Caffeic Acid Phenethyl Ester Reduces Ischemia‐Induced Kidney Mitochondrial Injury in Rats

Trumbeckaitė, Sonata; Paužienė, Neringa; Trumbeckas, Darius; Jievaltas, Mindaugas; Banienė, Rasa

doi:10.1155/2017/1697018

Cited by 18 publications

(16 citation statements)

References 30 publications

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“…It was also demonstrated by Feng et al that CAPE and its related phenolic compounds could protect the efficiency of oxidative phosphorylation (state 3 increased and state 4 decreased), as shown by the ADP/O ratio [ 48 ]. This is in agreement with our data and with our previous data from an in vitro kidney ischemia model [ 2 ] that showed an increase in the mitochondrial state 3 respiration (V ADP ) with glutamate/malate after pretreatment with two doses of CAPE (22 mg/kg and 34 mg/kg) as compared with the untreated group (ischemia/reperfusion).…”

Section: Discussionsupporting

confidence: 93%

“…Our recent in vitro study [ 2 ] has revealed that CAPE has a positive effect against ischemia-induced injury, namely that it partially protected rat kidney mitochondria from in vitro ischemia-induced damage. Since most studies, including our own, have been performed in vitro [ 2 ], the question remains open as to whether the same results will be observed in in vivo experiments. Such studies in kidney mitochondria have not yet been performed.…”

Section: Introductionmentioning

confidence: 99%

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Caffeic Acid Phenethyl Ester Protects Kidney Mitochondria against Ischemia/Reperfusion Induced Injury in an In Vivo Rat Model

et al. 2021

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To improve ischemia/reperfusion tolerance, a lot of attention has been focused on natural antioxidants. Caffeic acid phenethyl ester (CAPE), an active component of the resinous exudates of the buds and young leaves of Populus nigra L., Baccharis sarothroides A., etc., and of propolis, possesses unique biological activities such as anti-inflammatory, antioxidant, immunomodulating, and cardioprotective effects, among others. There is a lack of studies showing a link between the antioxidant potential of CAPE and the mechanism of protective action of CAPE at the level of mitochondria, which produces the main energy for the basic functions of the cell. In the kidney, ischemia/reperfusion injury contributes to rapid kidney dysfunction and high mortality rates, and the search for biologically active protective compounds remains very actual. Therefore, the aim of this study was to identify the antioxidant potential of CAPE and to investigate whether CAPE can protect rat kidney mitochondria from in vivo kidney ischemia/reperfusion induced injury. We found that CAPE (1) possesses antioxidant activity (the reducing properties of CAPE are more pronounced than its antiradical properties); CAPE effectively reduces cytochrome c; (2) protects glutamate/malate oxidation and Complex I activity; (3) preserves the mitochondrial outer membrane from damage and from the release of cytochrome c; (4) inhibits reactive oxygen species (ROS) generation in the Complex II (SDH) F site; (5) diminishes ischemia/reperfusion-induced LDH release and protects from necrotic cell death; and (6) has no protective effects on succinate oxidation and on Complex II +III activity, but partially protects Complex II (SDH) from ischemia/reperfusion-induced damage. In summary, our study shows that caffeic acid phenethyl ester protects kidney mitochondrial oxidative phosphorylation and decreases ROS generation at Complex II in an in vivo ischemia/reperfusion model, and shows potential as a therapeutic agent for the development of pharmaceutical preparations against oxidative stress-related diseases.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Caffeic Acid Phenethyl Ester Protects Kidney Mitochondria against Ischemia/Reperfusion Induced Injury in an In Vivo Rat Model

et al. 2021

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“…In addition, other previous studies have noted that phenolic acid and ester compounds play a positive role in amending lipid metabolism. For example, several studies have shown that CAPE has antioxidant, anti-inflammatory, and cytostatic properties and hepatorenal protective effects against the cytotoxic injuries linked to metabolic syndrome and vascular diseases [42][43][44][45]. CAPE can also reduce the activation of the nuclear factor κB pathway in high-fat diet-induced obesity mice [46].…”

