Dexmedetomidine suppresses bupivacaine-induced parthanatos in human SH-SY5Y cells via the miR-7-5p/PARP1 axis-mediated ROS

Zheng, Ting; Zheng, Changsong; Gao, Fei; Huang, Fei; Hu, Bin; Zheng, Xiaochun

doi:10.1007/s00210-020-01971-6

Cited by 5 publications

(3 citation statements)

References 42 publications

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“…Functionally, in this study, the mitochondrial membrane potential (Δ Ψm ) also decreased. Prior studies have suggested that dexmedetomidine can reverse bupivacaine-induced changes in mitochondrial membrane potential [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

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Dexmedetomidine attenuates postoperative spatial memory impairment after surgery by reducing cytochrome C

et al. 2023

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Background Anesthesia and surgery can induce perioperative neurocognitive disorders (PND). Mitochondrial dysfunction has been proposed to be one of the earliest triggering events in surgery-induced neuronal damage. Dexmedetomidine has been demonstrated to attenuate the impairment of cognition in aged rats induced by surgery in our previous study. Methods Male Sprague-Dawley rats underwent hepatic apex resection under anesthesia with propofol to clinically mimic human abdominal surgery. The rats were divided into three groups: Control group, Model group and Dexmedetomidine (Dex) group. Cognitive function was evaluated with the Morris water maze (MWM), Open Field Test (OFT)and Novel object recognition task (NOR). Ultrastructural change in neuronal mitochondria was measured by transmission electron microscopy. Mitochondrial function was measured by mitochondrial membrane potential and activities of mitochondrial complexes. Neuronal morphology was observed with H&E staining and the activation of glial cells was observed by immunohistochemistry in the hippocampus. Protein levels were measured by Western blot (WB) and immunofluorescence at 3 and 7 days after surgery. Results Surgery-induced cognitive decline lasts three days, but not seven days after surgery in the model group. Transmission electron microscope showed the mitochondrial structure damage in the model group, similar changes were not induced in the Dex group. Dexmedetomidine may reverse the decrease in mitochondrial membrane potential and mitochondrial complex activity. Compared with the Control group, the expression of cytochrome c was significantly increased in model group by Western blot and immunofluorescence on days 3, but not day 7. Rats from the Model group expressed significantly greater levels of Iba-1 and GFAP compared with the Control group and the Dex group. Conclusion Dexmedetomidine appears to reverse surgery-induced behavior, mitigate the higher density of Iba-1 and GFAP, reduce the damage of mitochondrial structure and function by alleviating oxidative stress and protect mitochondrial respiratory chain, thus increasing cytochrome c oxidase (COX) expression and downregulate the expression of cytochrome c protein in the hippocampus of rats.

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Section: Discussionmentioning

confidence: 99%

“…After treatment, 10 µg/mL JC-1 (Molecular Probes, Beyotime Biotech, China) was applied to the rat brain tissue [ 21 ], which were then analyzed using enzyme labeled instrument (Spectrum Max M5 microplate reader, molecular devices US) to measure the fluorescence value.…”

Section: Methodsmentioning

confidence: 99%

Dexmedetomidine attenuates postoperative spatial memory impairment after surgery by reducing cytochrome C

et al. 2023

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“…Meanwhile, dexmedetomidine suppresses bupivacaine-induced parthanatos in human SH-SY5Y cells via miR-7-5p/PARP1 axis-mediated ROS [99]. SH-SY5Y cell death and ropivacaine-induced apoptosis are related to parthanatos, ropivacaine induces NAD + depletion and PARP1 activation, and the result of treatment with the PARP1 inhibitor PJ-34 indicates that NAD + depletion is caused by PARP1 activation [100].…”

Section: Othersmentioning

confidence: 99%

Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases

Huang

Chen

Jin

et al. 2022

IJMS

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Differential evolution of apoptosis, programmed necrosis, and autophagy, parthanatos is a form of cell death mediated by poly(ADP-ribose) polymerase 1 (PARP1), which is caused by DNA damage. PARP1 hyper-activation stimulates apoptosis-inducing factor (AIF) nucleus translocation, and accelerates nicotinamide adenine dinucleotide (NAD+) and adenosine triphosphate (ATP) depletion, leading to DNA fragmentation. The mechanisms of parthanatos mainly include DNA damage, PARP1 hyper-activation, PAR accumulation, NAD+ and ATP depletion, and AIF nucleus translocation. Now, it is reported that parthanatos widely exists in different diseases (tumors, retinal diseases, neurological diseases, diabetes, renal diseases, cardiovascular diseases, ischemia-reperfusion injury...). Excessive or defective parthanatos contributes to pathological cell damage; therefore, parthanatos is critical in the therapy and prevention of many diseases. In this work, the hallmarks and molecular mechanisms of parthanatos and its related disorders are summarized. The questions raised by the recent findings are also presented. Further understanding of parthanatos will provide a new treatment option for associated conditions.

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Dexmedetomidine Inhibits Parthanatos in Cardiomyocytes and in Aortic Banded Mice by the ROS-Mediated NLRP3 Inflammasome Activation

Wang

Liu

Zhou

et al. 2022

J. of Cardiovasc. Trans. Res.

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Dexmedetomidine suppresses bupivacaine-induced parthanatos in human SH-SY5Y cells via the miR-7-5p/PARP1 axis-mediated ROS

Cited by 5 publications

References 42 publications

Dexmedetomidine attenuates postoperative spatial memory impairment after surgery by reducing cytochrome C

Dexmedetomidine attenuates postoperative spatial memory impairment after surgery by reducing cytochrome C

Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases

Dexmedetomidine Inhibits Parthanatos in Cardiomyocytes and in Aortic Banded Mice by the ROS-Mediated NLRP3 Inflammasome Activation

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