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Objective To evaluate the role of nuclear factor kappa B (NF-κB) in sevofluraneinduced release of inflammatory factors in mouse microglias.Methods Microglial cells obtained from newborn C57BL/6 mice (aged 2-3 days) were seeded in 24-well plates (density 1 × 105 cells/ml, 1 ml/well) , a total of 80 wells.The cells were randomly divided into 4 groups using a random number table (n =20 each) : control group (group C);sevoflurane group (group S);NF-κB selective inhibitor pyrrolidine dithiocarbamate (PDTC) group (group P);PDTC + sevoflurane group (group P +S).In S and P+S groups, 4.1％ sevoflurane was inhaled for 6 h.In P+S group, 10 μmol/L PDTC was added at 1 h before sevoflurane inhalation.At 6 h of incubation with sevoflurane, NF-κB activity and expression and levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were determined.Results Compared with group C, the NF-κB activity and levels of IL-6 and TNF-α were significantly increased in group S, and no significant change in the above parameters was found in the other two groups.Compared with group S, the NF-κB activity and levels of IL-6 and TNF-α were significantly decreased in group P+S.There was no significant difference in NF-κB expression between the four groups.Conclusion NF-κB mediates sevoflurane-induced release of inflammatory factors in mouse microglias.
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Objective To study the effects of lidocaine on inflammatory mediators and myocardial enzymes in patients undergoing off-pump coronary artery bypass grafting (OPCAB).Methods Twenty patients underging OPCAB were randomly divided into 2 groups of L and C with 10 cases each. After anesthesia induction, group L was given a bolus of lidocaine 2 mg/kg, which was followed by an infusion of lidocaine 2 mg·kg~(-1)·h~(-1) till the end of operation. Group C was given normal saline instead of lidocaine as the control. Blood samples were taken for the measurements of TNF-a, IL-8, SOD, MDA, cTnⅠ, CK-MB and MYO. The hemodynamics, early postoperative clinical informations and ICU and hospital stay were recorded. Results The increases of TNF-α and IL-8 were significiently less in group L than those in group C(P<0.01 or P<0.05). MDA at 24 h after operation was higher in group C than that in group L(P<0.05). The increases of CK-MB and cTnⅠ at 24 h and 48 h after operation were significiently less in group L than those in group C(P<0. 01 or P <0. 05). The ICU and hospital stays were shorter in group L than those in group C(P<0. 05). Conclusion Continuous infusion of lidocaine during OPCAB can decrease the inflammatory mediators and myocardial enzymes and protect the myocardium.
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Objective Role of melanocortin receptor 4 (MCAR) in excitatory amino acid release from rat astrocytes in spinal cord. Methods Astrocytes were isolated from the spinal cord of newborn pathogen-free Wistar rats ( 1-3 days after birth) and cultured in serum-free Neurobasal/B27 liquid culture medium. After 4 passages the primary cultured astrocytes were randomly divided into 3 groups (6 wells each): group Ⅰ control (group C); group Ⅱ the astrocytes were exposed to TNF-α 10 μg/L (group T) and group Ⅲ the astrocytes were exposed to TNF-α 10 μg/L and HS014 (selective MC4R antagonist) 1 μmol/L (group TH). The astrocytes were incubated at 37 ℃ for 3 h. The supernatant was collected for determination of glutamic acid (Glu) and aspartic acid (Asp)concentrations by HPLC-MS/MS. Results TNF-α significantly increased Glu and Asp release from astrocytes in group T as compared with group C. The Glu and Asp concentrations were significantly lower in group TH than in group T. Conclusion MG4R is involved in the excitatory amino acid release from astrocytes in the spinal cord.
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@#Recently studies have shown that ketamine given to patients under mechanical ventilation and background anesthetics without adversely altering cerebral hemodynamics. More studies have also shown ketamine has neuroprotective effects. The main mechanisms may involve changing the expression of apoptosis-regulating proteins, inhibiting the toxicibility of excitatory amino acid and decreasing Ca2+ influx by blockade of NMDA receptors activation. It can also inhibit proinflammatory cytokine production induced by tissue ischemia and affect the protein kinase phosphorylations related to cerebral ischemia, etc..