目的:探讨SPOCK2基因在高氧肺损伤新生儿支气管肺发育不良(bronchopulmonary dysplasia,BPD)大鼠模型中的表达意义。方法:利用高氧肺损伤诱导BPD动物模型,将新生SD大鼠随机分成空气对照组、高氧模型组。HE染色观察肺组织病理改变,q PCR...目的:探讨SPOCK2基因在高氧肺损伤新生儿支气管肺发育不良(bronchopulmonary dysplasia,BPD)大鼠模型中的表达意义。方法:利用高氧肺损伤诱导BPD动物模型,将新生SD大鼠随机分成空气对照组、高氧模型组。HE染色观察肺组织病理改变,q PCR法检测肺组织中SPOCK2 m RNA的表达水平,免疫组化法测定肺SPOCK2蛋白的表达。同时在体外利用高氧刺激A549人肺上皮细胞,q PCR法检测细胞SPOCK2 m RNA的表达水平。结果:成功构建BPD新生大鼠模型。HE染色显示高氧模型组肺组织均产生类似BPD的病理损伤,并且生后10、14 d高氧模型组大鼠肺组织辐射状肺泡计数(pulmonary radical alveolar counts,RAC)值较空气对照组显著减少,差异有统计学意义(P<0.05)。免疫组化显示空气对照组大鼠肺组织中SPOCK2蛋白表达量高于高氧模型组,生后10、14 d空气对照组肺组织SPOCK2蛋白表达呈阳性。q PCR结果示空气对照组大鼠肺组织中SPOCK2 m RNA表达量随时间递增,于生后18 d时表达量最高,生后24 d时仍处于高值(P<0.05),成年时下降;与空气对照组比较,高氧模型组大鼠肺组织中SPOCK2 m RNA表达量降低,生后10、14 d时两组差异有统计学意义(P<0.05)。高氧模型组A549细胞SPOCK2 m RNA表达量高于空气对照组(P<0.05),且有先上升后下降的趋势。结论:SPOCK2基因可能参与肺发育过程,并可能在高氧刺激时对肺组织起保护作用。展开更多
Matrix metalloproteinases（MMPs） are a family of proteases that are required for many biological processes and are also elevated in many pathological conditions. MMP inhibitors （MMPIs） may therefore be useful as th...Matrix metalloproteinases（MMPs） are a family of proteases that are required for many biological processes and are also elevated in many pathological conditions. MMP inhibitors （MMPIs） may therefore be useful as therapeutic agents in treating a number of diseases including cancer, cardiovascular diseases and arthritis. Attempts have been made to develop MMPIs. Recombinant MMPs have been used to screening MMPs in vitro assays. In this work, we report the expression of MMP-16 in E. coli and the characterization of the recombinant MMP-16 with a commonly used MMP substrate DQ-gelatin.展开更多
Cancer is cell fleeing from death by blocking the intrinsic and extrinsic programs of cell death. The six elements that shut down those programs are: muc-1, muc-4, muc-16, Bcl-2, MMPs and decoy R3. The nuclear factor-...Cancer is cell fleeing from death by blocking the intrinsic and extrinsic programs of cell death. The six elements that shut down those programs are: muc-1, muc-4, muc-16, Bcl-2, MMPs and decoy R3. The nuclear factor-kappa B (NF-Kb) stimulates the expression of genes responsible for the production of those elements, which are used by cells to block those two programs. In other words, the nuclear factor kappa B (NF-KB) is responsible for blocking both programs. Therefore, the nuclear factor kappa B (NF-Kb) is the true cause of cancer.展开更多
文摘目的:探讨SPOCK2基因在高氧肺损伤新生儿支气管肺发育不良(bronchopulmonary dysplasia,BPD)大鼠模型中的表达意义。方法:利用高氧肺损伤诱导BPD动物模型,将新生SD大鼠随机分成空气对照组、高氧模型组。HE染色观察肺组织病理改变,q PCR法检测肺组织中SPOCK2 m RNA的表达水平,免疫组化法测定肺SPOCK2蛋白的表达。同时在体外利用高氧刺激A549人肺上皮细胞,q PCR法检测细胞SPOCK2 m RNA的表达水平。结果:成功构建BPD新生大鼠模型。HE染色显示高氧模型组肺组织均产生类似BPD的病理损伤,并且生后10、14 d高氧模型组大鼠肺组织辐射状肺泡计数(pulmonary radical alveolar counts,RAC)值较空气对照组显著减少,差异有统计学意义(P<0.05)。免疫组化显示空气对照组大鼠肺组织中SPOCK2蛋白表达量高于高氧模型组,生后10、14 d空气对照组肺组织SPOCK2蛋白表达呈阳性。q PCR结果示空气对照组大鼠肺组织中SPOCK2 m RNA表达量随时间递增,于生后18 d时表达量最高,生后24 d时仍处于高值(P<0.05),成年时下降;与空气对照组比较,高氧模型组大鼠肺组织中SPOCK2 m RNA表达量降低,生后10、14 d时两组差异有统计学意义(P<0.05)。高氧模型组A549细胞SPOCK2 m RNA表达量高于空气对照组(P<0.05),且有先上升后下降的趋势。结论:SPOCK2基因可能参与肺发育过程,并可能在高氧刺激时对肺组织起保护作用。
文摘Matrix metalloproteinases（MMPs） are a family of proteases that are required for many biological processes and are also elevated in many pathological conditions. MMP inhibitors （MMPIs） may therefore be useful as therapeutic agents in treating a number of diseases including cancer, cardiovascular diseases and arthritis. Attempts have been made to develop MMPIs. Recombinant MMPs have been used to screening MMPs in vitro assays. In this work, we report the expression of MMP-16 in E. coli and the characterization of the recombinant MMP-16 with a commonly used MMP substrate DQ-gelatin.
文摘Cancer is cell fleeing from death by blocking the intrinsic and extrinsic programs of cell death. The six elements that shut down those programs are: muc-1, muc-4, muc-16, Bcl-2, MMPs and decoy R3. The nuclear factor-kappa B (NF-Kb) stimulates the expression of genes responsible for the production of those elements, which are used by cells to block those two programs. In other words, the nuclear factor kappa B (NF-KB) is responsible for blocking both programs. Therefore, the nuclear factor kappa B (NF-Kb) is the true cause of cancer.
