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目的观察附子、白及反药组合对乙酸诱导胃溃疡大鼠的毒效表现,并基于β2肾上腺素能受体(β2-AR)探讨其作用机制。方法大鼠随机分为对照组、模型组、沙丁胺醇组、普萘洛尔组、白及组、附子组和反药组合组。乙酸贴敷法制备胃溃疡模型,ig给药,观察溃疡面积、胃黏膜病理形态变化。利用Elisa试剂盒检测胃组织匀浆炎症相关指标髓过氧化物酶(MPO)、白细胞介素6(IL-6)、环磷酸腺苷(c AMP)水平变化。采用双荧光素酶报告基因技术评价附子、反药组合对β2-AR的激动作用。结果与模型组比较,附子组、反药组合组溃疡严重、自愈不佳,差异有统计学意义(P<0.05);白及组溃疡较轻,愈合明显,差异有极显著意义(P<0.01)。与模型组比较,反药组合组IL-6、MPO、c AMP水平均显著升高(P<0.05、0.01),附子组MPO水平显著升高(P<0.01)。附子具有明显的激动β2-AR作用,与白及联合使用后激动作用进一步增强(P<0.01)。结论附子、白及反药组合加重胃溃疡和炎症反应是其“相反”的主要表现,其机制可能与协同激动β2肾上腺素能受体有关。
Objective To observe the toxic effects of aconite, white and anti-drug combination on acetic-induced gastric ulcer in rats, and to explore the mechanism of action based on β2-adrenergic receptor (β2-AR). Methods The rats were randomly divided into control group, model group, salbutamol group, propranolol group, Baihe group, aconite group and anti-drug combination group. The model of gastric ulcer was prepared by the method of acetic acid sticking, and the administration of ig was performed. The ulcer area and pathological changes of gastric mucosa were observed. Elisa kit was used to detect changes of myeloperoxidase (MPO), interleukin-6 (IL-6) and cAMP in gastric tissue homogenate-related inflammation. Dual luciferase reporter gene assay was used to evaluate the agonistic effect of the combination of aconite and antidote on β2-AR. Results Compared with the model group, the aconite group and the anti-drug combination group had severe ulcer and poor self-healing, the difference was statistically significant (P <0.05). The ulcer of the white group and the group was lighter and the healing was obvious with significant difference (P < 0.01). Compared with the model group, the levels of IL-6, MPO and cAMP in the anti-drug combination group were significantly increased (P <0.05, 0.01), and the MPO level in the aconite group was significantly increased (P <0.01). The aconite had a significant effect of activating β2-AR, which was further enhanced by the combination of white and combination (P <0.01). Conclusion The aconite, white and anti-drug combination aggravate gastric ulcer and inflammatory reaction is its “opposite ” the main manifestation of the mechanism may be associated with co-activation of β2 adrenergic receptors.