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DCAMKL-1在小鼠结肠急性及慢性黏膜损伤中的表达
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作者 温泉 mahesh mahaseth +2 位作者 周李平 陈欢 张燕 《四川大学学报(医学版)》 CAS CSCD 北大核心 2012年第6期816-820,共5页
目的探讨微管相关蛋白-1(DCAMKL-1)在结肠上皮的表达,同时分析DCAMKL-1阳性细胞在急性结肠黏膜损伤〔葡聚糖硫酸钠(DSS)诱导的结肠炎〕及慢性结肠黏膜损伤(结肠炎相关结直肠癌)中的表达变化。方法取60只健康雌性C57BL/6J小鼠,其中40只用... 目的探讨微管相关蛋白-1(DCAMKL-1)在结肠上皮的表达,同时分析DCAMKL-1阳性细胞在急性结肠黏膜损伤〔葡聚糖硫酸钠(DSS)诱导的结肠炎〕及慢性结肠黏膜损伤(结肠炎相关结直肠癌)中的表达变化。方法取60只健康雌性C57BL/6J小鼠,其中40只用于DSS结肠炎模型实验,20只用于结肠炎相关结直肠癌模型实验。DSS结肠炎模型实验中小鼠分为4组,每组10只,其中3组饮用2.5%DSS溶液7d,再分别自由饮用自来水不同天数后处死,对照组小鼠仅自由饮用自来水,7d后处死;结肠炎相关结直肠癌模型实验中小鼠分为2组,每组10只,其中实验组小鼠腹腔内注射氧化偶氮甲烷(AOM)后给予3个周期DSS溶液和自来水饮用,对照组小鼠腹腔注射等量生理盐水,始终自由饮用自来水,两组小鼠均61d后处死。采用免疫组化观察DCAMKL-1、Musashi-1、增殖细胞核抗原(PCNA)和β-Catenin的表达,Westem blot分别检测2种模型实验中小鼠结肠上皮DCAMKL-1的表达。结果正常小鼠结肠上皮存在DCAMKL-1的表达,多数位于结肠隐窝的基底部。所有DCAMKL-1阳性细胞均表达Musashi-1。在DSS结肠炎模型中,DCAMKL-1阳性细胞在DSS作用7d后明显减少,停用DSS 3d后逐渐恢复正常;DCAMKL-1在结肠炎相关结直肠癌小鼠结肠上皮中表达明显增加,除隐窝底部以外,部分DCAMKL-1阳性细胞位于隐窝的中部,且部分DCAMKL-1阳性细胞胞浆内出现β-Catenin表达。结论DCAMKL-1可能是结肠干细胞的标志物之一。使用DCAMKL-1作为结肠干细胞的标记物,我们能够描述结肠干细胞在急慢性结肠黏膜损伤中的表达变化情况。 展开更多
关键词 微管相关蛋白 干细胞 DSS结肠炎 结肠炎相关结直肠癌
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Hyaluronic acid as a rescue therapy for trinitrobenzene sulfonica cid-induced colitis through Cox-2 and PGE_2 in a Toll-like receptor 4-dependent way
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作者 mahesh mahaseth 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2011年第9期712-719,共8页
We hypothesized whether systemic administration of high-molecular-weight hyaluronic acid(HMW HA) could rescue trinitrobenzene sulfonic acid(TNBS)-induced colitis through Toll-like receptor 4(TLR4) signal.C3H/HeN mice ... We hypothesized whether systemic administration of high-molecular-weight hyaluronic acid(HMW HA) could rescue trinitrobenzene sulfonic acid(TNBS)-induced colitis through Toll-like receptor 4(TLR4) signal.C3H/HeN mice and C3H/HeJ mice were used.Mice were divided into four groups:control,50% ethanol treatment group,TNBS treatment group,and TNBS plus HA treatment group.The weight changes,clinical scores,macroscopic scores,and histological scores were recorded.Cyclooxygenase 2(Cox-2) and prostaglandin E 2(PGE 2) expressions were measured both in colons and peritoneal macrophages from these mice.HA was a rescue therapy for the colitis induced by TNBS only in C3H/HeN mice.The clinical score,macroscopic score,and histological score were much lower in C3H/HeN mice receiving TNBS plus HA treatment.Cox-2 and PGE 2 expressions only increased in C3H/HeN mice.These Cox-2 expressing cells were macrophages.HA can also promote the production of Cox-2 and PGE 2 in peritoneal macrophages from C3H/HeN mice.Our data demonstrated that HMW HA can rescue TNBS-induced colitis through inducing Cox-2 and PGE 2 expressions in a TLR4-dependent way.Macrophages may be the effector cells of HMW HA. 展开更多
关键词 Trinitrobenzene sulfonic acid(TNBS) colitis Therapy Hyaluronic acid Toll-like receptor
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