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1.
Chinese Journal of Primary Medicine and Pharmacy ; (12): 1572-1574,1575, 2016.
Article in Chinese | WPRIM | ID: wpr-603979

ABSTRACT

Objective To explore the clinical efficacy of methylprednisolone injection and magnesium sulfate injection in the treatment of severe bronchial asthma and the impact on inflammatory cytokines.Methods 87 cases of severe bronchial asthma were selected for the study,and they were divided into two groups according to the order of admission,the control group (43 cases ) was given methylprednisolone treatment,while the observation group (44 cases)was given methylprednisolone injection and magnesium sulfate treatment.The clinical treatment and inflammatory cytokine levels before and after treatment were compared between the two groups.Results The effective rate of the observation group was 93.18%,which was higher than 74.42% of the control group,the difference was significant(χ2 =10.33,P <0.05 ).After treatment,pulmonary functions of the observation group [FVC (3.72 ± 0.42)L,FEV1 (2.72 ±0.32)L and PEF(3.48 ±0.49)L/s]were increased significantly than before treatment(t =7.87,7.81,8.41,all P <0.05),and had significant differences compared with the control group(t =6.93,7.44, 7.20,all P <0.05).After treatment,inflammatory cytokines indicators of the observation group[IL -6 (67.44 ± 0.43)μg/L,TNF -α(80.32 ±7.34)ng/L,hs -CRP(3.32 ±0.89)mg/L]were significantly increased than before treatment(t =6.85,7.41,7.33,all P <0.05),compared with the control group,the differences were significant(t =6.55,7.04,6.45,all P <0.05).Conclusion The methylprednisolone combination with magnesium sulfate in treat-ment of severe bronchial asthma had significant effect,and it can effectively improve the airway inflammation,promote lung function in patients'recovery,and it has great clinical value.

2.
Journal of Peking University(Health Sciences) ; (6): 777-782, 2016.
Article in Chinese | WPRIM | ID: wpr-502950

ABSTRACT

Objective:To investigate the anti-inflammation effects by activation of the cholinergic anti-inflammatory pathway and its mechanisms in non-alcoholic steatohepatitis (NASH)model mice.Me-thods:6-week-old male C57BL/6J (B6)mice were randomly divided into four groups:the first group was normal mice,injected with saline;the second group was normal mice,injected with nicotine;the third group was NASH model mice,injected with saline;the fourth group was NASH model mice,injec-ted with nicotine.The experimental mice were fed with either standard chow (SC)or high-fat and high-fructose (HFHF)for 17 weeks to generate an NASH model mice.The mice received injection once daily for 3 weeks [nicotine dose,400 μg/kg].Then,their pathological characteristics and function of the liver were assessed.The expressions of interleukin-6 (IL-6)and tumor necrosis factor-α(TNF-α)in se-rum were analyzed by enzyme linked immunosorbent assay (ELISA).The expressions of alpha 7 nicotinic acetylcholine receptors (α7nAChR),Toll-like receptors-4 (TLR-4)and nuclear factor κB of phosphory-lation (p-NF-κB)in Kupffer cells were determined by Western blot and immunofluorescence assays.Re-sults:We successfully generated NASH model mice by imitating the high-fat and high-fructose dietary style of NASH patients.The results of our investigation demonstrated that nicotine could reduce signifi-cantly the levels of IL-6,and TNF-αin serum (P <0.05).The expression of p-NF-κB protein in the group which was NASH model mice injected with nicotine declined significantly as compared with the group which was NASH model mice injected with saline (P <0.05).And the expression of α7nAChR protein elevated significantly conversely (P <0.05 ).Conclusion:Activation of the cholinergic anti-inflammatory pathway could inhibit the release of inflammatory factors as TNF-αand IL-6 in NASH model mice,and the mechanism for the inhibition of inflammatory was mediated by NF-κB pathway.

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