This study compared the wound-healing response and osteogenic gene expression profile of osteoblasts exposed to pediatric-equivalent concentrations of dexmedetomidine (DXMT) and propofol (POF). Human osteoblast-like SAOS-2 cells were assigned to control, low- and high-dose DXMT and POF groups based on pharmacokinetically derived free-drug levels. Scratch-wound closure was quantified over 24 h, and expression of osteogenesis- and cytoskeleton-related genes (RANKL, RUNX2, SP7, BMP2, VIM, VCL, OCN, ALP) was measured by SYBR Green quantitative Polymerase Chain Reaction (qPCR). Normality was assessed using the Shapiro-Wilk test, and group differences were analyzed with two-way ANOVA followed by Tukey's multiple comparisons test (p < 0.05). All groups demonstrated complete scratch closure by 24 h, with no differences at 6 h. At 18 h, POF did not differ from the control, whereas DXMT significantly accelerated closure at both doses in a dose-dependent fashion. High-dose DXMT significantly increased VIM (3.95 ± 3.12, p = 0.0144) and BMP2 (2.28 ± 0.70, p = 0.0002) expression, while RUNX2, SP7, and RANKL remained comparable to controls. ALP (1.68 ± 0.40, p = 0.0005) and OCN (3.31 ± 0.35, p = 0.0108) were significantly elevated only in the high-dose DXMT group, whereas POF showed no significant effects. At clinically relevant concentrations, DXMT was associated with enhanced scratch closure and increased expression of selected osteogenesis- and cytoskeleton-related genes in SAOS-2 cells, whereas POF showed limited effects under the tested conditions. These findings suggest that DXMT may influence early in vitro cellular responses relevant to bone healing and should be further validated in functional differentiation models and in vivo studies.

Diabetes-associated cognitive dysfunction represents a global health challenge, yet the mechanisms by which anesthetics modulate cognitive function in diabetic states remain poorly understood. We systematically compared the effects of 2-hour brief exposure to sevoflurane (SEV) and propofol (PRO) on cognitive function and neuropathology in streptozotocin (STZ) -induced diabetic mice. Morris water maze and Y-maze tests revealed that SEV significantly exacerbated spatial memory and learning deficits in mice, while PRO showed no significant effects. Additionally, diabetic mice exhibited reduced NeuN+ neurons, increased β-amyloid deposition, and decreased SYN expression in the hippocampal CA1 region as examined by Immuno-fluorescence staining. Neither short-term SEV nor PRO exposure aggravated neuronal structural damage. Further transcriptomics revealed both anesthetics affected hippocampal neuron differentiation, but SEV uniquely perturbed fatty acid metabolism pathways. Metabolomics identified SEV-induced disruptions in lipid metabolism, marked by elevated hippocampal free fatty acids, phospholipids, as well as reduced lysophospholipids and acylcarnitine. Integrated multi-omics analysis demonstrated that SEV impaired cognition by suppressing fatty acid oxidation and dysregulating glycerophospholipid metabolism. These findings highlight the critical impact of anesthetic selection in diabetic populations.

Introduction: The BIS monitor is an FDA approved multiprocessed EEG that can be used to guide general anesthesia, sedation procedures and ICU sedation. Over and under sedation can be avoided, allowing for a more efficient sedation process and reducing the risks of awareness. During sedation procedures the correct timing of titration is important to reduce the risk of over-sedation. If the sedatives are repeated before their peak effect has occurred this may result in respiratory depression. The aim of this study was to use the BIS monitor to determine the time to IV bolus peak effect for 3 sedative agents; Midazolam (MID), Fentanyl (FENT) and Propofol (PROP). The second aim was to determine the BIS value at which no movement to stimulus occurs, i.e. the ideal target depth. Methods: After IRB approval and informed consent meeting the inclusion criteria were patients of ages 10-17 undergoing a surgical dental extraction under deep intravenous sedation. All patients received the same sedative based regimen: Midazolam, Propofol and Fentanyl. Sedation doses were age and weight based. The only difference was the sequence of sedative administration prior to procedure start. On initial local anesthetic placement (a “sharp” stimulus of palatal LA), the BIS monitor to computer data stream was real-time highlighted. Patient movement in response to stimulation was assessed by two observers. Results: We have recruited 70 patients so far, ages ranged from 10 to 17 years, average procedure time of 16.6 minutes and recovery time of 34.3 minutes. The peak effect onset time for MID, PROP and FENT were ~ 95 seconds, ~ 55 seconds, Unable (FENT had a minimal BIS effect), these take into account a BIS recording delay of about 25 seconds for our model. About 25% patients moved with stimulus. The risk of movement was 4 x greater if the BIS was 50 or higher. Conclusions: The peak onset time for MID and PROP were identified which suggests that repeat dosing should be about 2 minutes apart for MID and 1 minute for PROP. Due to minimal FENT BIS effect no peak onset could be established. Movement was minimized with lower BIS, c/w deeper sedation, in GA territory. Deep sedation even with A BIS in the 50’s may not prevent patient movement to surgical stimulation.

