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目的:探讨脾虚型功能性消化不良(FD)大鼠胃组织PERK蛋白表达及脾虚一号方干预。方法:60只10日龄雄性SD大鼠随机分为正常对照组(10只)、脾虚型FD模型组(50只)。正常组给予2%蔗糖溶液灌胃,脾虚型FD模型组给予0.1%蔗糖碘乙酰胺蔗糖溶液灌胃,每天0.2m L/只,连续6d。脾虚型FD模型组正常饲料喂养至6周龄后叠加改良小平台站立,连续14d。造模结束后随机分为模型组,多潘立酮组,脾虚一号方低、中、高剂量组,每组10只,分别给予蒸馏水1m L·100g-1·d-1,多潘立酮0.3125mg·100g-1·d-1,脾虚一号方0.1275、0.255、0.51g·100g-1·d-1,正常组给予等体积蒸馏水,灌胃14d。采用Western blot和免疫组化方法检测大鼠胃窦组织PERK蛋白表达量。结果:与模型组比较,Western blot方法检测中,脾虚一号方中、高剂量组大鼠胃组织PERK蛋白表达量显著降低(P<0.05);免疫组织化学方法检测中,脾虚一号方中剂量组大鼠胃组织PERK蛋白光密度值降低(P<0.05)。结论:脾虚型FD大鼠存在内质网应激(ERS)现象,脾虚一号方能够减少PERK蛋白的表达,减轻ERS。
Objective: To investigate the PERK protein expression in gastric tissue of spleen deficiency type dyspepsia (FD) rats and intervention of spleen deficiency one. Methods: Sixty male SD rats (10 days old) were randomly divided into normal control group (n = 10) and spleen deficiency model group (n = 50). The normal group was given 2% sucrose solution by gavage. The spleen deficiency model group was given intragastric administration of 0.1% sucrose solution of iodoacetamide and 0.2m L / day for 6 days. Spleen-deficient FD model group fed normal diet until 6 weeks of age, superimposed to improve the small platform to stand for 14 days. After modeling, rats were randomly divided into model group, domperidone group, spleen deficiency one low, medium and high dose group, 10 rats in each group were given distilled water 1m L · 100g-1 · d-1, domperidone 0.3125mg · 100g- 1 · d-1, spleen deficiency one side 0.1275,0.255,0.51g · 100g-1 · d-1, the normal group were given equal volume of distilled water, gavage 14d. The expression of PERK protein in gastric antrum was detected by Western blot and immunohistochemistry. Results: Compared with the model group, the expression of PERK protein in gastric tissue of middle and high dose Spleen deficiency No.1 group was significantly lower than that of the model group (P <0.05) by Western blot. In immunohistochemical method, The optical density of PERK protein in gastric tissue of rats in the dose group decreased (P <0.05). Conclusion: There is endoplasmic reticulum stress (ERS) in spleen deficiency type rats. Spleen No.1 can reduce the expression of PERK protein and reduce ERS.