关键词: beta-conglycinin quantity-dependent nonlinear model sodium cromoglycate suppression transport

Mesh : Globulins / metabolism pharmacology chemistry Seed Storage Proteins / metabolism pharmacology chemistry Antigens, Plant / metabolism Soybean Proteins / metabolism chemistry Animals Cromolyn Sodium / pharmacology Chlorpromazine / pharmacology Endocytosis / drug effects beta-Cyclodextrins / pharmacology chemistry Cell Line Biological Transport / drug effects Glycine max / metabolism chemistry Intestinal Mucosa / metabolism drug effects Swine

来  源:   DOI:10.3390/ijms25126636   PDF(Pubmed)

Abstract:
Understanding the transport mechanism is crucial for developing inhibitors that block allergen absorption and transport and prevent allergic reactions. However, the process of how beta-conglycinin, the primary allergen in soybeans, crosses the intestinal mucosal barrier remains unclear. The present study indicated that the transport of beta-conglycinin hydrolysates by IPEC-J2 monolayers occurred in a time- and quantity-dependent manner. The beta-conglycinin hydrolysates were absorbed into the cytoplasm of IPEC-J2 monolayers, while none were detected in the intercellular spaces. Furthermore, inhibitors such as methyl-beta-cyclodextrin (MβCD) and chlorpromazine (CPZ) significantly suppressed the absorption and transport of beta-conglycinin hydrolysates. Of particular interest, sodium cromoglycate (SCG) exhibited a quantity-dependent nonlinear suppression model on the absorption and transport of beta-conglycinin hydrolysates. In conclusion, beta-conglycinin crossed the IPEC-J2 monolayers through a transcellular pathway, involving both clathrin-mediated and caveolae-dependent endocytosis mechanisms. SCG suppressed the absorption and transport of beta-conglycinin hydrolysates by the IPEC-J2 monolayers by a quantity-dependent nonlinear model via clathrin-mediated and caveolae-dependent endocytosis. These findings provide promising targets for both the prevention and treatment of soybean allergies.
摘要:
了解转运机制对于开发阻止过敏原吸收和转运并防止过敏反应的抑制剂至关重要。然而,β-伴大豆球蛋白的过程,大豆中的主要过敏原,穿过肠粘膜屏障仍不清楚。本研究表明,IPEC-J2单层对β-伴大豆球蛋白水解产物的转运以时间和数量依赖性的方式发生。β-伴大豆球蛋白水解产物被吸收到IPEC-J2单层的细胞质中,而在细胞间隙中没有检测到。此外,甲基-β-环糊精(MβCD)和氯丙嗪(CPZ)等抑制剂可显着抑制β-伴大豆球蛋白水解产物的吸收和转运。特别感兴趣的是,色甘酸钠(SCG)对β-伴大豆球蛋白水解产物的吸收和转运表现出数量依赖性非线性抑制模型。总之,β-伴大豆球蛋白通过跨细胞途径穿过IPEC-J2单层,涉及网格蛋白介导的和caveolae依赖性的内吞机制。SCG通过网格蛋白介导的和Caveolae依赖性内吞作用,通过数量依赖性非线性模型抑制IPEC-J2单层对β-伴大豆球蛋白水解产物的吸收和转运。这些发现为大豆过敏的预防和治疗提供了有希望的目标。
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