[Retracted] Effect of Dexmedetomidine Combined with Ropivacaine on Cognitive Dysfunction and Inflammatory Response in Patients Undergoing Craniocerebral Surgery

Yang, Licong; Zhang, Hongwei; Zhang, Wenhua

doi:10.1155/2021/4968300

Cited by 10 publications

(12 citation statements)

References 24 publications

(19 reference statements)

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“…Most of the trials did not report on our outcomes. A total of 106 RCTs and one sub‐study of an included RCT provided data for quantitative synthesis 43–149 . Six of the included trials reported a total of 15 eligible comparisons 60,62,82,124,145,147 .…”

Section: Resultsmentioning

confidence: 99%

Dexmedetomidine for the prevention of delirium in adults admitted to the intensive care unit or post‐operative care unit: A systematic review of randomised clinical trials with meta‐analysis and Trial Sequential Analysis

Maagaard

Barbateskovic

Andersen-Ranberg

et al. 2023

Acta Anaesthesiol Scand

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Objectives: To assess any benefit or harm, we conducted a systematic review of randomised clinical trials (RCTs) allocating adults to dexmedetomidine versus placebo/no intervention for the prevention of delirium in intensive care or post-operative care units.Data Sources: We searched Medline, Embase, CENTRAL and other databases. The last search was 9 April 2022.Data Extraction: Literature screening, data extraction and risk of bias volume 2 assessments were performed independently and in duplicate. Primary outcomes were occurrences of serious adverse events (SAEs), delirium and all-cause mortality.We used meta-analysis, Trial Sequential Analysis, and GRADE (Grading Recommendations Assessment, Development and Evaluation).Data Synthesis: Eighty-one RCTs (15,745 patients) provided data for our primary outcomes. Results from trials at low risk of bias showed that dexmedetomidine may reduce the occurrence of the most frequently reported SAEs (relative risk[RR] 0.69; 95% CI 0.43-1.09), cumulated SAEs (RR 0.70; 95% CI 0.52-0.95) and the occurrence of delirium (RR 0.62; 95% CI 0.43-0.89). The certainty of evidence was very low for delirium. Mortality was very low in trials at low risk of bias (0.4% in the dexmedetomidine groups and 1.0% in the control groups) and meta-analysis did not

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Section: Resultsmentioning

confidence: 99%

Dexmedetomidine for the prevention of delirium in adults admitted to the intensive care unit or post‐operative care unit: A systematic review of randomised clinical trials with meta‐analysis and Trial Sequential Analysis

Maagaard

Barbateskovic

Andersen-Ranberg

et al. 2023

Acta Anaesthesiol Scand

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“…Consistently, our results revealed that DEX pretreatment notably reduced LDH release and repressed cell apoptosis. DEX combined with ropivacaine potently alleviates postoperative pain and improves cognitive function in patients receiving craniocerebral surgery [ 30 ]. DEX combined with ropivacaine not only prolongs the sensory and motor block duration of sciatic nerve in rats but also mitigates ropivacaine-induced neurotoxicity by suppressing caspase-3-dependent apoptosis of sciatic nerve cells [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

“…It has been recognized that ropivacaine can cause neurotoxicity during the perioperative period, especially at a high concentration and/or for prolonged use [6]. DEX, a kind of α2 adrenergic receptor agonist, has been commonly used as an adjuvant of ropivacaine and has shown neuroprotective properties in multiple experimental models [28][29][30]. To the best of our knowledge, our study is the first-of-its-kind to demonstrate that DEX pretreatment alleviated ropivacaine-induced neurotoxicity via the miR-10b-5p/BDNF axis.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine pretreatment alleviates ropivacaine-induced neurotoxicity via the miR-10b-5p/BDNF axis

