目的:研究链脲佐菌素(streptozocin, STZ)所致Ⅰ型糖尿病大鼠肠系膜淋巴管收缩性情况,以及肠管血流灌注情况。方法:将健康SPF级12周龄成年Wistar大鼠16只,体重为190~220 g,随机分为正常组和Ⅰ型糖尿病组,腹腔注射STZ制备Ⅰ型糖尿病大鼠...目的:研究链脲佐菌素(streptozocin, STZ)所致Ⅰ型糖尿病大鼠肠系膜淋巴管收缩性情况,以及肠管血流灌注情况。方法:将健康SPF级12周龄成年Wistar大鼠16只,体重为190~220 g,随机分为正常组和Ⅰ型糖尿病组,腹腔注射STZ制备Ⅰ型糖尿病大鼠模型。一周后,利用激光散点动态血流监测系统(PeriCam PSI)观察大鼠肠管血流灌注量,利用动态可视化微循环研究系统(Gene&Ⅰ)观察大鼠肠系膜淋巴管收缩性,测量肠组织湿干比用以明确水肿情况。结果:糖尿病组大鼠的肠管血液灌注量相比正常组大鼠的肠管血液灌注量有着明显的提高(243.21±9.19 vs 199.33±10.33,P<0.05),同时其肠组织湿干比也有明显提高(5.10±0.09 vs 4.43±0.08,P<0.05),Ⅰ型糖尿病大鼠肠系膜淋巴管的收缩性无显著性变化(P>0.05),IndexⅠ收缩分数、IndexⅡ总收缩活性指数和L.D-Index肠系膜淋巴管动力学指数无统计学差异。结论:STZ诱导Ⅰ型糖尿病一周后会导致大鼠的肠道发生组织水肿,肠管血液灌注量增加,而对肠系膜淋巴管收缩性影响不大。展开更多
AIM： To study the effect of oxymatrine-baicalin combination （OB） against HBV replication in 2.2.15 cells and α smooth muscle actin （ α SMA） expression, type I, collagen synthesis in HSC-T6 cells. METHODS： The ...AIM： To study the effect of oxymatrine-baicalin combination （OB） against HBV replication in 2.2.15 cells and α smooth muscle actin （ α SMA） expression, type I, collagen synthesis in HSC-T6 cells. METHODS： The 2.2.15 cells and HSC-T6 cells were cultured and treated respectively. HBsAg and HBeAg in the culture supernatants were detected by ELISA and HBV DNA levels were determined by fluorescence quantitative PCR. Total RNA was extracted from HSC-T6 cells and reverse transcribed into cDNA. The cDNAs were amplified by PCR and the quantities were expressed in proportion to β actin. The total cellular proteins extracted from HSC-T6 cells were separated by electrophoresis. Resolved proteins were electrophoretically transferred to nitrocellulose membrane. Protein bands were revealed and the quantities were corrected by β actin. RESULTS： In the 2.2.15 cell culture system, the inhibitory rate against secretion of HBsAg and HBeAg in the OB group was significantly stronger than that in the oxymatrine group （HBsAg, P = 0.043; HBeAg, P = 0.026; respectively）; HBV DNA level in the OB group was significantly lower than that in the oxymatrine group （P = 0.041）. In HSC-T6 cells the mRNA and protein expression levels of α SMA in the OB group were significantly lower as compared with those in the oxymatrine group （mRNA, P = 0.013; protein, P = 0.042; respectively）; The mRNA