A novel ultrasensitive derivatization-free synchronous fluorescence approach for the simultaneous analysis of propofol and nalbuphine in human plasma and dosage forms: Compliance with greenness and blueness metrics.

While different anesthetic drugs induce distinct electrical characteristics in the anesthetized brain, the effects of different anesthetics on the activity of single neurons in the central nervous system remain unclear. In this study, mice were anesthetized with different agents (Remimazolam [REM], dexmedetomidine [DEX], and propofol [PRO]), and cortical electroencephalogram (EEG) and neuronal calcium signals were recorded before, during, and after anesthesia, followed by analysis of the changes in the power spectra of the EEG signals and the intensities of the neuronal calcium signals. Compared with awake mice, mice under PRO-induced anesthesia primarily exhibited changes in low-frequency range brain electrical activity, whereas mice under REM-induced anesthesia exhibited significant increases in the power density in the low- and mid-frequency ranges (δ, θ, and α) postanesthesia, with minimal impact on the high-frequency (β) range. DEX not only suppressed brain cortical activity in the low-frequency range but also affected the mid-frequency range, indicating a broader effect. Reduced rates of transient calcium frequencies per minute were observed, as were reductions in the peak amplitudes of calcium activity (ΔF/F) and total signal intensity of calcium activity (ΔF/F) in anesthetized mice, with PRO showing more pronounced inhibition of neuronal calcium activity than REM and DEX did. These results demonstrate that propofol (PRO) exerts the strongest inhibitory effect on neuronal calcium activity during anesthesia, significantly suppressing transient calcium frequencies, peak amplitudes (ΔF/F), and total signal intensity (ΔF/F) compared to REM and DEX. PRO primarily enhanced low-frequency δ oscillations in EEG during anesthesia, while REM increased low- to mid-frequency (δ, θ, α) power, and DEX broadly suppressed both low- and mid-frequency bands (δ, θ, α, β). These findings highlight PRO as the most potent suppressor of neuronal excitability during the maintenance phase of anesthesia.

Postoperative nausea and vomiting (PONV) is a frequent adverse event after bariatric surgery and is associated with patient dissatisfaction and increased health care burden. Aggressive multimodal antiemetic prophylaxis and the use of propofol infusion during anesthesia are associated with the reduction of PONV. In this study, we examined the use of rescue antiemetics following bariatric surgery performed with 3 different anesthetic strategies designed to reduce PONV: (1) primary volatile (VOL) anesthetic and propofol (PROP) infusion (VOL+PROP), (2) volatile anesthetic with propofol and dexmedetomidine (DEX) infusions (VOL+PROP+DEX), or (3) opioid-sparing total intravenous anesthesia (PROP+DEX). In this retrospective observational study, we included patients undergoing bariatric surgery from 2018-2022 who received 1 of 3 anesthetics: (1) VOL+PROP, (2) VOL+PROP+DEX, or (3) opioid-sparing PROP+DEX without a VOL. Inverse probability of treatment weighting analysis determined the association between the need for rescue-antiemetics in the postanesthesia care unit (PACU) and following PACU discharge. Three hundred thirty-two patients received VOL+PROP, 354 VOL+PROP+DEX, and 166 PROP+DEX, and all received prophylactic antiemetics during surgery. After surgery, the PROP+DEX patients received fewer rescue antiemetics in the PACU compared with VOL+PROP (11% vs. 24%, P =0.002), and VOL+PROP+DEX fewer compared with VOL+PROP (16% vs. 24%, P =0.023). This differential antinausea effect was limited to PACU stay only. Rescue antiemetic use increased across all anesthetic management groups following PACU discharge until midnight on the day of surgery (ranging from 38% to 46% across groups, P =0.71) and through the first postoperative day (ranging from 47% to 57% across groups, P =0.20). The benefit associated with anesthetic strategies designed to reduce PONV was present but did not persist past PACU discharge. This finding suggests that aggressive perioperative multimodal antiemetic prophylaxis combined with anesthetic strategies designed to prevent PONV after bariatric surgery have only a short-lived effect, thus health care staff in hospital wards may expect to encounter high rates of PONV in these patients. There is a need for the development of novel antinausea treatments to reduce the rate of this frequent postoperative complication.