Chen

et al. 2022

BMC Anesthesiol

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Background Ropivacaine is commonly applied for local anesthesia and may cause neurotoxicity. Dexmedetomidine (DEX) exhibits neuroprotective effects on multiple neurological disorders. This study investigated the mechanism of DEX pretreatment in ropivacaine-induced neurotoxicity. Methods Mouse hippocampal neuronal cells (HT22) and human neuroblastoma cells (SH-SY5Y) were treated with 0.5 mM, 1 mM, 2.5 mM, and 5 mM ropivacaine. Then the cells were pretreated with different concentrations of DEX (0.01 μM, 0.1 μM, 1 μM, 10 μM, and 100 μM) before ropivacaine treatment. Proliferative activity of cells, lactate dehydrogenase (LDH) release, and apoptosis rate were measured using CCK-8 assay, LDH detection kit, and flow cytometry, respectively. miR-10b-5p and BDNF expressions were determined using RT-qPCR or Western blot. The binding of miR-10b-5p and BDNF was validated using dual-luciferase assay. Functional rescue experiments were conducted to verify the role of miR-10b-5p and BDNF in the protective mechanism of DEX on ropivacaine-induced neurotoxicity. Results Treatment of HT22 or SH-SY5Y cells with ropivacaine led to the increased miR-10b-5p expression (about 1.7 times), decreased BDNF expression (about 2.2 times), reduced cell viability (about 2.5 times), elevated intracellular LDH level (about 2.0–2.5 times), and enhanced apoptosis rate (about 3.0–4.0 times). DEX pretreatment relieved ropivacaine-induced neurotoxicity, as evidenced by enhanced cell viability (about 1.7–2.0 times), reduced LDH release (about 1.7–1.8 times), and suppressed apoptosis rate (about 1.8–1.9 times). DEX pretreatment repressed miR-10b-5p expression (about 2.5 times). miR-10b-5p targeted BDNF. miR-10b-5p overexpression or BDNF silencing reversed the protective effect of DEX pretreatment on ropivacaine-induced neurotoxicity, manifested as reduced cell viability (about 1.3–1.6 times), increased intracellular LDH level (about 1.4–1.7 times), and elevated apoptosis rate (about 1.4–1.6 times). Conclusions DEX pretreatment elevated BDNF expression by reducing miR-10b-5p expression, thereby alleviating ropivacaine-induced neurotoxicity.

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“…Surgery-induced tissue trauma and ischemia-reperfusion damage can activate the immune system, and then an in ammatory cascade response can be triggered (1)(2)(3). Neuroin ammation, which has catastrophic effects after both craniocerebral surgery and neurological diseases, such as epilepsy and Alzheimer's disease, is caused by a variety of in ammatory cytokines and in ammatory pathways (4,5). However, it is not entirely clear how these in ammatory cytokines have an impact on the brain when the surgical site is not in the brain.…”

Section: Introductionmentioning

confidence: 99%

NLRP3 inflammasome-IL-1β-IL-1R1 signaling pathway is involved in surgery- induced neuroinflammation in mice

Jiang

Liu

Ren

et al. 2023

Preprint

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OBJECTIVE Previous studies have shown that the activation of NLRP3 inflammasome and associated IL-1β/IL-1R1 pathway plays a crucial role in the occurrence and development of inflammation-induced impairment of diverse diseases, inflammation-induced pulmonary fibrosis pathological process. However, the impact of NLRP3 inflammasome-IL-1β-IL-1R1 signaling pathway in surgery-induced neuroinflammation still remains unknown. METHODS Firstly, male C57BL/6J mice were adopted to randomly devided into control group and different time point group (0.5h, 6h, 12h, 18h, 24h) after surgery treated with carotid artery exploration surgery. Moreover, to further investigate the effect of blockage of NLRP3, 4 groups including control group, surgery group, surgery + AAV group and surgery + NEG group, were added to our experiments. After the surgery, the levels of proteins related to the NLRP3 inflammasome, IL-1R1, IL-1β, and IL-18 in diverse groups were measured by immunofluorescence assay, quantitative polymerase chain reaction (qPCR), western blot, and enzyme-linked immunosorbent assay (ELISA), respectively. Microglia and monocytes were separately determined by flow cytometry. The pathological changes in the brain were detected by Nissl staining. RESULTS Peripheral surgery resulted in monocyte activation and an increase in the expression of IL-1β in the circulatory system. IL-1R1, NLRP3, activated caspase-1 (caspase-1 P10), IL-1β, and IL-18 were upregulated in the hippocampus. Subsequently, the expression of microglia cells considerably increased and neuronal damage was observed. These effects were attenuated by AAV-NLRP3 treatment. CONCLUSIONS The peripheral surgery induced an increase of IL-1β, IL-1R1, NLRP3, and neuron injury in the hippocampus, inhibiting the expression of NLRP3 can alleviate inflammatory factors expression and neuron damage. We assumed that there is a feedback mechanism about IL-1β-IL-1R1-NLRP3 inflammasome existing in the brain after peripheral surgery.

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[Retracted] Effect of Dexmedetomidine Combined with Ropivacaine on Cognitive Dysfunction and Inflammatory Response in Patients Undergoing Craniocerebral Surgery

Cited by 10 publications

References 24 publications

Dexmedetomidine for the prevention of delirium in adults admitted to the intensive care unit or post‐operative care unit: A systematic review of randomised clinical trials with meta‐analysis and Trial Sequential Analysis

Dexmedetomidine for the prevention of delirium in adults admitted to the intensive care unit or post‐operative care unit: A systematic review of randomised clinical trials with meta‐analysis and Trial Sequential Analysis

Dexmedetomidine pretreatment alleviates ropivacaine-induced neurotoxicity via the miR-10b-5p/BDNF axis

NLRP3 inflammasome-IL-1β-IL-1R1 signaling pathway is involved in surgery- induced neuroinflammation in mice

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