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目的观察CXC趋化因子受体3(CXCR3)及配体IFN-γ诱导蛋白-10(IP-10)在哮喘小鼠肺组织中的表达,探讨地塞米松(DEX)、卡介苗(BCG)干预对其表达的影响。方法健康雄性昆明小鼠40只,分为哮喘组、DEX组、BCG组和对照组,每组10只。哮喘组分别于实验第1、3、5、7、9、11、13天腹腔注射卵清蛋白(OVA)10μg致敏,第21天起予10g/LOVA5mL雾化吸入30min,1次/d,连续7d,激发哮喘。DEX组在雾化吸入前30min,按2mg/kg腹腔注射DEX溶液。BCG组在致敏前7、3、1d分别皮内注射BCG0.025mg。对照组用9g/L盐水代替OVA。各组小鼠于末次雾化吸入24h后麻醉并处死,取其肺组织置于40g/L多聚甲醛中固定,48h后取出,石蜡包埋、切片、HE染色。免疫组织化学法检测各组小鼠肺组织中CXCR3、IP-10蛋白的表达。结果4组间小鼠肺组织中CXCR3蛋白表达有显著性差异(F=4.602P=0.008),IP-10表达亦有显著性差异(F=4.207P=0.012)。哮喘组小鼠肺组织CXCR3、IP-10蛋白表达较对照组明显增加(Pa=0.002);DEX组CXCR3、IP-10蛋白表达较哮喘组明显降低(P=0.029,0.019);BCG组CXCR3、IP-10蛋白表达较哮喘组降低,但均无统计学意义。结论趋化因子受体CXCR3及配体IP-10参与哮喘发病过程,DEX与BCG可不同程度干预CXCR3、IP-10的表达。
Objective To investigate the expression of CXCR3 and IP-10 in the lung tissue of asthmatic mice and to explore the effects of dexamethasone (DEX), BCG intervention The impact on their expression. Methods Forty healthy male Kunming mice were divided into asthma group, DEX group, BCG group and control group, with 10 mice in each group. Asthma group were sensitized by intraperitoneal injection of 10μg ovalbumin (OVA) on the 1st, 3rd, 5th, 7th, 9th, 11th and 13th day of the experiment respectively, and inhaled 10g / LOVA5mL for 30min, Continuous 7d, stimulate asthma. DEX group 30min before inhalation, according to 2mg / kg intraperitoneal injection of DEX solution. BCG group were intradermal injection of BCG0.025mg 7,3,1 d before sensitization. The control group replaced OVA with 9 g / L saline. The mice in each group were anesthetized and killed 24 hours after the last inhalation. The lung tissues were fixed in 40g / L paraformaldehyde, removed after 48h, embedded in paraffin, sliced and stained with HE. Immunohistochemistry was used to detect the expression of CXCR3 and IP-10 in the lung tissue of each group. Results There was a significant difference in the expression of CXCR3 protein between the 4 groups (F = 4.602 P = 0.008) and IP-10 (F = 4.207 P = 0.012). The expression of CXCR3 and IP-10 protein in lung tissue of asthmatic mice was significantly increased compared with control group (Pa = 0.002); the expression of CXCR3 and IP-10 protein in DEX group was significantly lower than that in asthma group (P = 0.029,0.019); CXCR3, IP-10 protein expression decreased compared with the asthma group, but no statistically significant. Conclusion CXCR3 and IP-10 are involved in the pathogenesis of asthma. DEX and BCG may interfere with the expression of CXCR3 and IP-10 to some extent.