ObjectiveThis study aims to compare the effects of sevoflurane (SEV) and propofol (PRO) on postoperative cognitive dysfunction (POCD) in patients undergoing cardiac surgery (CS) under cardiopulmonary bypass (CPB), with a focus on evaluating the efficacy of these anesthetic agents in preventing POCD.MethodsA total of 113 patients undergoing CS with CPB were grouped into two: PRO group (n = 58) and SEV group (n = 55). Baseline data, anesthesia effects (CPB duration, anesthesia time, respiratory recovery time, and anesthesia recovery time), Montreal Cognitive Assessment (MoCA) scores, POCD incidence, neurological function markers (NSE, S-100β, MMP9), and serum inflammatory markers (IL-6, IL-8, TNF-α) were analyzed. The study was conducted between March 2018 and May 2021.ResultsThe PRO group showed significantly shorter anesthesia time (P < 0.05), respiratory recovery time (P < 0.05), and anesthesia recovery time (P < 0.05) compared to the SEV group. The postoperative MoCA score in the PRO group reduced markedly compared with the baseline, but still higher than that in the SEV group (P < 0.05). The incidence of POCD was significantly lower in the PRO group (5.17% vs. 27.27%, P = 0.001). The levels of NSE, S-100β, MMP9, IL-6, IL-8, and TNF-α were significantly elevated compared to baseline values, but still lower than those in the SEV group (P < 0.05 for all comparisons).ConclusionPRO is more effective than SEV in preventing POCD in patients undergoing CS with CPB. It provides superior anesthetic effects and offers better protection against neuronal damage and serum inflammation compared to SEV.Clinical trial numberNot applicable.

The ventrolateral preoptic nucleus (VLPO) is a crucial regulator of sleep, and its neurons are implicated in both sleep-wake regulation and anesthesia-induced loss of consciousness. Propofol (PRO), a widely used intravenous anesthetic, modulates the activity of VLPO neurons, but the underlying mechanisms, particularly the role of dopaminergic receptors, remain unclear. This study aimed to investigate the effects of PRO on NA (-) neurons in the VLPO and to determine the involvement of D1 and D2 dopaminergic receptors in mediating these effects. Using in vitro patch-clamp techniques, we identified and characterized NA (-) and NA (+) neurons in the VLPO based on their morphological, pharmacological, and electrophysiological properties. We assessed the effects of PRO on spontaneous excitatory postsynaptic currents (sEPSCs) and inhibitory postsynaptic currents (sIPSCs) in NA (-) neurons, both in the presence and absence of dopaminergic receptor modulators. PRO significantly increased the firing frequency of NA (-) neurons while decreasing the firing frequency of NA (+) neurons. This activation of NA (-) neurons was mediated through GABA_A receptors, as evidenced by the increased frequency of sEPSCs and altered sIPSCs dynamics. Dopamine (DA) attenuated the PRO-induced increase in sEPSCs frequency and suppression of sIPSCs frequency in NA (-) neurons via D1 receptors, but not D2 receptors. Blocking D1 receptors with SCH23390 reversed the effects of DA on PRO-induced changes, while D2 receptor antagonist sulpiride had minimal impact. Our findings demonstrate that PRO excites sleep-promoting NA (-) neurons in the VLPO, primarily through GABA_A receptors, with dopaminergic modulation occurring via D1 receptors. These results provide new insights into the neural mechanisms underlying general anesthesia and highlight the potential role of dopaminergic signaling in modulating anesthetic effects on sleep-related neural circuits.

