Dexmedetomidine reduces the neuronal apoptosis related to cardiopulmonary bypass by inhibiting activation of the JAK2&amp;ndash;STAT3 pathway

Chen, Yanhua; Xu, Zhendong; Zhang, Bingdong; He, Guodong; Zhou, Lifang; Xie, Yubo

doi:10.2147/dddt.s140644

Cited by 21 publications

(15 citation statements)

References 43 publications

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“…These findings suggest that propofol, midazolam and dexmedetomidine are effective and safe for the sedative treatment of ICU patients with sepsis, but dexmedetomidine has the best effect. This is similar to the findings of Chen et al (23) and Sonneville et al (24), both of which support the results of this study. There was no difference in HR among the three groups, suggesting that the three sedation methods had the same effect on patients' cardiac function.…”

Section: Discussionsupporting

confidence: 93%

Effect of propofol, midazolam and dexmedetomidine on ICU patients with sepsis and on arterial blood gas

2019

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Effects of propofol, midazolam and dexmedetomidine on patients with sepsis in intensive care unit (ICU) and on arterial blood gas (ABG) were studied. In total 429 ICU patients with sepsis, admitted to Renji Hospital, School of Medicine, Shanghai Jiaotong University from May 2015 to January 2019, were selected as research subjects for a prospective analysis. All patients received basic treatment, such as anti-infection treatment, correction of shock and improvement of microcirculation. One hundred and fifty-two patients who were treated with propofol for sedation served as group A, 146 patients who were treated with midazolam for sedation served as group B, and 131 patients who were treated with dexmedetomidine for sedation served as group C. The three groups of patients were compared in terms of diastolic blood pressure (DBP), systolic blood pressure (SBP), heart rate (HR), arterial partial pressure of oxygen (PaO2), arterial partial pressure of carbon dioxide (PaCO2), cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB) before and after treatment. APACHE II score was used to evaluate the sedative effects. The wake-up time of the patients, the length of ICU stay and the adverse reactions were recorded. There was no significant difference among groups A, B and C in terms of HR, SBP, DBP, PaO2, PaCO2, cTnT, CK-MB and APACHE II score before treatment, and SBP, DBP, cTnT and HR after treatment (P>0.050). After treatment, there was no significant difference between groups A and B with respect to CK-MB and APACHE II score (P>0.050). The wake-up time in group A was significantly longer than that in groups B and C (P<0.001). In conclusion, propofol, midazolam and dexmedetomidine are effective and safe in the sedative treatment of ICU patients with sepsis, but dexmedetomidine has the best effect on protecting blood pressure and cardiac functions, which is worthy of use in the clinic.

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Section: Discussionsupporting

confidence: 93%

Effect of propofol, midazolam and dexmedetomidine on ICU patients with sepsis and on arterial blood gas

2019

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“…Dexmedetomidine is a α 2 adrenoceptor agonist first licenced for clinical use in 1999 by FDA, with an initial use for sedation. In animal models of SIRS and surgical insult, dexmedetomidine has been shown to reduce the severity of neuroinflammation and neuroapoptosis [ [82] , [83] , [84] , [85] , [86] ]. Dexmedetomidine administration is associated with reduced hippocampal expression of IL-1β, IL-6, TNF-α and TLR-4, as well as reduced astrocyte and microglial activities [ 83 , 87 ].…”

Section: Therapeutic Options For Post-operative Neurological Complicamentioning

confidence: 99%

Surgery, neuroinflammation and cognitive impairment

et al. 2018

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Trauma experienced during surgery can contribute to the development of a systemic inflammatory response that can cause multi-organ dysfunction or even failure. Post-surgical neuroinflammation is a documented phenomenon that results in synaptic impairment, neuronal dysfunction and death, and impaired neurogenesis. Various pro-inflammatory cytokines, such as TNFα, maintain a state of chronic neuroinflammation, manifesting as post-operative cognitive dysfunction and post-operative delirium. Furthermore, elderly patients with post-operative cognitive dysfunction or delirium are three times more likely to experience permanent cognitive impairment or dementia. We conducted a narrative review, considering evidence extracted from various databases including Pubmed, MEDLINE and EMBASE, as well as journals and book reference lists. We found that further pre-clinical and well-powered clinical studies are required to delineate the precise pathogenesis of post-operative delirium and cognitive dysfunction. Despite the burden of post-operative neurological sequelae, clinical studies investigating therapeutic agents, such as dexmedetomidine, ibuprofen and statins, have yielded conflicting results. In addition, evidence supporting novel therapeutic avenues, such as nicotinic and HMGB-1 targeting and remote ischaemic pre-conditioning, is limited and necessitates further investigation.

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“…In an experimental study, Sancaktar et al reported that there was a signifi cant decrease in renal apoptotic index in the DEX group compared to the I/R damage group (29). Again Chen et al showed that use of DEX reduces apoptosis in cardiopulmonary bypass related neuronal apoptosis (31). In another experimental study, Cakir et al reported that DEX has been shown to reduce histological damage on large tubular necrosis and glomerular damage secondary to I/R injury (32).…”

Section: Discussionmentioning

confidence: 99%

Acute acetaminophene-induced hepatotoxicity and nephrotoxicity; therapeutic effect of dexmedetomidine

Taş¹,

Altınbaş²,

Noyan³

et al. 2019

BLL

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OBJECTIVE AND BACKGROUND: Acute acetaminophen (APAP) overdose has been shown to cause toxicity and the primary treatment medication is N-acetylcysteine (NAC). Dexmedetomidine (DEX) is a sedative drug with known antioxidant properties. We researched whether DEX has an injury-reducing effect on toxicity. METHODS: Rats were divided into: Group I (control), Group II (APAP) Group III (NAC) Group IV (DEX) and Group V (NAC+DEX). Histopathologic investigations of tissues were performed and glutathione peroxidase (GSH-Px), catalase (CAT), malondialdehyde (MDA), myeloperoxidase (MPO) and beta trace protein (PGD2S) levels were studied in blood samples. RESULTS: DEX administration for hepatotoxicity and nephrotoxicity induced with APAP, caused a signifi cant reduction in oxidative injury markers like MDA and MPO, a signifi cant increase in GSH-Px level and a signifi cant degree of amelioration in liver histopathologic scores. CONCLUSION: DEX administration for APAP toxicity causes a reduction in oxidative injury biomarkers, increased antioxidant biomarker levels and signifi cant reduction in liver histopathologic scores. The benefi cial effect of DEX use for detection of toxicity induced by acute APAP overdose, was shown in this study for the fi rst time (Tab. 5, Fig. 2, Ref. 41).

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Dexmedetomidine reduces the neuronal apoptosis related to cardiopulmonary bypass by inhibiting activation of the JAK2–STAT3 pathway

Cited by 21 publications

References 43 publications

Effect of propofol, midazolam and dexmedetomidine on ICU patients with sepsis and on arterial blood gas

Effect of propofol, midazolam and dexmedetomidine on ICU patients with sepsis and on arterial blood gas

Surgery, neuroinflammation and cognitive impairment

Acute acetaminophene-induced hepatotoxicity and nephrotoxicity; therapeutic effect of dexmedetomidine

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