CAJ | 학술논문

探讨不同维生素对P. y17XL感染BALB/c小鼠的免疫调节作用。将6~8周龄,雌性BALB/c小鼠,随机分为维生素( V)处理组和对照组。 V处理组小鼠分别经50 mg/kg VA、600 mg/kg VE 或1 g/只VC连续10 d灌胃,0.2 mL/只；对照组小鼠分别给予相同剂量的溶剂(大豆油或生理盐水)处理。之后,各组小鼠分别经腹腔接种1×106 P. y17XL寄生的红细胞,动态观察感染小鼠原虫血症水平和生存率；流式细胞术检测感染后第0、3和5天小鼠脾细胞树突状细胞( DCs)亚群( pDCs与mDCs)百分比及功能分子( TLR9和MHC域)的表达。与对照组相比,VA和VE处理组小鼠原虫血症水平升高,生存率降低；感染后第5天脾细胞中pDCs与mDCs亚群水平以及DCs表面受体TLR9和表面分子MHC域的表达水平显著下降。相反,VC处理组小鼠原虫血症水平降低,生存率延长,pDCs与mDCs亚群以及TLR9和MHC域的表达水平显著升高。结果表明,不同维生素对疟疾感染产生不同的调控作用,VA和VE通过抑制DCs数量和功能,加重疟疾感染,而VC则促进DCs数量和功能,推迟感染进程。
탐토불동유생소대P. y17XL감염BALB/c소서적면역조절작용。장6~8주령,자성BALB/c소서,수궤분위유생소( V)처리조화대조조。 V처리조소서분별경50 mg/kg VA、600 mg/kg VE 혹1 g/지VC련속10 d관위,0.2 mL/지；대조조소서분별급여상동제량적용제(대두유혹생리염수)처리。지후,각조소서분별경복강접충1×106 P. y17XL기생적홍세포,동태관찰감염소서원충혈증수평화생존솔；류식세포술검측감염후제0、3화5천소서비세포수돌상세포( DCs)아군( pDCs여mDCs)백분비급공능분자( TLR9화MHC역)적표체。여대조조상비,VA화VE처리조소서원충혈증수평승고,생존솔강저；감염후제5천비세포중pDCs여mDCs아군수평이급DCs표면수체TLR9화표면분자MHC역적표체수평현저하강。상반,VC처리조소서원충혈증수평강저,생존솔연장,pDCs여mDCs아군이급TLR9화MHC역적표체수평현저승고。결과표명,불동유생소대학질감염산생불동적조공작용,VA화VE통과억제DCs수량화공능,가중학질감염,이VC칙촉진DCs수량화공능,추지감염진정。
Immuno-regulation of different vitamins on BALB/c mouse malaria infected by P. y17XL was investigated. Female BALB/c mice at the ages of 6~8 weeks were randomly divided into vitamin ( V) treated groups and the con-trol groups. V treated groups were administered by oral gavage with 50 mg/kg VA, 600 mg/kg VE or 1 g/VC in 0.2 mL per mouse, respectively, for 10 d successively;the control groups were given the same dose of solvent ( soybean oil or saline). Then each group of mice was intraperitoneally inoculated with 1 í106 P. y l7XL parasitized erythro-cytes. Parasitemia levels and survival rate were dynamically observed. Flow cytometry was performed to detect the per-centage of dendritic cells subsets ( pDCs and mDCs) expression of functional molecules ( TLR9 and MHCII) at 0 d, 3 d and 5 d after the infection. The results showed that as compared with the control groups, the parasitemia levels in VA and VE treated mice was elevated, and the survival rate dampened. Splenic pDCs and mDCs were also significant-ly decreased companied with lower level of TLR9 and MHCIImolecules at 5 d after infection. In contrast, VC trea-ted mice showed reduced levels of parasitemia, with survival rate extended, and the expression of pDCs and mDCs subgroup as well as the expression levels of TLR9 and MHCIIwere significantly elevated. Therefore, it could be con-cluded that different vitamins have different regulation on malaria infection. VA and VE could promote plasmodium in-fection by inhibition of the numbers and functions of DCs and worsen the malaria infection, whereas VC could delay the infection process by promote the numbers and functions of DCs.