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.
Sevoflurane is a commonly used inhalation anesthetic. Sevoflurane-induced neuroapoptosis and cognitive impairments in animals are widely reported, however, the underlying molecular mechanisms remain largely unknown. The results of the present study demonstrated that sevoflurane anesthesia induced spatial memory impairments in rats, as determined by the Morris water maze test. Mechanistically, the current study demonstrated that sevoflurane administration significantly enhanced the expression of microRNA (miR)-188-3p. Furthermore, inhibition of miR-188-3p using lentiviral miR-188-3p inhibitors attenuated sevoflurane-induced cognitive impairments in rats. The present study also demonstrated that miR-188-3p targeted MDM2 proto-oncogene (MDM2) and negatively regulated the expression of MDM2, as determined by luciferase assays, reverse transcription-quantitative polymerase chain reaction and western blot analysis. Furthermore, decreased abundance of MDM2 following transfection with miR-188-3p mimics was associated with increased stability of p53 protein. Suppression of p53 activity using the specific p53 inhibitor pifithrin-α alleviated sevoflurane-induced neuroapoptosis. These results indicate that the miR-188-3p-MDM2-p53 axis may have a critical role in sevoflurane-induced cognitive dysfunction. Therefore, miR-188-3p may be a potential target for the treatment of sevoflurane-induced cognitive impairment.
Background: Pressure-regulated capacity control volume controlled (PRVC) ventilation mode is a new type of ventilation mode, which could reduce the occurrence of ventilator-related lung injury. The aim of this study was to explore PRVC mode on airway pressure, oxygenation index, pulmonary inflammatory index and prognosis in patients with one-lung ventilation during pulmonary segmentectomy.Methods: Eighty ASA Ⅱ-Ⅲ Patients with moderate to severe pulmonary dysfunction, ready to receive segmentectomy were randomly divided into VC and PRVC group, which included 40 patients in each group. PRVC ventilation mode was performed for patients in VC-group in the first 5 minutes after OLV, and then ventilation mode was transformed into VC ventilation mode till the end of operation. In PRVC-group, ventilation modes were performed in opposite order. The changes of airway peak pressure, airway platform pressure, pulmonary static compliance, blood gas analysis results and hemodynamics in the two groups under different ventilation modes were recorded. The whole blood samples and bronchoalveolar lavage fluid (BALF) in ventilated lung were collected to determine the level of TNF-α, IL-1β, IL-6 and IL-8 after the surgery. Results: Both static lung compliance and the peak expiratory pressure in PRVC-group were significantly lower than those in VC-group (P=0.023). But there were no difference in hemodynamic parameters such as heart rate, blood pressure. The arterial blood gas analysis (pH, pO2 and pCO2) between the two groups during, as well as postoperative pulmonary complications and length of hospital stay also did not show difference. However, the levels of TNF-α, IL-6, IL-8 and IL-10 in BALF in VC-group were significantly higher than that in PRVC-group (P=0.01). Conclusion: PRVC ventilation mode during intraoperative one-lung ventilation can effectively relieve airway pressure and reduce the secretion of inflammatory factors in the lung, which is a safe and protective ventilation mode for patients with poor preoperative pulmonary function who undergo pulmonary segmentectomy.
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