With antibiotic resistance increasing in the global population every year, efforts to discover new strategies against microbial diseases are urgently needed. One of the new therapeutic targets is the bacterial cell membrane since, in the event of a drastic alteration, it can cause cell death. We propose the utilization of hydrophobic molecules, namely, propofol (PFL) and cannabidiol (CBD), dissolved in nanodroplets of oil, to effectively strike the membrane of two well-known pathogens: Escherichia coli and Staphylococcus aureus. First, we carried out calorimetric measurements to evaluate the effects of these drugs on model membranes formed by lipids from these bacteria. We found that the drugs modify their transition temperature, enthalpy of cohesion, and cooperativity, which indicates a strong alteration of the membranes. Then, inhibition of colony-forming units is studied in incubation experiments. Finally, we demonstrate, using atomic force and fluorescence microscopy, that the drugs, especially propofol, produce a visible disruption in real bacterial membranes, explaining the observed inhibition. These findings may have useful implications in the global effort to discover new ways to effectively combat the growing threat of drug-resistant pathogens, especially in skin infections.

Propofol administration for induction is associated with peri-intubation instability in trauma critical care unit patients

The purpose of this study is to explore the shared molecular pathogenesis of traumatic brain injury (TBI) and high-grade glioma and investigate the mechanism of propofol (PF) as a potential protective agent. By analyzing the Chinese glioma genome atlas (CGGA) and The Cancer Genome Atlas (TCGA) databases, we compared the transcriptomic data of high-grade glioma and TBI patients to identify common pathological mechanisms. Through bioinformatics analysis, in vitro experiments and in vivo TBI model, we investigated the regulatory effect of PF on extracellular matrix (ECM)-related genes through Prrx1 under oxidative stress. The impact of PF on BBB integrity under oxidative stress was investigated using a dual-layer BBB model, and we explored the protective effect of PF on tight junction proteins and ECM-related genes in mice after TBI. The study found that high-grade glioma and TBI share ECM instability as an important molecular pathological mechanism. PF stabilizes the ECM and protects the BBB by directly binding to Prrx1 or indirectly regulating Prrx1 through miRNAs. In addition, PF reduces intracellular calcium ions and ROS levels under oxidative stress, thereby preserving BBB integrity. In a TBI mouse model, PF protected BBB integrity through up-regulated tight junction proteins and stabilized the expression of ECM-related genes. Our study reveals the shared molecular pathogenesis between TBI and glioblastoma and demonstrate the potential of PF as a protective agent of BBB. This provides new targets and approaches for the development of novel neurotrauma therapeutic drugs.

Icaritin is a prenylflavonoid derivative of the genus Epimedium (Berberidaceae) and has a variety of pharmacological actions. Icaritin is approved by the National Medical Products Administration as an anticancer drug that exhibits efficacy and safety advantages in patients with hepatocellular carcinoma cells. This study aimed to evaluate the inhibitory effects of icaritin on UDP-glucuronosyltransferase (UGT) isoforms. 4-Methylumbelliferone (4-MU) was employed as a probe drug for all the tested UGT isoforms using in vitro human liver microsomes (HLM). The inhibition potentials of UGT1A1 and 1A9 in HLM were further tested by employing 17β-estradiol (E2) and propofol (PRO) as probe substrates, respectively. The results showed that icaritin inhibits UGT1A1, 1A3, 1A4, 1A7, 1A8, 1A10, 2B7, and 2B15. Furthermore, icaritin exhibited a mixed inhibition of UGT1A1, 1A3, and 1A9, and the inhibition kinetic parameters (Ki) were calculated to be 3.538, 2.117, and 0.306 (μM), respectively. The inhibition of human liver microsomal UGT1A1 and 1A9 both followed mixed mechanism, with Ki values of 2.694 and 1.431 (μM). This study provides supporting information for understanding the drug-drug interaction (DDI) potential of the flavonoid icaritin and other UGT-metabolized drugs in clinical settings. In addition, the findings provide safety evidence for DDI when liver cancer patients receive a combination therapy including icaritin.

