Effects of propofol-dexmedetomidine combination on ischemia reperfusion-induced cerebral injury

Wang, Zhun; Kou, Dang-pei; Li, Zhao-duan; He, Yan; Yu, Wenli; Du, Hongyin

doi:10.3233/nre-141177

Cited by 27 publications

(20 citation statements)

References 40 publications

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“…Numerous anesthetics are used for cancer surgery, such as propofol, remifentanil and sevoflurane (26,27); however, their effects on the potential behaviors of cancer remain unknown. Propofol is an anesthetic agent that exerts numerous anesthetic, neuroprotective and myocardial-protective effects (18,28,29). Previous studies have demonstrated an association between propofol use and antitumor effects (20,21).…”

Section: Discussionmentioning

confidence: 99%

Propofol exhibits a tumor‑suppressive effect and regulates cell viability, migration and invasion in bladder carcinoma by targeting the microRNA‑10b/HOXD10 signaling pathway

Yuan

Sun

2019

Oncol Lett

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2,6-diisopropylphenol (propofol) is a commonly used intravenous anesthetic drug, which has been reported to serve an antitumor role in human cancers. The current study aimed to assess the effects of propofol on the biological behaviors of human bladder cancer cells and to elucidate its potential molecular mechanism. The results of MTT, wound healing and Matrigel invasion assays demonstrated that propofol significantly inhibited the viability, migration and invasion of bladder cancer T24 cells in vitro. Reverse transcription-quantitative PCR and western blotting revealed that propofol decreased the expression levels of microRNA (miR)-10b and increased the expression levels of homeobox D10 (HOXD10) in T24 cells. Luciferase reporter assay revealed that HOXD10 was a direct target of miR-10b in T24 cells. T24 cells transfected with a miR-10b mimic significantly reduced the mRNA and protein expression levels of HOXD10. In addition, overexpression of miR-10b partly reversed the inhibitory effect of propofol on T24 cell viability, migration and invasion induced by upregulation of HOXD10. In summary, the present study focused on the role of propofol in the treatment of bladder cancer and demonstrated that propofol may serve a tumor-suppressive role and control cell viability, migration and invasion of T24 cells by targeting the miR-10b/HOXD10 signaling pathway, which indicated that propofol may be used as an effective therapeutic drug for the treatment of bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Propofol exhibits a tumor‑suppressive effect and regulates cell viability, migration and invasion in bladder carcinoma by targeting the microRNA‑10b/HOXD10 signaling pathway

Yuan

Sun

2019

Oncol Lett

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“…Isoflurane (Iso) exerted neuroprotection by reducing the expression of the TLR4-mediated NF-κB signalling pathway and alleviating microglial activation after cerebral I/R injury in vitro and in vivo [ 21 ]. In addition, perioperative treatment with propofol (Pro) and Dex significantly suppressed cerebral I/R injury and upregulation of TNF-α and IL-1β in rats [ 22 ]. Thus, we hypothesised that there might be a link between Dex-induced spinal cord neuroprotection and both TLR4 activity and microglial activation.…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine attenuates spinal cord ischemia–reperfusion injury through both anti-inflammation and anti-apoptosis mechanisms in rabbits

Sun

Zhao

et al. 2018

J Transl Med

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BackgroundDexmedetomidine (Dex) can improve neuronal viability and protect the spinal cord from ischemia–reperfusion (I/R) injury, but the underlying mechanisms are not fully understood. This study investigated the effects of dexmedetomidine on the toll-like receptor 4 (TLR4)-mediated nuclear factor κB (NF-κB) inflammatory system and caspase-3 dependent apoptosis induced by spinal cord ischemia–reperfusion injury.MethodsTwenty-four rabbits were divided into three groups: I/R, Dex (10 µg/kg/h prior to ischemia until reperfusion), and Sham. Abdominal aortic occlusion was carried out for 30 min in the I/R and Dex groups. Hindlimb motor function was assessed using the Tarlov scoring system for gait evaluation. Motor neuron survival and apoptosis in the ventral grey matter were assessed by haematoxylin–eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labelling staining. The expression and localisation of ionised calcium-binding adaptor molecule 1, TLR4, NF-κB and caspase-3 were assessed by immunoreactivity analysis. The levels of interleukin 1β and tumour necrosis factor α were assessed using enzyme-linked immunosorbent assays.ResultsPerioperative treatment with dexmedetomidine was associated with a significant preservation of locomotor function following spinal cord ischemia–reperfusion injury with increased neuronal survival in the spinal cord compared to control. In addition, dexmedetomidine suppressed microglial activation, inhibited the TLR4-mediated NF-κB signalling pathway, and inhibited the caspase-3 dependent apoptosis.ConclusionsDexmedetomidine confers neuroprotection against spinal cord ischemia–reperfusion injury through suppression of spinal cord inflammation and neuronal apoptosis. A reduction in microglial activation and inhibition of both the TLR4-mediated NF-κB signalling pathway and caspase-3 dependent apoptosis are implicated.

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“…Dexmedetomidine (Dex), a highly selective α 2 -adrenoceptor agonist, previously provided neuroprotection against ischemia reperfusion-induced cerebral injury ( 20 , 21 ), transient spinal ischemia ( 22 ) and isoflurane-induced neuroapoptosis ( 23 ). However, the underlying mechanisms of these processes have not been fully determined.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression

et al. 2018

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The aim of the present study was to investigate the protective effect of dexmedetomidine (Dex) on traumatic brain injury (TBI), and further evaluate whether the underlying neuroprotective mechanisms are associated with neurological apoptosis and the expression of 70 kDa heat shock protein (HSP70) in the hippocampus. A total of 90 adult male Sprague-Dawley rats were randomly assigned into 3 groups (n=30/group): Sham, TBI and Dex groups. The rat models of TBI were established using a modified weight-drop device and Dex (15 µg/kg) was intravenously administered immediately following TBI. The brain edema and neurological function outcomes of TBI were assessed using wet-dry weight analysis and the Neurological Severity Score method. The expression levels of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) in the rat hippocampus were evaluated using immunohistochemical staining and western blot analysis. The protein levels of HSP70 in the hippocampal region were analyzed using western blot analysis. The results of the present study revealed that administration of Dex post-TBI improved brain edema and neurological outcomes, due to the attenuation of the TBI-induced reduction of Bax expression and increase of Bcl-2 and HSP70 expression. In conclusion, the results of the present study suggested that administration of Dex may serve as a neuroprotective agent against brain injury, at least partially via the inhibition of neuronal apoptosis and upregulation of HSP70 expression in the hippocampus.

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Effects of propofol-dexmedetomidine combination on ischemia reperfusion-induced cerebral injury

Cited by 27 publications

References 40 publications

Propofol exhibits a tumor‑suppressive effect and regulates cell viability, migration and invasion in bladder carcinoma by targeting the microRNA‑10b/HOXD10 signaling pathway

Propofol exhibits a tumor‑suppressive effect and regulates cell viability, migration and invasion in bladder carcinoma by targeting the microRNA‑10b/HOXD10 signaling pathway

Dexmedetomidine attenuates spinal cord ischemia–reperfusion injury through both anti-inflammation and anti-apoptosis mechanisms in rabbits

Neuroprotective effects of dexmedetomidine on traumatic brain injury: Involvement of neuronal apoptosis and HSP70 expression

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