Deletion of HAX1 in mice causes a severe reduction in the numbers of lymphocytes in the bone marrow and in the spleen. Additionally, B220＋ B progenitor cells in the bone marrow are reduced, suggesting an important fu...Deletion of HAX1 in mice causes a severe reduction in the numbers of lymphocytes in the bone marrow and in the spleen. Additionally, B220＋ B progenitor cells in the bone marrow are reduced, suggesting an important function of HAX1 in B cell development. HAX1 is thought to play a protective role in apoptotic processes; therefore, we investigated the role of HAX1 in bone marrow B progenitor cells and splenic B cells. We did not observe an effect on the survival of Hax1-/- bone marrow cells but detected enhanced survival of splenic Hax1-/- B cells upon in vitro starvation/ growth-factor withdrawal. To explain this apparent inconsistency with previous reports of HAX1 function, we also studied the B cell receptor （BCR）-induced apoptosis of IgM-stimulated splenic naive B cells and found that apoptosis decreased in these cells. We further found impaired internalization of the BCR from Hax1-/- splenic B cells after IgM crosslinking; this impaired internalization may result in decreased BCR signaling and, consequently, decreased BCR-mediated apoptosis. We measured HAX1 binding to the cytoplasmic domains of different Ig subtypes and identified KVKWI（V）F as the putative binding motif for HAX1 within the cytoplasmic domains. Because this motif can be found in almost all Ig subtypes, it is likely that HAX1 plays a general role in BCR-mediated internalization events and BCR-mediated apoptosis.展开更多
目的探讨脑缺血再灌注损伤（I／R）大鼠丹红注射液干预后胶质原纤维酸性蛋白（GFAP）的表达变化。方法96只SD大鼠随机分为：正常对照8只（N组），不做任何处理；假手术组8只（S组），仅分离出血管，不做其他处理；缺血再灌注损伤组40只...目的探讨脑缺血再灌注损伤（I／R）大鼠丹红注射液干预后胶质原纤维酸性蛋白（GFAP）的表达变化。方法96只SD大鼠随机分为：正常对照8只（N组），不做任何处理；假手术组8只（S组），仅分离出血管，不做其他处理；缺血再灌注损伤组40只（I／R组），丹红注射液干预组40只（DI／R组），两组均采用大脑中动脉闭塞方法制作大鼠脑缺血再灌注模型。模型成功后，DI／R组从实验前一天开始腹腔注射丹红注射液（8 mL／kg ，Qd）；I／R组在相同时间点注射生理盐水。并于再灌注后6h、24h、48h、72h、7d的各时间点分批处死动物，免疫组织化学方法检测各组大鼠脑内GFAP的表达情况；各组大鼠在处死前行神经功能缺损评分。结果 N组和S组神经细胞中GFAP阳性细胞较少；I／R组缺血再灌注6 h GFAP的表达开始增加，72 h GFAP表达增加达到高峰，缺血再灌注7 d表达减少，DI／R组GFAP表达趋势同缺血再灌注组，但各时间点阳性细胞数明显低于I／R组（ P ＜0．05）；除6 h外的其余各时间点，DI／R组大鼠神经功能缺损均小于I／R组（ P ＜0．05），且DI／R组缺血再灌注时间越长，神经功能缺损程度越轻（ P＜0．05）。结论大鼠脑缺血再灌注损伤后，GFAP的表达上调，但丹红注射液下调GFAP的表达，抑制星形胶质细胞过度增生，减轻脑缺血后损伤。展开更多
文摘Deletion of HAX1 in mice causes a severe reduction in the numbers of lymphocytes in the bone marrow and in the spleen. Additionally, B220＋ B progenitor cells in the bone marrow are reduced, suggesting an important function of HAX1 in B cell development. HAX1 is thought to play a protective role in apoptotic processes; therefore, we investigated the role of HAX1 in bone marrow B progenitor cells and splenic B cells. We did not observe an effect on the survival of Hax1-/- bone marrow cells but detected enhanced survival of splenic Hax1-/- B cells upon in vitro starvation/ growth-factor withdrawal. To explain this apparent inconsistency with previous reports of HAX1 function, we also studied the B cell receptor （BCR）-induced apoptosis of IgM-stimulated splenic naive B cells and found that apoptosis decreased in these cells. We further found impaired internalization of the BCR from Hax1-/- splenic B cells after IgM crosslinking; this impaired internalization may result in decreased BCR signaling and, consequently, decreased BCR-mediated apoptosis. We measured HAX1 binding to the cytoplasmic domains of different Ig subtypes and identified KVKWI（V）F as the putative binding motif for HAX1 within the cytoplasmic domains. Because this motif can be found in almost all Ig subtypes, it is likely that HAX1 plays a general role in BCR-mediated internalization events and BCR-mediated apoptosis.
