The Effect of Dexmedetomidine on Oxidative Stress Response Following Cerebral Ischemia-Reperfusion in Rats and the Expression of Intracellular Adhesion Molecule-1 (ICAM-1) and S100B

Li, Yanwen; Liu, Shikun

doi:10.12659/msm.899855

Cited by 27 publications

(15 citation statements)

References 21 publications

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“…Furthermore, we found that APE1 knockdown induced by APE1 shRNA abolished resveratrol-induced the increases in the cell viability and decreases in the LDH release, indicating the contribution of APE1 to the protective effect of resveratrol against OGD/R injury. Increasing evidence confirms that inhibition of oxidative stress of and promotion of antioxidant signaling contributes to neuroprotective agent against ischemia-reperfusion damage to rat brains (35,36). APE1 is a multifunctional protein that plays a vital role in the cellular response to DNA injury and redox regulation against oxidative stress through the inhibition of reactive oxygen species (ROS) production (37).…”

Section: Discussionmentioning

confidence: 99%

Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol-induced neuroprotection against oxygen-glucose deprivation and re-oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage

Jia

Tan

Liu

et al. 2017

Molecular Medicine Reports

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Resveratrol, a naturally occurring polyphenolic compound, exhibits a neuroprotective role in models of central nervous system diseases, including cerebral ischemia/reperfusion injury. Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional enzyme that contributes to base excision repair of oxidative DNA damage and redox activation of transcription factors, associated with neuronal survival against hypoxic‑ischemic injury. It was hypothesized that resveratrol protects HT22 cells against oxygen‑glucose deprivation and re‑oxygenation (OGD/R)‑induced injuries through upregulation of APE1. It was demonstrated that resveratrol pretreatment significantly increased the viability of HT22 cells and decreased the release of lactate dehydrogenase (LDH), accompanied by the upregulation of APE1 mRNA, and protein levels, as well as the activity of APE1 under OGD/R conditions. In addition, resveratrol reversed OGD/R‑induced oxidative DNA damage as evidenced by the decreases in the levels of 8‑hydroxy‑2'‑deoxyguanosine and APE sites. However, APE1 knockdown using short hairpin RNA sequence targeting APE1 abolished resveratrol‑elicited beneficent effects against OGD/R‑induced cytotoxicity and oxidative stress. This was indicated by decreased cell viability, superoxide dismutase activity and glutathione levels, and increased LDH release and reactive oxygen species levels. The results of the present study indicate that APE1 contributes to the protective effects of resveratrol against neonatal hypoxic‑ischemic brain injuries, and suggest that DNA repair enzymes, including APE1, may be a unique strategy for neuroprotection against this disease.

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Section: Discussionmentioning

confidence: 99%

Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol-induced neuroprotection against oxygen-glucose deprivation and re-oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage

Jia

Tan

Liu

et al. 2017

Molecular Medicine Reports

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“…Furthermore, thiopental pretreatment reduced renal IR injury induced by free radicals [46, 47]. Reinforcing this finding, dexmedetomidine has been shown to decrease brain IR injury and inhibit nuclear factor-κB and intercellular adhesion molecule 1 expression through the inhibition of oxidative stress and inflammation, which are pathogenic factors of IR injury [48]…”

Section: General Anesthesiamentioning

confidence: 94%

A Review of Anesthetic Effects on Renal Function: Potential Organ Protection

et al. 2017

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Background: Renal protection is a critical concept for anesthesiologists, nephrologists, and urologists, since anesthesia and renal function are highly interconnected and can potentially interfere with one another. Therefore, a comprehensive understanding of anesthetic drugs and their effects on renal function remains fundamental to the success of renal surgeries, especially transplant procedures. Some experimental studies have shown that some anesthetics provide protection against renal ischemia/reperfusion (IR) injury, but there is limited clinical evidence. Summary: The effects of anesthetic drugs on renal failure are particularly important in the context of kidney transplantation, since the conditions of preservation following removal profoundly influence the recovery of organ function. Currently, preservation procedures are typically based on the usage of a cold-storage solution. Some anesthetic drugs induce anti-inflammatory, anti-necrotic, and anti-apoptotic effects. A more thorough understanding of anesthetic effects on renal function can present a novel approach for developing organ-protective strategies. The aim of this review is to discuss the effects of different anesthetic drugs on renal function, with particular focus on IR injury. Many studies have demonstrated the organ-protective effects of some anesthetic drugs, specifically propofol, which indicate the potential of some anesthetics to introduce novel organ protective targets. This is not surprising, since lipid emulsions are major components of propofol, which accumulating data show provide organ protective effects against IR injury. Key Messages: Thorough understanding of the interaction between anesthetic drugs and renal function remains fundamental to the delivery of safe perioperative care and to optimizing outcomes after renal surgeries, particularly transplant procedures. Anesthetics can be repurposed for organ protection with more information about their effects, especially during transplant procedures. Here, we review the effects of different anesthetic drugs – specifically those that contain lipids in their structure, with special reference to IR injury.

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“…Simultaneously, inflammatory cells that accumulate in the ischemic area release large amounts of toxic oxygen free radicals, proteolytic enzymes, and related molecules, thus increasing vascular permeability, destroying the blood-brain barrier, and causing toxic damage to neurons (Yang et al, 2018). Dexmedetomidine alleviates ischemia-reperfusion damage to rat brains and inhibits NF-κB and ICAM-1 expression in brain tissues (Li and Liu, 2017).…”

Section: Icam-1mentioning

confidence: 99%

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

326

197

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The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.

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The Effect of Dexmedetomidine on Oxidative Stress Response Following Cerebral Ischemia-Reperfusion in Rats and the Expression of Intracellular Adhesion Molecule-1 (ICAM-1) and S100B

Cited by 27 publications

References 21 publications

Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol-induced neuroprotection against oxygen-glucose deprivation and re-oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage

Apurinic/apyrimidinic endonuclease 1 (APE1) contributes to resveratrol-induced neuroprotection against oxygen-glucose deprivation and re-oxygenation injury in HT22 cells: Involvement in reducing oxidative DNA damage

A Review of Anesthetic Effects on Renal Function: Potential Organ Protection

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

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