HS-1793, a recently developed resveratrol analogue protects rat heart against hypoxia/reoxygenation injury via attenuating mitochondrial damage

Jeong, Sang Hoon; Hanh, Tran My; Kim, Hyoung Kyu; Lee, Sung Ryul; Song, In-Sung; Noh, Su Jin; Song, Suhee; Suh, Hongsuk; Kim, Nari; Rhee, Byoung Doo; Ko, Kyung Soo; Han, Jin

doi:10.1016/j.bmcl.2013.05.010

Cited by 12 publications

(8 citation statements)

References 27 publications

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“…Rat hearts were mounted as previously described [40,41]. After a 15-min stabilization period in NT solution, hearts were perfused with Ca 2+ -free NT solution for 7 min, followed by Ca 2+ -free NT solution plus 0.01% collagenase (Yakult, Tokyo, Japan) for 9–13 min.…”

Section: Methodsmentioning

confidence: 99%

Echinochrome A Protects Mitochondrial Function in Cardiomyocytes against Cardiotoxic Drugs

et al. 2014

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Echinochrome A (Ech A) is a naphthoquinoid pigment from sea urchins that possesses antioxidant, antimicrobial, anti-inflammatory and chelating abilities. Although Ech A is the active substance in the ophthalmic and cardiac drug Histochrome®, its underlying cardioprotective mechanisms are not well understood. In this study, we investigated the protective role of Ech A against toxic agents that induce death of rat cardiac myoblast H9c2 cells and isolated rat cardiomyocytes. We found that the cardiotoxic agents tert-Butyl hydroperoxide (tBHP, organic reactive oxygen species (ROS) inducer), sodium nitroprusside (SNP; anti-hypertension drug), and doxorubicin (anti-cancer drug) caused mitochondrial dysfunction such as increased ROS level and decreased mitochondrial membrane potential. Co-treatment with Ech A, however, prevented this decrease in membrane potential and increase in ROS level. Co-treatment of Ech A also reduced the effects of these cardiotoxic agents on mitochondrial oxidative phosphorylation and adenosine triphosphate level. These findings indicate the therapeutic potential of Ech A for reducing cardiotoxic agent-induced damage.

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Section: Methodsmentioning

confidence: 99%

Echinochrome A Protects Mitochondrial Function in Cardiomyocytes against Cardiotoxic Drugs

et al. 2014

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“…During muscle contraction, ATP utilization is accelerated to meet the energy demand. Under ischemia, the production of reactive oxidative species (ROS) inhibits ATPase activity in the mitochondria, and therefore, reduces intracellular ATP utilization (Dobrota et al, 1999;Simao et al, 2011;Jeong et al, 2013). Apart from the suppressed intracellular ATP utilization, during the ischemia condition, the muscular cells are swollen, and thus, the permeability and efflux of the cytoplasmic soluble molecules including ATP is increased (Boudreault and Grygorczyk, 2002).…”

Section: Discussionmentioning

confidence: 99%

One-Time Acute Heat Treatment Is Effective for Attenuation of the Exaggerated Exercise Pressor Reflex in Rats With Femoral Artery Occlusion

Qin

2020

Front. Physiol.

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The purpose of this study was to determine the effects of one-time acute heat treatment (HT) on the exaggerated exercise pressor reflex in a model of peripheral arterial insufficiency induced by ligation of the femoral artery and was to further examine the underlying mechanism of ATP-P2X 3 signal activity during this process. The blood pressure (BP) response to static muscle contraction and muscle tendon stretch was recorded to determine the exercise pressor reflex. Also, αβ-methylene ATP (αβ-me ATP) was injected into the arterial blood supply of the hindlimb muscles to stimulate P2X 3 receptors in the muscle afferent nerves. To process one-time acute HT, a heating pad was placed locally on the hindlimb and the muscle temperature (Tm) was increased by ~1.5°C and maintained for 5 min. Compared with control rats, a greater mean arterial pressure (MAP) response to muscle contraction was observed in rats with femoral occlusion in a pre-heat control session (28 ± 2 mmHg in occluded rats/n = 12 vs. 18 ± 2 mmHg in control rats/n = 9; p < 0.05). The one-time acute HT attenuated the amplification of the BP response in rats with femoral artery occlusion (MAP response: 19 ± 8 mmHg in occluded rats + HT/n = 11; p < 0.05 vs. occluded rats). In contrast, HT did not significantly attenuate amplification of MAP response to muscle stretch and αβ-me ATP injection in rats with femoral artery occlusion and controls (all p > 0.05). Our data suggest that one-time acute HT selectively attenuates the amplified pressor response induced by activation of the metabolic and mechanical components of the reflex in rats after femoral artery occlusion. The suppressing effects of acute HT on the exaggerated exercise pressor reflex are likely mediated through a reduction in metabolites (e.g., ATP) stimulating the muscle afferent nerves in contracting muscle, but unlikely through direct alteration of P2X receptors per se.

