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目的探讨大麻素受体2在重症急性胰腺炎(SAP)导致的肺损伤中的作用。方法雄性SPF级SD大鼠96只按数字表法随机分成4组。对照组:开腹翻动胰腺组织后关腹;SAP组:4%牛磺胆酸钠建立SAP模型;HU-308组:腹腔注射HU-308 2.5mg/kg,1h后建立SAP模型;AM-630组:腹腔注射AM-630 2.5mg/kg,1h后建立SAP模型。分别在3、6、12h检测各组血清中TNF-α和IL-6水平。取左肺下叶肺组织匀浆后检测髓过氧化物酶水平,右肺下叶组织制作成HE病理切片并进行病理学评分。其余肺组织称重后烘干处理,测量湿干重之比。结果各时间点SAP组、AM-630组、HU-308组中TNF-α、IL-6、MPO、肺组织湿干重比值和病理学评分均高于对照组(P<0.05),HU-308组水平低于SAP组水平(P<0.05)。AM-630组中TNF-α、IL-6、MPO水平均大于SAP组(P<0.05)。AM-630组中肺组织湿干重比值和病理学评分与SAP组比较,在3h无统计学差异(P>0.05),在6、12h大于SAP组水平(P<0.05)。结论激活CB2受体能够抑制SAP导致的肺损伤的形成和发展,抑制CB2受体加重SAP导致的肺损伤。
Objective To investigate the role of cannabinoid receptor 2 in lung injury induced by severe acute pancreatitis (SAP). Methods Ninety-nine male Sprague-Dawley (SD) SD rats were randomly divided into 4 groups according to the digital table method. The rats in the control group were transabdominal with open pancreas. SAP group: 4% sodium taurocholate (SAP) was used to establish SAP model; HU-308 group was injected intraperitoneally with HU-308 2.5 mg / Group: The intraperitoneal injection of AM-630 2.5mg / kg, SAP model after 1h. The levels of TNF-α and IL-6 in each group were detected at 3, 6, 12 h respectively. Myeloperoxidase level was measured in lung tissue of left lower lobe lung tissue and HE pathology in lower lobe of right lung was made and pathological score was taken. The remaining lungs were weighed and dried, and the ratio of wet to dry weight was measured. Results The wet-to-dry weight ratio and pathological score of lung tissue in SAP group, AM-630 group and HU-308 group at each time point were higher than those in control group (P <0.05) 308 group was lower than SAP group (P <0.05). The levels of TNF-α, IL-6 and MPO in AM-630 group were significantly higher than those in SAP group (P <0.05). Compared with the SAP group, the wet-to-dry weight ratio and pathological score of lung tissue in AM-630 group were not significantly different at 3h (P> 0.05), and were higher at 6h and 12h than that of SAP group (P <0.05). Conclusion Activation of CB2 receptor can inhibit the formation and development of lung injury induced by SAP and inhibit the increase of SAP induced lung injury by CB2 receptor.