Vitexin is a bioactive compound extracted from hawthorn leaves, which reduces blood pressure and has anti‑inflammatory and potential anticancer effects. However, the mechanisms underlying the protective effects of vitexin against isoflurane‑induced neurotoxicity remain elusive. Therefore, the aim of the present study was to investigate these mechanisms further. Sprague Dawley rats received 1.4% isoflurane in a 100% oxygen environment for 2 h. Human PC12 pheochromocytoma neurosecretory cells were exposed to 2% isoflurane for 12 h before they were treated with 1, 10 or 100 µM vitexin for a further 24 h. Vitexin inhibited the isoflurane-induced cell cytotoxicity and weakened isoflurane-induced neuroinflammation and oxidative stress pathways in PC12 cells. In addition, treatment with vitexin suppressed isoflurane‑induced caspase‑3 activation and increased β-secretase 1 levels in PC12 cells. Furthermore, vitexin treatment decreased the levels of isoflurane‑induced cytosolic calcium and reactive oxygen species, and downregulated the expression of transient receptor potential cation channel subfamily V member 1 (TRPV1) and glutamate ionotropic receptor NMDA type subunit 2B (NR2B) protein expression in isoflurane-treated PC12 cells. These results suggest that vitexin mediates its protective effects against isoflurane-induced neurotoxicity by targeting the TRPV1 and NR2B signaling pathways.

The effect of sulforaphane on nuclear factor erythroid 2-related factor 2 (Nrf2) and its protective mechanism for lung injury in rabbits with acute respiratory distress syndrome (ARDS) were investigated. Thirty rabbits were randomly divided into control (n=10), model (n=10) and experimental groups (n=10). Rabbits in model group and experimental group were treated with femoral venous injection of oleic acid to establish the ARDS model, while those in control group were injected with the same volume of normal saline. The experimental group received intravenous injection of sulforaphane. Twelve hours after modeling, the clinical manifestations and deaths of rabbits in each group were recorded and compared, including blood gas indexes, lung index (LI), alveolar damage coefficient, serum Nrf2 expression, as well as messenger ribonucleic acid (mRNA) and protein expression of Nrf2 in lung tissues. Pink frothy sputum and death were observed in rabbits in model group and experimental group, but the number of such cases in experimental group was smaller than that in the model group (p<0.05). Compared with those in control group, LI and IQA in model group and experimental group were increased, but LI and IQA in the experimental group were significantly decreased compared with those in the model group. Compared with those in the model group, the blood gas indexes (PaO2, PaCO2 and SaO2) in the experimental group were significantly increased (p<0.05). Nrf2 in serum and lung tissues of rabbits in experimental group was significantly increased compared with that in model group (p<0.05). Sulforaphane significantly inhibits ARDS in rabbits and plays a protective role in ARDS through upregulating Nrf2.

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Background: Double-lumen bronchial tubes (DLBT) and bronchial blockers (BB) are commonly used in the anesthesia for clinical thoracic surgery. But there are few systematic clinical comparisons between them. In this study, the effects of BB and DLBT on one-lung ventilation (OLV) are studied.Methods: The 200 patients with thoracic tuberculosis undergoing thoracic surgery, were randomly assigned to group A (DLBT) and group B (BB). Intubation time, hemodynamic changes (mean arterial pressure [MAP], heart rate [HR]), and arterial blood gas indicators (arterial partial pressure of carbon dioxide [PaCO2], arterial partial pressure of oxygen [PaO2], airway plateau pressure [Pplat], and airway peak pressure [Ppeak]) at 4 time points were recorded. Complications such as hoarseness, pulmonary infection, pharyngalgia, and surgical success rate were also evaluated postoperatively.Results: Intubation times were shorter in group B. Both MAP and HR in group A were significantly higher 1 minute after intubation than before, but also higher than those in group B. PaO2 levels were lower in both groups during (OLV) than immediately after anesthesia and after two-lung ventilation (TLV), with PaO2 being lower after 60 minutes of OLV than after 20 minutes of OLV. Furthermore, at both points during OLV, PaO2 was lower in group A than in group B. No significant differences in PaCO2 were found between the 2 groups. Ppeak and Pplat were increased in both groups during OLV, with both being higher in group A than in group B. The incidence of postoperative hoarseness, pulmonary infection, and pharyngalgia were lower in group B. There was no significant difference in the success rate of operation between the 2 groups.Conclusions: Compare with using DLBT, implementation of BB in general anesthesia has less impact on hemodynamics, PaO2 and airway pressures, and achieves lower incidence of postoperative complication.

Mechanical ventilation (MV) can contribute to ventilator-induced lung injury (Vili); dexmedetomidine (dex) treatment attenuates MV-related pulmonary inflammation, but the mechanisms remain unclear. Therefore, the present study aimed to explore the protective effect and the possible molecular mechanisms of dex in a Vili rodent model. adult male Sprague-dawley rats were randomly assigned to one of seven groups (n=24 rats/group). rats were euthanized after 4 h of continuous MV, and pathological changes, lung wet/dry (W/D) weight ratio, the levels of inflammatory cytokines (il-1β, TnF-α and il-6) in the bronchoalveolar lavage fluid (BALF), and the expression levels of Bcl-2 homologous antagonist/killer (Bak), Bcl-2, pro-caspase-3, cleaved caspase-3 and the phosphorylation of erK1/2 in the lung tissues were measured. Propidium iodide uptake and Tunel staining were used to detect epithelial cell death. The dex pretreatment group exhibited fewer pathological changes, lower W/d ratios and lower expression levels of inflammatory cytokines in BALF compared with the VILI group. Dex significantly attenuated the ratio of Bak/Bcl-2, cleaved caspase-3 expression levels and epithelial cell death, and increased the expression of phosphorylated erK1/2. The protective effects of dex could be partially reversed by Pd98059, which is a mitogen-activated protein kinase (upstream of erK1/2) inhibitor. overall, dexmedetomidine was found to reduce the inflammatory response and epithelial cell death caused by Vili, via the activation of the erK1/2 signaling pathway.