Section: Discussionmentioning

confidence: 99%

Phenolic Compounds of Propolis Alleviate Lipid Metabolism Disorder

Kong

Zhang

Feng

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Lipid metabolism disorder is one of the significant risk factors for a multitude of human diseases and has become a serious threat to human health. The present study aimed to evaluate the effects of phenolics from poplar-type propolis on regulating lipid metabolism by using cell models of steatosis induced by palmitic acid (PA). Our study shows that phenolic esters have higher lipid-lowering activities than phenolic acids, especially for three caffeic acid esters, including caffeic acid phenethyl ester (CAPE), caffeic acid cinnamyl ester (CACE), and caffeic acid benzyl ester (CABE). Most notably, CACE presents prominent properties to prevent intracellular lipid accumulation and to amend extracellular adipokine secretion abnormalities. In addition, our results firstly reveal that CACE can alleviate lipid metabolism disorder through mediating protein kinase RNA-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6) signaling pathway-associated protein expression, suppressing endoplasmic reticulum (ER) stress, and activating peroxisome proliferator-activated receptors (PPARs) by distinct upregulation of PPARα and downregulation of PPARγ.

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“…Mitochondrial oxygen consumption rates was measured using Oroboros oxygraph-2 k in 2 mL incubation medium containing 10 mM Tris·Cl, 5 mM KH 2 PO4, 150 mM KCl, 1 mM MgCl 2 × 6H 2 O, pH 7.2, 37°C with 5 mM glutamate + 5 mM malate, or 15 mM succinate + 2 mM amytal (an inhibitor of complex I) as respiratory substrates. All experimental conditions are described in [ 10 ]. The mitochondrial routine respiration rate ( V 0 ) was recorded in the medium supplemented with mitochondria and substrates (complex I-dependent substrate: glutamate 5 mM + malate 5 mM, or complex II-dependent substrate: succinate 15 mM + 2 mM amytal as complex I inhibitor); original curves of mitochondrial respiration are seen in Figure 1 .…”

Section: Methodsmentioning

confidence: 99%

Increased Succinate Accumulation Induces ROS Generation in In Vivo Ischemia/Reperfusion‐Affected Rat Kidney Mitochondria

Kamarauskaitė

Banienė

Trumbeckas

et al. 2020

BioMed Research International

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Mitochondria are recognized as main reactive oxygen species (ROS) producers, involving ROS generation by mitochondrial complexes I and III. Lately, the focus has been shifting to the ROS generation by complex II. Contribution of complex II (SDH) to ROS generation still remains debatable, especially in in vivo settings. Moreover, it is not completely defined at what time of ischemia the first alterations in mitochondria and the cell begin, which is especially important with renal arterial clamping in vivo during kidney surgery, as it predicts the postischemic kidney function. The aim of this study on an in vivo rat kidney ischemia/reperfusion model was to determine if there is a connection among (a) duration of kidney ischemia and mitochondrial dysfunction and (b) succinate dehydrogenase activity, succinate accumulation, and ROS generation in mitochondria at low and saturating succinate concentrations. Our results point out that (1) mitochondrial disturbances can occur even after 30 min of kidney ischemia/reperfusion in vivo and increase progressively with the prolonged time of ischemia; (2) accumulation of succinate in cytosol after ischemia/reperfusion correlated with increased H2O2 generation mediated by complex II, which was most noticeable with physiological succinate concentrations; and (3) ischemia/reperfusion induced cell necrosis, indicated by the changes in LDH activity. In conclusion, our new findings on the accumulation of succinate in cytosol and changes in SDH activity during kidney ischemia/reperfusion may be important for energy production after reperfusion, when complex I activity is suppressed. On the other hand, an increased activity of succinate dehydrogenase is associated with the increased ROS generation, especially with physiological succinate concentrations. All these observations play an important role in understanding the mechanisms which occur in the early phase of ischemia/reperfusion injury in vivo and may provide new ideas for novel therapeutic approaches or injury prevention; therefore, more detailed studies are necessary in the future.

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Caffeic Acid Phenethyl Ester Reduces Ischemia‐Induced Kidney Mitochondrial Injury in Rats

Cited by 18 publications

References 30 publications

Caffeic Acid Phenethyl Ester Protects Kidney Mitochondria against Ischemia/Reperfusion Induced Injury in an In Vivo Rat Model

Caffeic Acid Phenethyl Ester Protects Kidney Mitochondria against Ischemia/Reperfusion Induced Injury in an In Vivo Rat Model

Phenolic Compounds of Propolis Alleviate Lipid Metabolism Disorder

Increased Succinate Accumulation Induces ROS Generation in In Vivo Ischemia/Reperfusion‐Affected Rat Kidney Mitochondria

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