BackgroundBalanced propofol sedation is extensively used in endoscopic retrograde cholangiopancreatography (ERCP), but sedation-related adverse events (SRAEs) are common. In various clinical settings, the combination of dexmedetomidine with opioids and benzodiazepines has provided effective sedation with increased safety. The aim of this investigation was to compare the efficacy and safety of dexmedetomidine and propofol for sedation during ERCP.MethodsForty-one patients were randomly divided into two groups: the dexmedetomidine (DEX) group and the propofol (PRO) group. Patients in the DEX group received an additional bolus of 0.6 μg kg−1 dexmedetomidine followed by a dexmedetomidine infusion at 1.2 μg kg−1 h−1, whereas the PRO group received 1–2 mg kg−1 of propofol bolus followed by a propofol infusion at 2–3 mg kg−1 h−1. During ERCP, the primary outcome was the incidence of hypoxemia (SpO2 < 90% for > 10 s). Other intraoperative adverse events were also recorded as secondary outcomes, including respiratory depression (respiratory rate of < 10 bpm min−1), hypotension (MAP < 65 mmHg), and bradycardia (HR < 45 beats min−1).ResultsThe incidence of hypoxemia was significantly reduced in the DEX group compared to the PRO group (0% versus 28.6%, respectively; P = 0.032). Patients in the PRO group exhibited respiratory depression more frequently than patients in the DEX group (35% versus 81%, respectively; P = 0.003). There were no significant differences in terms of hypotension and bradycardia episodes between groups. During the procedures, the satisfaction scores of endoscopists and patients, as well as the pain and procedure memory scores of patients were comparable between groups.ConclusionIn comparison with propofol, dexmedetomidine provided adequate sedation safety with no adverse effects on sedation efficacy during ERCP.Trial registrationChinese Clinical Trial Registry, ChiCTR2200061468, 25/06/2022.

The water microstructure around propofol plays a crucial role in controlling their solubility in the binary mixture. The unusual nature of such a water microstructure can influence both translational and reorientational dynamics, as well as the water hydrogen bond network near propofol. We have carried out all-atom molecular dynamics simulations of five different compositions of the propylene glycol (PG)/water binary mixture containing propofol (PFL) molecules to investigate the differential behavior of water microsolvation shells around propofol, which is likely to control the propofol solubility. It is evident from the simulation snapshots for various compositions that the PG at high molecular ratio favors the water cluster and extended chainlike network that percolates within the PG matrix, where the propofol is in the dispersed state. We estimated that the radial distribution function indicates higher ordered water microstructure around propofol for high PG content, as compared to the lower PG content in the PG/water mixture. So, the hydrophilic PG regulates the stability of the water micronetwork around propofol and its solubility in the binary mixture. We observed that the translational and rotational mobility of water belonging to the propofol microsolvation shell is hindered for high PG content and relaxed toward the low PG molecular ratio in the PG/water mixture. It has been noticed that the structural relaxation of the hydrogen bond formed between the propofol and the water molecules present in the propofol microsolvation shell for all five compositions is found to be slower for high PG content and becomes faster on the way to low PG content in the mixture. Simultaneously, we calculated the intermittent residence time correlation function of the water molecules belonging to the microsolvation shell around the propofol for five different compositions and found a faster short time decay followed up with long time components. Again, the origin of such long time decay is primarily from the structural relaxation of the microsolvation shell around the propofol, where the high PG content shows the slower structural relaxation that turns faster as the PG content approaches to the other end of the compositions. So, our studies showed that the slower structural relaxation of the microsolvation shell around propofol for a high PG molecular ratio in the PG/water mixture correlate well with the extensive ordering of the water microstructure and restricted water mobility and facilitates the dissolution process of propofol in the binary mixture.

