目的探讨中国西南地区汉族人群中PRDM16、TRPM8、TSPAN2及MMP16等基因多态性与无先兆偏头痛遗传易感性关系。方法共收集512例无先兆偏头痛和535例健康正常对照,运用病例-对照分析,荟萃分析目前国内外报道的全基因组关联分析(genome-wide...目的探讨中国西南地区汉族人群中PRDM16、TRPM8、TSPAN2及MMP16等基因多态性与无先兆偏头痛遗传易感性关系。方法共收集512例无先兆偏头痛和535例健康正常对照,运用病例-对照分析,荟萃分析目前国内外报道的全基因组关联分析(genome-wide association studies,GWAS),单碱基延伸法(SNa Pshot)进行多个基因11个SNP位点的基因分型。结果 rs2651899(PRDM16),rs10166942(TRPM8),rs12134493(TSPAN2)和rs10504861(MMP16)与无先兆偏头痛发病具相关性。结论本研究重复了以前GWAS结果,PRDM16,TRPM8,TSPAN2,MMP16基因的SNP位点与无先兆偏头痛发病相关。展开更多
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
Crocus sativus and its bioactive constituent crocin are well known for anti-tumor potential in different models.However, the efficacy of crocin on in-vivo melanoma metastasis is not yet reported. In this study, melano...Crocus sativus and its bioactive constituent crocin are well known for anti-tumor potential in different models.However, the efficacy of crocin on in-vivo melanoma metastasis is not yet reported. In this study, melanoma metastatic model was developed by tail vein injection of B16 F-10 cells in to C57 BL/6 mice. Metastatic mice treated with two different doses of crocin（250 and 500 μg/kg of bodyweight） for 10 days and parameters such as lung metastasis inhibition, mean survival time, lung hydroxyproline, uronic acid and hexosamine levels were analyzed after 21 days of treatment. Then blood was collected and serum gamma glutamyl transpeptidase（γ-GGT）, sialic acid,tumor necrosis factor alpha（TNF-a）, interleukin 10（IL-10）, IL-6, IL-2, and TIMP-1 levels were measured. Further, a lung histological examination was done in crocin treated metastatic mice. Subsequently hallmark metastatic parameters such as matrix metalloproteinases（MMPs）, extracellular regulated kinase 2（ERK2）, vascular endothelial growth factor（VEGF）, and K-ras gene expression were investigated in the lungs of crocin treated metastatic mice.Further, in-vitro adhesion, invasion and migration of B16 F-10 cells were examined after 24 hours of crocin（5 and 10μg/mL） treatment. Administration of crocin to tumor bearing C57 BL/6 mice reduced the lung metastasis by 85%.Elevated levels of hydroxyproline, uronic acid, hexosamine, serum sialic acid and y-GGT in metastatic control were found to be significantly reduced in crocin treated mice. Crocin also inhibited expression of MMP-2, MMP-9, ERK-2,K-ras, and VEGF. Crocin reduced the ability of B16 F-10 cells invasion（P〈0.05）, migration（P〈0.05） and adhesion by upregulating E-cadherin expression. In conclusion, crocin elicited marked anti-metastatic potential by regulating the metastasis induced biomarkers.展开更多
文摘目的探讨中国西南地区汉族人群中PRDM16、TRPM8、TSPAN2及MMP16等基因多态性与无先兆偏头痛遗传易感性关系。方法共收集512例无先兆偏头痛和535例健康正常对照,运用病例-对照分析,荟萃分析目前国内外报道的全基因组关联分析(genome-wide association studies,GWAS),单碱基延伸法(SNa Pshot)进行多个基因11个SNP位点的基因分型。结果 rs2651899(PRDM16),rs10166942(TRPM8),rs12134493(TSPAN2)和rs10504861(MMP16)与无先兆偏头痛发病具相关性。结论本研究重复了以前GWAS结果,PRDM16,TRPM8,TSPAN2,MMP16基因的SNP位点与无先兆偏头痛发病相关。
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Crocus sativus and its bioactive constituent crocin are well known for anti-tumor potential in different models.However, the efficacy of crocin on in-vivo melanoma metastasis is not yet reported. In this study, melanoma metastatic model was developed by tail vein injection of B16 F-10 cells in to C57 BL/6 mice. Metastatic mice treated with two different doses of crocin（250 and 500 μg/kg of bodyweight） for 10 days and parameters such as lung metastasis inhibition, mean survival time, lung hydroxyproline, uronic acid and hexosamine levels were analyzed after 21 days of treatment. Then blood was collected and serum gamma glutamyl transpeptidase（γ-GGT）, sialic acid,tumor necrosis factor alpha（TNF-a）, interleukin 10（IL-10）, IL-6, IL-2, and TIMP-1 levels were measured. Further, a lung histological examination was done in crocin treated metastatic mice. Subsequently hallmark metastatic parameters such as matrix metalloproteinases（MMPs）, extracellular regulated kinase 2（ERK2）, vascular endothelial growth factor（VEGF）, and K-ras gene expression were investigated in the lungs of crocin treated metastatic mice.Further, in-vitro adhesion, invasion and migration of B16 F-10 cells were examined after 24 hours of crocin（5 and 10μg/mL） treatment. Administration of crocin to tumor bearing C57 BL/6 mice reduced the lung metastasis by 85%.Elevated levels of hydroxyproline, uronic acid, hexosamine, serum sialic acid and y-GGT in metastatic control were found to be significantly reduced in crocin treated mice. Crocin also inhibited expression of MMP-2, MMP-9, ERK-2,K-ras, and VEGF. Crocin reduced the ability of B16 F-10 cells invasion（P〈0.05）, migration（P〈0.05） and adhesion by upregulating E-cadherin expression. In conclusion, crocin elicited marked anti-metastatic potential by regulating the metastasis induced biomarkers.
