目的研究IL-32γ可否诱导肝星状细胞LX-2表达Ⅰ型胶原(CollagenⅠ)。方法不同浓度的IL-32γ与LX-2共培养,分别收集培养上清液、提取细胞总RNA,real-time PCR检测CollagenⅠmRNA表达水平,ELISA法检测CollagenⅠ蛋白质表达水平。用不同浓...目的研究IL-32γ可否诱导肝星状细胞LX-2表达Ⅰ型胶原(CollagenⅠ)。方法不同浓度的IL-32γ与LX-2共培养,分别收集培养上清液、提取细胞总RNA,real-time PCR检测CollagenⅠmRNA表达水平,ELISA法检测CollagenⅠ蛋白质表达水平。用不同浓度的人重组磷酸化p38α蛋白(recombinant human active p38α蛋白)与LX-2细胞共培养,48 h后收集细胞培养上清液,ELISA法检测CollagenⅠ蛋白质表达水平。再用不同浓度的p38MAPK抑制剂SB203580加入LX-2细胞与IL-32γ共培养的培养液中,分别收集培养上清液,采用ELISA检测CollagenⅠ蛋白质表达水平,同时提取细胞总RNA采用real-time PCR检测CollagenⅠmRNA表达水平。结果 IL-32γ诱导人LX-2细胞表达CollagenⅠ,且其表达水平随IL-32γ浓度的增加而增强;人重组磷酸化p38α蛋白可诱导LX-2细胞表达CollagenⅠ增高,阻断p38MAPK可降低IL-32γ诱导的CollagenⅠ表达。结论 IL-32γ通过活化p38MAPK通路诱导LX-2细胞表达CollagenⅠ,IL-32γ可能通过诱导肝星状细胞表达CollagenⅠ而参与肝纤维化的形成。展开更多
Objective: To study the role of macrophage inflammatory protein (MIP)-2γ in myocarditis pathogenesis in BALB/c mice. Methods: The relationship between the progression of Coxsarckie virus B3(CVB3) viral myocarditis an...Objective: To study the role of macrophage inflammatory protein (MIP)-2γ in myocarditis pathogenesis in BALB/c mice. Methods: The relationship between the progression of Coxsarckie virus B3(CVB3) viral myocarditis and experimental autoimmune myocarditis and MIP-2γ mRNA expression in mouse was studied by TaqMan real-time fluorescent quantitative RT-PCR. Results: MIP-2γ mRNA expression rose on 3 to 5 d after CVB3 infection, reached peak on 7 d, and returned to normal level until 14 d, which corresponded well with the disease course. The MIP-2γ mRNA expression level rose significantly on the day 18 d after immunization with porcine cardiac myosin, which was consistent with pathological examination. Conclusion: MIP-2γ may be involved in the pathogenesis of myocarditis.展开更多
目的研究srGAP2(Slit-Robo GTPase activating Protein 2)、γ-氨基丁酸以及单核细胞趋化蛋白-1(MCP-1)在难治性癫痫患儿脑组织中的表达情况及意义。方法选取11例患儿的颞叶脑组织和同期11例正常标本的颞叶脑组织,使用免疫组化和免疫印...目的研究srGAP2(Slit-Robo GTPase activating Protein 2)、γ-氨基丁酸以及单核细胞趋化蛋白-1(MCP-1)在难治性癫痫患儿脑组织中的表达情况及意义。方法选取11例患儿的颞叶脑组织和同期11例正常标本的颞叶脑组织,使用免疫组化和免疫印迹等方法检测srGAP2、γ-氨基丁酸以及MCP-1的表达情况。结果难治性癫痫患儿脑组织中,srGAP2的阳性表达率显著高于正常脑组织。难治性癫痫患儿脑组织和正常脑组织可以看到染成棕褐色的神经元,但难治性癫痫患儿脑组织γ-氨基丁酸能神经元表达量明显低于正常脑组织。正常脑组织中MCP-1的表达较弱,而难治性癫痫患儿脑组织中MCP-1的表达较强。结论难治性癫痫患儿脑组织srGAP2和MCP-1表达上升而γ-氨基丁酸表达下降,srGAP2、γ-氨基丁酸及MCP-1与难治性癫痫发病密切相关,可能作为潜在治疗靶标。展开更多
文摘目的研究IL-32γ可否诱导肝星状细胞LX-2表达Ⅰ型胶原(CollagenⅠ)。方法不同浓度的IL-32γ与LX-2共培养,分别收集培养上清液、提取细胞总RNA,real-time PCR检测CollagenⅠmRNA表达水平,ELISA法检测CollagenⅠ蛋白质表达水平。用不同浓度的人重组磷酸化p38α蛋白(recombinant human active p38α蛋白)与LX-2细胞共培养,48 h后收集细胞培养上清液,ELISA法检测CollagenⅠ蛋白质表达水平。再用不同浓度的p38MAPK抑制剂SB203580加入LX-2细胞与IL-32γ共培养的培养液中,分别收集培养上清液,采用ELISA检测CollagenⅠ蛋白质表达水平,同时提取细胞总RNA采用real-time PCR检测CollagenⅠmRNA表达水平。结果 IL-32γ诱导人LX-2细胞表达CollagenⅠ,且其表达水平随IL-32γ浓度的增加而增强;人重组磷酸化p38α蛋白可诱导LX-2细胞表达CollagenⅠ增高,阻断p38MAPK可降低IL-32γ诱导的CollagenⅠ表达。结论 IL-32γ通过活化p38MAPK通路诱导LX-2细胞表达CollagenⅠ,IL-32γ可能通过诱导肝星状细胞表达CollagenⅠ而参与肝纤维化的形成。
文摘Objective: To study the role of macrophage inflammatory protein (MIP)-2γ in myocarditis pathogenesis in BALB/c mice. Methods: The relationship between the progression of Coxsarckie virus B3(CVB3) viral myocarditis and experimental autoimmune myocarditis and MIP-2γ mRNA expression in mouse was studied by TaqMan real-time fluorescent quantitative RT-PCR. Results: MIP-2γ mRNA expression rose on 3 to 5 d after CVB3 infection, reached peak on 7 d, and returned to normal level until 14 d, which corresponded well with the disease course. The MIP-2γ mRNA expression level rose significantly on the day 18 d after immunization with porcine cardiac myosin, which was consistent with pathological examination. Conclusion: MIP-2γ may be involved in the pathogenesis of myocarditis.
文摘目的研究srGAP2(Slit-Robo GTPase activating Protein 2)、γ-氨基丁酸以及单核细胞趋化蛋白-1(MCP-1)在难治性癫痫患儿脑组织中的表达情况及意义。方法选取11例患儿的颞叶脑组织和同期11例正常标本的颞叶脑组织,使用免疫组化和免疫印迹等方法检测srGAP2、γ-氨基丁酸以及MCP-1的表达情况。结果难治性癫痫患儿脑组织中,srGAP2的阳性表达率显著高于正常脑组织。难治性癫痫患儿脑组织和正常脑组织可以看到染成棕褐色的神经元,但难治性癫痫患儿脑组织γ-氨基丁酸能神经元表达量明显低于正常脑组织。正常脑组织中MCP-1的表达较弱,而难治性癫痫患儿脑组织中MCP-1的表达较强。结论难治性癫痫患儿脑组织srGAP2和MCP-1表达上升而γ-氨基丁酸表达下降,srGAP2、γ-氨基丁酸及MCP-1与难治性癫痫发病密切相关,可能作为潜在治疗靶标。