The use of two or more drugs carries the potential risk of drug-drug interactions (DDIs), which may result in adverse reactions. Some human immunodeficiency virus (HIV)-infected patients who receive antiretroviral therapy (ART) may require general anesthesia with propofol (PRL) before undergoing surgical treatment. Both PRL and ART drugs may lead to neuronal dysfunction, which can be accompanied by energy metabolism disorders. Neurons take in glucose mainly through glucose transporter 3 (Glut3) which is specifically expressed on the cell membranes of neurons. However, to date, no study has examined whether the DDIs of PRL and ART drugs interfere with glucose metabolism and Glut3 expression in neurons. An in vitro model was constructed using the primary cultures of neurons. PRL and ART drugs (EFV, AZT, and 3TC), were added at different concentrations (low, medium, and high). The neurons were exposed to the drugs for 1, 4, 8, and 12 h. The optimal drug concentration and exposure time were selected. The cellular survival rate, glucose concentration, electrophysiology, and the expression of Glut3 were detected. There were no significant changes in the cellular survival rates of the neurons that were exposed to both PRL and ART drugs at low concentrations for 1 h. However, the survival rates of the neurons decreased significantly as the drug concentrations and durations increased. The glucose concentration of the neurons that were exposed to both PRL and the ART drugs was significantly decreased. The glucose concentration of the neurons was not affected by any individual drug. The amplitude of the action potential and the expression of Glut3 were decreased in the neurons that were exposed to both PRL and ART drugs. The main adverse reactions induced by the DDIs between PRL and the ART drugs were decreased glucose metabolism and neuronal damage, which were caused by inhibiting the expression of Glut3. More importantly, we found that decreases in glucose metabolism predated neuronal damage.

Purpose: To examine the association of propofol (PRO) with related key genes that may serve as potential biomarkers for alleviation of PRO-induced toxicity in neural stem cells (NSCs).&#x0D; Methods: Differentially expressed genes (DEGs) were screened based on GEO database, using the analysis platform of Metaboanalyst, GEO2R, DAVID and Ehbio. NSCs were purchased and treated with 3 μM of propofol (PRO). NR4A1 was transfected into NSCs, and the NR4A1 expression, apoptosis-related protein and AMPK pathway-related protein were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting. Cell viability and apoptosis were evaluated by methylthiazolyldiphenyl-tetrazolium bromid (MTT) assay and flow cytometry.&#x0D; Results: A total of 278 DEGs were analyzed on GSE106799 microarray, and finally screened for differentially expressed down-regulated gene, NR4A1, which is a hubgene. NR4A1 expression decreased in PRO-induced NSCs. Furthermore, NR4A1 attenuated the PRO-induced decrease in the viability of NSCs and the increase in apoptosis. Moreover, NR4A1 increased p-AMPK/AMPK level.&#x0D; Conclusion: NR4A1 attenuates the toxicity in NSCs induced by PRO by regulating AMPK pathways, and thus provides a theoretical basis for the treatment of nerve damage caused by anesthetics.

Liver ischemia reperfusion (IR) injury induces hepatic stellate cell (HSC) activation and liver fibrosis. Propofol (PRO) possesses a positive protective effect on liver ischemia reperfusion injury. We aimed to investigate PRO function and mechanism in IR-induced liver fibrosis. A mice model of liver IR was established. Hematoxylin-eosin (HE) staining was utilized to evaluate liver tissue's pathological changes. Masson staining was applied to evaluate liver fibrosis. The expression level of α-SMA was measured by immunohistochemical (IHC). The expressions of lncRNA HOXA11-AS (HOXA11-AS), PTBP1, HDAC4, α-SMA, COL1A1 and Fibronectin were tested by qRT-PCR or Western blot. The commercial kits detected alanine aminotransferase (ALT) and aspartate aminotransferase (AST) concentrations in serum. Enzyme-linked immunosorbent assay (ELISA) measured TNF-α and IL-6 levels. The binding relationship between HOXA11-AS, PTBP1 and HDAC4 was verified by RNA immunoprecipitation (RIP). Our results showed that PRO alleviated liver fibrosis and the inflammation in IR-induced mice. PRO decreased the expression levels of HOXA11-AS, PTBP1 and HDAC4. Furthermore, HOXA11-AS overexpression abolished the protective effect of PRO against liver fibrosis in mice with IR-disposed. HOXA11-AS interacted with PTBP1 to regulate HDAC4 level and prevented its degradation in JS-1 cells. HDAC4 silencing eliminated the regulatory of HOXA11-AS overexpression on fibrosis and inflammation in IR-induced mice PRO inhibited HOXA11-AS expression to regulate HDAC4, thereby influencing liver fibrosis and inflammation induced by IR. It suggesting that PRO plays a protective role in liver fibrosis induced by ischemia-reperfusion in mice by regulating HOXA11-AS/PTBP1/HDAC4 axis.

