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Objective To explore effects of dizocilpine (MK-801) preconditioning on excitatory amino acids and inflammatory response in rats induced by cardiac arrest-cardiopulmonary resuscitation (CACPR).Methods 18 male Sprague Dawley (SD) rats were randomly divided into three groups:control group,CA group and CA + MK-801 group.To establish rat models of CA-CPR and keep samples of serum and specimens of brain tissues for following detection.The injury of neurons was observed by HE staining and expression of N-methyl-D-aspartic acid receptor (NMDAR) in brain tissues was detected by Western blot.The concentrations of interleukin 1 beta (IL-1 β) and tumor necrosis factor (TNF)-α in serum were detected by enzyme linked immunosorbent assay (ELISA).Results Neurons in CA group were disorganized,cells shrank,nuclei pyknosis,and cytoplasmic eosinophilia,accompanied by inflammatory cell infiltration.Preconditioning with MK-801 reduced the pathological damage of neuron and degree of macrophage infiltration.The relative expression of NMDAR protein in CA group were significantly higher than that in control group (907.9 ±24.9 vs 321.6 ± 18.4,P ＜0.001).Preconditioning with MK-801 significantly decreased the expression of NMDAR in CA + MK-801 group compared with that in CA group (512.4 ± 21.1 vs 907.9 ± 24.9).The CA group showed significantly increased concentrations of IL-1 β and TNF-α than that in control group (P ＜ 0.001),and this effect was abolished by preconditioning with MK-801.CA rats treated with MK-801 showed higher concentrations of IL-1 β and TNF-α than the control group.Conclusions Cardiac arrest causes pathological injury of neurons,up-regulates expression of NMDAR and aggravates inflammatory response.These results induce the apoptosis of nerve cells.Blocking glutamate receptor with MK-801 can inhibit expression of NMDAR,decrease level of cytokines,down-regulate inflammatory reaction degree therefore to protect the brain.
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Objective To investigate which cells persistantly express interleukin (IL)-1β during the transition of acute neuroinflammaiton to chronic neuroinflammaiton and therefore to provide the evidences of targeted therapy for blocking neuroinflammation.Methods A single does of lipopolysaccharide (LPS) (2 mg/kg,LPS group) or 0.9％ saline (Control group) was intraperitoneally injected in aged rats.Level and gene expression of IL-1β in hippocampual tissue were measured by enzyme-linked immunosorbent assay (ELISA) and real time polymerase chain reaction (RT-PCR),respectively.Cells secreted IL-1β in hippocampus was detected via double fluorescence.Results Glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule-1 (IBA-1) positive cells were significantly increased day 1 (P ＜ 0.05) and latee on,gradually return to base level 30 days after LPS exposure.These changes were consistent with mRNA expressions of IL-1β and astrocytes-derived IL-1β in hippocampus.Neither IL-1β expressed in microglia nor in neurons was observed at any time point following LPS-treated.Conclusions LPS induces prolonged activation of glial cells and sustained expression of astrocytes-derived IL-1β,which may play an important role in the transition of acute neuroinflammation to chronic neuroinflammation.
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Objective To investigate which cells persistantly express interleukin (IL)-1β during the transition of acute neuroinflammaiton to chronic neuroinflammaiton and therefore to provide the evidences of targeted therapy for blocking neuroinflammation.Methods A single does of lipopolysaccharide (LPS) (2 mg/kg,LPS group) or 0.9％ saline (Control group) was intraperitoneally injected in aged rats.Level and gene expression of IL-1β in hippocampual tissue were measured by enzyme-linked immunosorbent assay (ELISA) and real time polymerase chain reaction (RT-PCR),respectively.Cells secreted IL-1β in hippocampus was detected via double fluorescence.Results Glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule-1 (IBA-1) positive cells were significantly increased day 1 (P ＜ 0.05) and latee on,gradually return to base level 30 days after LPS exposure.These changes were consistent with mRNA expressions of IL-1β and astrocytes-derived IL-1β in hippocampus.Neither IL-1β expressed in microglia nor in neurons was observed at any time point following LPS-treated.Conclusions LPS induces prolonged activation of glial cells and sustained expression of astrocytes-derived IL-1β,which may play an important role in the transition of acute neuroinflammation to chronic neuroinflammation.
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ObjectiveTo investigate the effect of immunological and inflammatory reactions on type 2 diabetic macrovascular disease.Methods120 patients with type 2 diabetes mellitus and 60 health controls were enrolled in this study.The patients were divided into two sub - groups,type 2 diabetes mellitus group and type 2 diabetic macrovascular disease group.The markers of immunological and inflammatory reactions were detected,and the main associated factors were collected and analyzed by one -way ANOVA and logistic regression.ResultsThe level of FBG,PPG,HbA1c,Hs-CRP and TNF-αt [ (9.86 ± 1.79)mmol/L,( 14.45 ±5.48) mmol/L,( 11.43 ±3.25) ％,(6.79 ±3.71 )mg/L,( 1.99 ±0.65) ng/ml] in the group of type 2 diabetic macrovascular disease group were higher than type 2 diabetes mellitus group [ (7,25±0.64)mmol/L,(10.45 t2.89) mmol/L,(8.56 ±1.58)％,(4.72 ±2.39) ag/L,(1.24 ±0.44) ng/ml,P ＜ 0.05 ].The risk factors in type 2 diabetic macrovascular disease were TNF-α,Hs-CRP and HbA1 c.ConclusionsImmunological and inflammatory reactions play a key role in type 2 diabetic macrovascular disease.
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Objective To study the Sheng Mai San on the levels of cell factors induced by lipopolysaccharide in acute liver failure rats. Methods The models of chronic liver failure were constructed by injecting CCl4 in the abdomen of rats. The serum levels of lipopolysaccharide and cell factors were determined after treating with LPS and Sheng Mai San for 2 hours. Results The serum level of IL-6［(64.50±18.79)pg/ml vs (4.79±0.57)pg/ml］, ICAM-1［(25100.00±5258.85)pg/ml vs (4215.50±942.79)pg/ml］ and TNF-α［(17.55±2.39)pg/ml vs (10.92±5.02)pg/ml］ was increased by CCl4 (P＜0.05), but there is no effect on the serum level of LPS in rats ［(0.058±0.007)EU/ml vs (0.040±0.002)EU/ml,P＞0.05］. Sheng Mai San can significantly reduce the serum level of IL-6, ICAM-1 and TNF-α in rats with acute liver failure induced by CCl4 ［(17.20±3.12)pg/ml,(9490.00±2725.78)pg/ml,(3.00±1.00)pg/ml,P＜0.05］. After treating with LPS for 2 hours, the serum level of LPS, TNF-α, IL-6, ICAM-1 markedly increased ［(0.501±0.019)EU/ml,(19750.00±9655.17)pg/ml,(5615.00±490.50)pg/ml,(41000.00±589.88)pg/ml,P＜0.01］. Sheng Mai San could reduce the serum levels of LPS, TNF-α, IL-6, ICAM-1 and in rats with chronic liver failure (P＜0.01). Conclusions SD Rats in the state of chronic liver fail-ure, existing serious serum endotoxin, can induce the levels of cell factors by diversification inflammation reaction and. ShengMaiSan can regulating the levels of cell factors in rats with chronic liver failure.