms of action include the enhanced expression of SIRT3, Bcl-2 and MnSOD, and the decreased protein expression of Bax and cleaved caspase-3 (Park et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

SIRT3 in Neural Stem Cells Attenuates Microglia Activation-Induced Oxidative Stress Injury Through Mitochondrial Pathway

Jiang

Wang

et al. 2017

Front. Cell. Neurosci.

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Sirtuin 3 (SIRT3), a mitochondrial protein, is involved in energy metabolism, cell apoptosis and mitochondrial function. However, the role of SIRT3 in neural stem cells (NSCs) remains unknown. In previous studies, we found that microglia activation-induced cytotoxicity negatively regulated survival of NSCs, along with mitochondrial dysfunction. The aim of this study was to investigate the potential neuroprotective effects of SIRT3 on the microglia activation-induced oxidative stress injury in NSCs and its possible mechanisms. In the present study, microglia-NSCs co-culture system was used to demonstrate the crosstalk between both cell types. The cytotoxicity of microglia activation by Amyloid-β (Aβ) resulted in the accumulation of reactive oxygen species (ROS) and down-regulation of SIRT3, manganese superoxide dismutase (MnSOD) gene expression in NSCs, concomitant to cell cycle arrest at G0/G1 phase, increased cell apoptosis rate and opening of the mitochondrial permeability transition pore (mPTP) and enhanced mitochondrial membrane potential (ΔΨm) depolarization. Furthermore, SIRT3 knockdown in NSCs via small interfering RNA (siRNA) accelerated cell injury, whereas SIRT3 overexpression provided resistance to microglia activation-induced oxidative stress cellular damage. The mechanisms of SIRT3 attenuated activated microglia-induced NSC dysfunction included the decreased mPTP opening and cyclophilin D (CypD) protein expression, inhibition of mitochondrial cytochrome C (Cyt C) release to cytoplasm, declined Bax/B-cell lymphoma 2 (Bcl-2) ratio and reduced caspase-3/9 activity. Taken together, these data imply that SIRT3 ameliorates microglia activation-induced oxidative stress injury through mitochondrial apoptosis pathway in NSCs, these results may provide a novel intervention target for NSC survival.

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“…Caffeic acid (CA; found in the eucalyptus bark) and gallic acid (GA; found in black tea and many plants), including derivatives thereof, for instance, reportedly induce autophagy (Doan et al, 2015), AMPK activation (Doan et al, 2015;Tyszka-Czochara et al, 2017), protein deacetylation (Pietrocola et al, 2012), extended longevity across species, and anti-diabetes effects (Eid et al, 2017). While GA was found to inhibit EP300 (Lee et al, 2015c), CA might activate SIRTs, namely SIRT3 (Mu et al, 2015). Moreover, CA has been shown to induce autophagy and improve glucose and lipid metabolism as well as renal function in a diabetic rat model (Matboli et al, 2017).…”

Section: Resveratrol and Other Sirt1 Activatorsmentioning

confidence: 99%

Caloric Restriction Mimetics against Age-Associated Disease: Targets, Mechanisms, and Therapeutic Potential

et al. 2019

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Caffeic acid attenuates rat liver reperfusion injury through sirtuin 3-dependent regulation of mitochondrial respiratory chain

Cited by 35 publications

References 50 publications

Inhibitory effect of caffeic acid on ADP-induced thrombus formation and platelet activation involves mitogen-activated protein kinases

Inhibitory effect of caffeic acid on ADP-induced thrombus formation and platelet activation involves mitogen-activated protein kinases

SIRT3 in Neural Stem Cells Attenuates Microglia Activation-Induced Oxidative Stress Injury Through Mitochondrial Pathway

Caloric Restriction Mimetics against Age-Associated Disease: Targets, Mechanisms, and Therapeutic Potential

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