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“…The increasing of cell membrane permeability could further lead to and external environment imbalance internal of the cells, accelerating cell apoptosis. It was found that the generation of mitochondrial ROS can be reduced during IRI by inhibiting Ca 2+ overload (Jeong et al, 2013, Bround et al, 2013), thus improving mitochondrial dysfunction. Therefore, the variations of ATP content and ATPase activity in mitochondria can be applied as an index to reflect the severity of IRI, which is also an important target to mitigate or prevent the occurrence and development of IRI.…”

Section: Discussionmentioning

confidence: 99%

Effect of propofol on mitochondrial ATP content and ATPase activity in hippocampus of rats with cerebral ischemia-reperfusion injury

Gao

2017

Saudi Journal of Biological Sciences

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ObjectiveStudy on the influence of the cerebral Ischemia-reperfusion Injury (IRI) on mitochondrial adenosine triphosphate (ATP) content and ATPase activity in hippocampus of rats, as well as the protective effect of propofol on IRI in rats.MethodsA total of 40 male SD rats were randomly divided into 5 groups: sham operation group (Group A), ischemia reperfusion control group (Group B) and ischemic reperfusion with propofol pretreatment group (C group). Group C was further divided into three sub groups according to the different doses of propofol: Group C1 (50 mg/kg), Group C2 (100 mg/kg) and Group C3 (150 mg/kg). The rats from Groups B and C were applied for the IRI model preparation by blockage of the blood flow in arteria carotis communis. For the Groups A, arteria carotis communis were separated without blockage of the blood flow. Before preparation of IRI model for rats in Group C, different doses of propofol were intraperitoneally injected into the rats. For rats in Groups A and B, only saline solution with same volume was intraperitoneally injected at the same time. The ultra-structures of mitochondria in hippocampus of rats were observed under transmission electron microscope, and the mitochondrial degeneration rate was counted. The contents of ATP were determined by HPLC and the ATPase activity was characterized by ATPase activity assay kit.Results(1) Mitochondria in the hippocampus from Groups B and C showed different degrees of ultrastructural damage and more significant mitochondrial degeneration than those from Group A. The degree of damage and the rate of degeneration were in the order of B > C1 > C2 > C3 and the difference was statistically significant (P < 0.01). (2) The contents of ATP and the ATPase activity in hippocampus from Groups B and C were significantly lower than those of Group A, while these indices from Group C were significantly higher than those in the B group, and the sequence was C3 > C2 > C1, indicating that the ATP content and ATPase activity were significantly correlated with the dose of propofol, and the difference was statistically significant (P < 0.05).ConclusionIn summary, the contents of ATP and ATPase activity in hippocampus of rats can be decreased by cerebral IRI. The structure and function of the impaired mitochondria in IRI rats could be significantly improved by propofol, and the improvement effect is related to the dose of propofol.

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HS-1793, a recently developed resveratrol analogue protects rat heart against hypoxia/reoxygenation injury via attenuating mitochondrial damage

Cited by 12 publications

References 27 publications

Echinochrome A Protects Mitochondrial Function in Cardiomyocytes against Cardiotoxic Drugs

Echinochrome A Protects Mitochondrial Function in Cardiomyocytes against Cardiotoxic Drugs

One-Time Acute Heat Treatment Is Effective for Attenuation of the Exaggerated Exercise Pressor Reflex in Rats With Femoral Artery Occlusion

Effect of propofol on mitochondrial ATP content and ATPase activity in hippocampus of rats with cerebral ischemia-reperfusion injury

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