Dexmedetomidine attenuates neuronal injury induced by cerebral ischemia‑reperfusion by regulating miR‑199a

Zhu, Yong‐Guan; Zhao, Huihui; Zhang, Wenshan; Ma, Xingang; Liu, Ye

doi:10.3892/mmr.2021.12213

Cited by 10 publications

(9 citation statements)

References 40 publications

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“…The regulation of DEX on miRs has been extensively studied. [25][26][27] However, there is no literature on the serum expression of miR-10a after DEX intervention. This study was the first time to put forward that DEX reduced serum miR-10a in lung cancer patients during the perioperative period.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine Can Reduce the Level of Oxidative Stress and Serum miR-10a in Patients with Lung Cancer after Surgery

Zhou¹,

Xia

Zhang³

2022

Thorac Cardiovasc Surg

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Objective Lung cancer is a primary cause of cancer death. This study assessed the action of dexmedetomidine (DEX) on oxidative stress (OS) and microRNA 10a (miR-10a) in patients with lung cancer. Methods Patients were given 1 µg/kg DEX before anesthesia and control patients were given saline. The duration of intraoperative one-lung ventilation (OLV) and fluid intake were determined, and mean arterial pressure, heart rate and bispectral index were observed at the time of before anesthesia (T0), immediately after endotracheal intubation (T1), 1 hour after OLV (T2), and 10 minutes before the end of surgery (T3). The expressions and correlations of miR-10a, inflammation and OS levels in the serum were analyzed. The effects of DEX intervention and miR-10a level on pulmonary complications were analyzed. Results Patients with DEX intervention had lower levels of inflammation and OS during perioperative period than the controls. DEX intervention reduced miR-10a levels in patients during perioperative period. miR-10a in serum of patients with DEX intervention after surgery was positively-correlated with the concentrations of malondialdehyde, and inflammatory factors, while negatively-correlated with superoxide dismutase. The total incidence of postoperative pulmonary complications after DEX intervention was lowered. Patients with high miR-10a expression had a higher cumulative incidence of pulmonary complications than those with low miR-10a expression. Conclusion DEX can reduce postoperative OS and plasma miR-10a level in patients with lung cancer, and high expression of miR-10a predicts a high incidence of postoperative pulmonary complications.

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Section: Discussionmentioning

confidence: 99%

Dexmedetomidine Can Reduce the Level of Oxidative Stress and Serum miR-10a in Patients with Lung Cancer after Surgery

Zhou¹,

Xia

Zhang³

2022

Thorac Cardiovasc Surg

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“…To analyze apoptosis in brain tissues at 24 h after HI, TUNEL staining was performed using TUNEL Apoptosis Detection Kit (11684817910, Roche, Basel, Switzerland). Briefly, the sections of brain tissues were dewaxed and hydrated, and incubated with the reaction solution in a humid chamber at 37°C for 1 h ( Zhu Y et al, 2021 ). The stained images were captured using a fluorescence microscope, and the number of TUNEL positive cells and DAPI positive staining nuclei were counted using Image J software.…”

Section: Methodsmentioning

confidence: 99%

Myricetin attenuates hypoxic-ischemic brain damage in neonatal rats via NRF2 signaling pathway

Chen

Hu²,

Lu³

et al. 2023

Front. Pharmacol.

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Introduction: Hypoxic-ischemic encephalopathy (HIE) is a crucial cause of neonatal death and neurological sequelae, but currently there is no effective therapy drug for HIE. Both oxidative stress and apoptosis play critical roles in the pathological development of HIE. Myricetin, a naturally extracted flavonol compound, exerts remarkable effects against oxidative stress, apoptosis, and inflammation. However, the role and underlying molecular mechanism of myricetin on HIE remain unclear.Methods: In this study, we established the neonatal rats hypoxic-ischemic (HI) brain damage model in vivo and CoCl2 induced PC12 cell model in vitro to explore the neuroprotective effects of myricetin on HI injury, and illuminate the potential mechanism.Results: Our results showed that myricetin intervention could significantly reduce brain infarction volume, glia activation, apoptosis, and oxidative stress marker levels through activating NRF2 (Nuclear factor-E2-related factor 2) and increase the expressions of NRF2 downstream proteins NQO-1 and HO-1. In addition, the NRF2 inhibitor ML385 could significantly reverse the effects of myricetin.Conclusion: This study found that myricetin might alleviate oxidative stress and apoptosis through NRF2 signaling pathway to exert the protective role for HI injury, which suggested that myricetin might be a promising therapeutic agent for HIE.

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“…Moreover, DEX has been reported to reduce autophagy effect and improve learning and memory dysfunction in rodent MCAO model [ 163 ]. A recent study showed that regulation of miR-199 was a potential mechanism by which DEX inhibited autophagy and promoted neurological recovery after ischemic stroke [ 164 ]. Propofol administration reduced the infarct size and improves the outcome of acute ischemic stroke [ 165 , 166 ].…”

Section: Potential Therapeutic Strategies For Ischemic Stroke Targeti...mentioning

confidence: 99%

Novel Therapeutic Strategies for Ischemic Stroke: Recent Insights into Autophagy

Zhang

Ding

et al. 2022

Oxidative Medicine and Cellular Longevity

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Stroke is one of the leading causes of death and disability worldwide. Autophagy is a conserved cellular catabolic pathway that maintains cellular homeostasis by removal of damaged proteins and organelles, which is critical for the maintenance of energy and function homeostasis of cells. Accumulating evidence demonstrates that autophagy plays important roles in pathophysiological mechanisms under ischemic stroke. Previous investigations show that autophagy serves as a “double-edged sword” in ischemic stroke as it can either promote the survival of neuronal cells or induce cell death in special conditions. Following ischemic stroke, autophagy is activated or inhibited in several cell types in brain, including neurons, astrocytes, and microglia, as well as microvascular endothelial cells, which involves in inflammatory activation, modulation of microglial phenotypes, and blood-brain barrier permeability. However, the exact mechanisms of underlying the role of autophagy in ischemic stroke are not fully understood. This review focuses on the recent advances regarding potential molecular mechanisms of autophagy in different cell types. The focus is also on discussing the “double-edged sword” effect of autophagy in ischemic stroke and its possible underlying mechanisms. In addition, potential therapeutic strategies for ischemic stroke targeting autophagy are also reviewed.

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Dexmedetomidine attenuates neuronal injury induced by cerebral ischemia‑reperfusion by regulating miR‑199a

Cited by 10 publications

References 40 publications

Dexmedetomidine Can Reduce the Level of Oxidative Stress and Serum miR-10a in Patients with Lung Cancer after Surgery

Dexmedetomidine Can Reduce the Level of Oxidative Stress and Serum miR-10a in Patients with Lung Cancer after Surgery

Myricetin attenuates hypoxic-ischemic brain damage in neonatal rats via NRF2 signaling pathway

Novel Therapeutic Strategies for Ischemic Stroke: Recent Insights into Autophagy

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