Objective To evaluate the regulatory role of acetylcholine receptor in muramyl dipeptide (MDP)-induced activation of Nod-like receptor 2/receptor-interacting protein 2 (2NLR2/RIP2) pathway in macrophages of mice.Methods RAW264.7 cells at the logarithmic growth phase were seeded in 12-well plates (density 1 × 106 cells/ml,2 ml/well),a total of 108 wells.The cells were randomly divided into 3 groups (n =36 each) using a random number table:control group (group C),MDP group (group M),and GTS-21 (a7nAChR specific agonist) group (group G).The cells were routinely cultured in group C.MDP with the final concentration of 10 μg/ml was added to the culture medium in group M.MDP with the final concentration of 10μg/ml and GTS21 with the final concentration of 50 μg/ml were added to the culture medium in group G.The cells were incubated for 24 h.At 1,6 and 24 h of incubation with MDP,12 wells were chosen and the cell suspension was obtained for measurement of NLR2 mRNA expression (by real-time fluorescent quantitative PCR),RIP2 expression (by Western blot),and concentrations of tumor necrosis factor-alpha (TNF-α) and high mobility group box-1 (HMGB1) in the culture media (by ELISA).Results Compared with group C,the levels of NLR2 mRNA,RIP2,TNFα and HMGB1 were significantly increased at each time point in group M (P ＜ 0.05).Compared with group M,the levels of NLR2 mRNA,RIP2,TNF-α and HMGB1 were significantly decreased at each time point in group G (P ＜ 0.05).Conclusion Acetylcholine receptor can suppress MDP-induced transduction of NLR2/RIP2 pathway in macrophages of mice.

Objective To investigate the therapeutic effect of esomeprazole,a new type 0f proton pump inhibitor(PPI),on patients with reflux esophagitis(RE).Methods 80 cases with RE diagnosed by endoscope were randomly divided into treatmeat group(n=40)and control group(n=40).The treatmeat group was treated with esomeprazole 20 mg bid,compared with the control group famotidine 20mg bid.The two courses of treatment both persisted for four weeks and included mosapride 5mg tid.At the end of therapy,the rate of relief of heartburn,acid reflux and substernal burning symptom,and the total effective rate confirmed by endoscope were recorded.ResuIts The clinical symptoms relief rates were 92.5%in the treatment and 62.5%in the control group raspectively and had obviously statistical difference(P＜0.05).The total effective rate was confirmed by endoscope were 82.5%and 55.0%respectively in two groups(P＜0.05).Conclusion Esomeprazole is a type of effective drug for patients with RE.

Objective To investigate the effect of electro-acupuncture at zusanli on Severe thermal injury-induced acute lung injury in rats.Methods Forty male SD rats weighing 200-250 g were used in this study.Thirty percent of the total body surface (TBS) was shaved chemically with 20% sodium sulfate and then exposed to 99-100℃ water for 12 s.The animals with third degree thermal injury involving 30% TBS were randomly divided into 5 groups(n=8 each):group Ⅰ control(group C);groupⅡ thermal injury;group Ⅲ electro-acupuncture at zusanli;group Ⅳ electric stimulation of non-acupoint and group Ⅴ electro-acupuncture at zusanli+α-bungarotoxin α-BGT).In group Ⅲ,Ⅳ,and Ⅴ electro-stimulation(3 v,2 ms,3 Hz) of zusanli or non-acupoint was performed for 12 min immediately after thermal injury model was established and every 8 h.hung specimens were obtained at 48 h after thermal injury for microscopic examination.The pulmonary HMGB-l protein level was measured by ELISA.The expression of HMGB-1 mRNA and protein in the lung was determined by RT-PCR and immuno-histochemistry respectively.Results Thermal injury induced leucocytosis in the interstitial capillaries,interstitial edema,intra-alveolar fibrin deposit,blebbing of type Ⅱ alveolar lining cells and decrease in lamellar body.Both expression of HMGB-1 mRNA and protein in the lung was significantly enhanced at 48 h after thermal injury.Electrical stimulation of zusanli significantly down-regalated the expression of HMGB-1 mRNA and protein in the lung.However,α-BGT pretreatment reversed the effects of electrical stimulation of zusanli.Conclusion Electrical stimulation of zusanli could significantly ameliorate severe thermal injury-induced acute lung injury through inhibition of HMGB-1 mRNA and protein expression and activation of cholinergic anti-inflammatory pathway mediated by nicotinic acetylcholine receptor α7 subunit.