文摘目的探讨脑缺血再灌注损伤（I／R）大鼠丹红注射液干预后胶质原纤维酸性蛋白（GFAP）的表达变化。方法96只SD大鼠随机分为：正常对照8只（N组），不做任何处理；假手术组8只（S组），仅分离出血管，不做其他处理；缺血再灌注损伤组40只（I／R组），丹红注射液干预组40只（DI／R组），两组均采用大脑中动脉闭塞方法制作大鼠脑缺血再灌注模型。模型成功后，DI／R组从实验前一天开始腹腔注射丹红注射液（8 mL／kg ，Qd）；I／R组在相同时间点注射生理盐水。并于再灌注后6h、24h、48h、72h、7d的各时间点分批处死动物，免疫组织化学方法检测各组大鼠脑内GFAP的表达情况；各组大鼠在处死前行神经功能缺损评分。结果 N组和S组神经细胞中GFAP阳性细胞较少；I／R组缺血再灌注6 h GFAP的表达开始增加，72 h GFAP表达增加达到高峰，缺血再灌注7 d表达减少，DI／R组GFAP表达趋势同缺血再灌注组，但各时间点阳性细胞数明显低于I／R组（ P ＜0．05）；除6 h外的其余各时间点，DI／R组大鼠神经功能缺损均小于I／R组（ P ＜0．05），且DI／R组缺血再灌注时间越长，神经功能缺损程度越轻（ P＜0．05）。结论大鼠脑缺血再灌注损伤后，GFAP的表达上调，但丹红注射液下调GFAP的表达，抑制星形胶质细胞过度增生，减轻脑缺血后损伤。
文摘目的:探讨竹荪多糖对砷中毒大鼠肝损伤的影响。方法:将24只清洁级健康SD大鼠均分为对照组、模型组、竹荪干预组3组,每组雌雄各半;对照组以常规饲料饲养,竹荪干预组和模型组喂饲砷含量50 mg/kg的饲料,竹荪干预组每日以10 g/L的竹荪多糖20 m L/kg灌胃,各组大鼠喂养3个月时取血检测血清谷草转氨酶(AST)及谷丙转氨酶(ALT)活力、总蛋白(TP)及白蛋白(ALB)水平、白蛋白与球蛋白比值(A/G)、粘连蛋白(LN)、透明质酸酶(HA)、Ⅲ型前胶原(PCⅢ)以及Ⅳ型胶原(PCIV)的水平;取大鼠同一肝小叶行HE及Masson染色,观察肝组织病理学改变,并计算肝纤维化增生面积。结果:与对照组相比,竹荪干预组和模型组大鼠血清内AST的活力均升高,ALB水平降低,LN、HA、PCIV水平增高,差异有统计学意义(P<0.05);与模型组相比,竹荪干预组大鼠血清内AST和ALT的活力均降低,TP、A/G、ALB水平升高,LN、PCIV水平降低,差异有统计学意义(P<0.05);HE和Masson染色结果显示,竹荪干预组和模型组均出现不同程度的肝损伤;通过图像分析系统测量,对照组、竹荪干预组、模型组大鼠肝脏增生纤维面积呈增加趋势,竹荪干预组和模型组与对照组相比胶原纤维沉积面积差异均有统计学意义(P<0.05)。结论:竹荪多糖对砷中毒大鼠肝脏有一定的保护作用。