Previous pairwise meta-analyses demonstrated the efficacy and safety of dexmedetomidine in preventing postoperative delirium (POD) after cardiac surgery; however, the optimal time of applying dexmedetomidine remains unclear. This network meta-analysis aimed to determine the optimal time of using dexmedetomidine to reduce the incidence of POD following cardiac surgery. We first retrieved eligible randomized controlled trials (RCTs) from previous meta-analyses, and then an updated search was performed to identify additional RCTs in PubMed, Embase, and the Cochrane library from January 1, 2021 to October 31, 2021. Two authors screened literature, collected data, and evaluated bias risk of eligible studies. Finally, we performed Bayesian network analysis using R version 3.6.1 with the "gemtc" and "rjags" package. Eighteen studies with 2636 patients were included, and all studies were identified from previous meta-analyses. Results showed that postoperative dexmedetomidine reduced the risk of POD compared with normal saline (NS) (odds ratio [OR], 0.13; 95% credible interval [CrI], 0.03-0.35) and propofol (PRO) (OR, 0.19; 95%CrI, 0.04-0.66). Postoperative dexmedetomidine was associated with a lower incidence of POD compared with perioperative dexmedetomidine (OR, 0.21; 95% CrI, 0.04-0.82). Moreover, postoperative dexmedetomidine had the highest probability of ranking best (90.98%), followed by intraoperative dexmedetomidine (46.83%), PRO (36.94%), perioperative dexmedetomidine (30.85%), and NS (60.02%). Dexmedetomidine reduces the incidence of POD compared with PRO and NS in patients undergoing cardiac surgery, and postoperative application of dexmedetomidine is the optimal time.

Background General anesthesia in early childhood may affect all aspects of neurodevelopment, resulting in learning and behavior defects. Therefore, there is an urgent need to find safe anesthetics or put forward more comprehensive anesthesia schemes to solve the negative effects caused by existing anesthetics. The objective of this study is to explore the impact of dexmedetomidine (Dex) incorporated with low-dose propofol (PRO) on learning and memory ability and neural cells in developing rats. Methods Eighty SD rats were randomly divided into 4 groups including the Sham group, Lipid group, L-PRO group, and Dex + L-PRO group. After treatment, the spatial learning and memory ability of rats in each group were assessed by the water maze test and the passive avoidance test. The damage of hippocampal tissues was assessed by Nissl staining; the apoptosis, the levels of inflammatory factors, and the level of oxidative stress were measured by Tunel staining, ELISA, and biochemical assays, respectively. Besides, qRT-PCR and Western Blot determined the expression of apoptosis-related proteins, neurotrophic factors, and MAPK signaling pathway-related proteins in the hippocampus. Results Compared with the L-PRO group, the Dex + L-PRO group had better spatial learning and memory ability. Administration of Dex and L-PRO greatly alleviated neural cell damage in the hippocampus and decreased the levels of IL-6, IL-1β, and TNF-α. Besides, it significantly decreased the content of ROS and malondialdehyde (MDA), glutathione (GSH), when up-regulating the levels of IL-10, antioxidant superoxide dismutase (SOD) and BDNF, receptor tyrosine kinase B (TrkB), and neurotrophin-3 (NT-3) related to hearing function and significantly lower activity of MAPK signaling pathway. Conclusion Dex combined with low-dose PRO can significantly inhibit inflammation, oxidative stress response, neuronal apoptosis, MAPK signaling pathway activity and promote the secretion of neurokines in hippocampus to reduce neural cell damage and avoid the learning and memory impairment caused by anesthetics in developing rats.

Dexmedetomidine versus propofol for operator-directed nurse-administered procedural sedation during catheter ablation of atrial fibrillation: A randomized controlled study.