and protein expression levels of type I collagen in the OB group were significantly lower as compared with those in the oxymatrine group （mRNA, P 〈 0.01; protein, P 〈 0.01; respectively）.CONCLUSION： OB combination has a better effect against HBV replication in 2.2.15 cells and is more effective against α SMA expression and type I collagen synthesis in HSC-T6 cells than oxymatrine in vitro.展开更多
目的:研究NADPH氧化酶4(NOX-4)调控PI3K信号通路在转化生长因子β1(TGF-β1)诱导肺癌细胞表达Ⅰ型胶原蛋白(collagen Ⅰ)的作用及分子机制。方法:体外培养人肺癌A549细胞,予TGF-β1刺激后,观察NOX家族和collagen家族的mRNA和蛋白表达的...目的:研究NADPH氧化酶4(NOX-4)调控PI3K信号通路在转化生长因子β1(TGF-β1)诱导肺癌细胞表达Ⅰ型胶原蛋白(collagen Ⅰ)的作用及分子机制。方法:体外培养人肺癌A549细胞,予TGF-β1刺激后,观察NOX家族和collagen家族的mRNA和蛋白表达的变化,以及PI3K class I催化亚基的表达和PI3K信号通路活化的变化;NOX-4抑制剂二亚苯基碘鎓(DPI)预先处理肺癌细胞,观察TGF-β1刺激后collagen Ⅰ的mRNA和蛋白表达的变化以及PI3K class I催化亚基表达和PI3K信号通路活化。结果:TGF-β1可以诱导肺癌细胞中NOX-4和collagen Ⅰ的mRNA和蛋白表达升高,并诱导PI3K class I催化亚基中PIK3CD表达升高和PI3K信号通路的活化。NOX-4抑制剂DPI可以抑制TGF-β1诱导的collagen Ⅰ表达升高;抑制NOX-4并不影响TGF-β1诱导的PI3K催化亚基PIK3CD表达,但可以降低TGF-β1诱导PI3K信号通路的活化程度。结论:NOX-4经调控PI3K信号通路的活化参与了TGF-β1诱导肺癌细胞表达collagen Ⅰ的分子机制。TGF-β1/NOX-4/PI3K信号通路轴在肺癌细胞collagen Ⅰ的表达中发挥了调控作用。展开更多
目的探讨高剂量维生素D补充剂治疗前、后骨质疏松症患者骨代谢标志物水平变化及意义。方法骨质疏松症患者100例,随机分为对照组和维生素D组各50例,对照组口服钙尔奇D 600mg/d;维生素D组在对照组基础上口服维生素D滴剂,1滴/d;2组均连续治...目的探讨高剂量维生素D补充剂治疗前、后骨质疏松症患者骨代谢标志物水平变化及意义。方法骨质疏松症患者100例,随机分为对照组和维生素D组各50例,对照组口服钙尔奇D 600mg/d;维生素D组在对照组基础上口服维生素D滴剂,1滴/d;2组均连续治疗6个月。分别于治疗前,治疗3、6个月时检测2组L_(2-4)、股骨颈及大转子骨密度(bone mineral density,BMD),采用电化学发光法检测血清Ⅰ型胶原羧基端肽β特殊序列(βisomer of C-terminal telopeptide of typeⅠcollagen,β-CTX)和Ⅰ型前胶原氨基端肽(procollagenⅠN-terminal peptide,PⅠNP)水平,并进行比较。结果维生素D组、对照组治疗前BMD在L_(2-4)[(0.683±0.006)、(0.681±0.007)g/cm^2]、股骨颈[(0.559±0.009)、(0.555±0.021)g/cm^2]、大转子[(0.421±0.011)、(0.418±0.011)g/cm^2]比较差异均无统计学意义(P>0.05);治疗6个月时维生素D组BMD在L_(2-4)、肢骨颈、大转子[(0.784±0.172)、(0.679±0.007)、(0.507±0.091)g/cm^2],对照组BMD在L_(2-4)、肢骨颈、大转子[(0.701±0.080)、(0.611±0.163)、(0.457±0.079)g/cm^2]均高于治疗前,且维生素D组高于对照组(P<0.05);2组治疗3个月时L_(2-4)、股骨颈、大转子BMD与治疗前比较差异均无统计学意义(P>0.05);维生素D组治疗前血清β-CTX[(0.74±0.05)μg/L]、PⅠNP[(42.10±3.50)μg/L]与对照组[(0.76±0.12)、(42.40±3.60)μg/L]比较差异无统计学意义(P>0.05);维生素D组及对照组治疗3个月β-CTX[(0.57±0.11)、(0.63±0.14)μg/L]、PⅠNP[(30.20±6.50)、(36.90±10.30)μg/L],治疗6个月β-CTX[(0.33±0.12)、(0.54±0.11)μg/L]、PⅠNP[(24.50±0.90)、(29.60±2.40)μg/L]均低于治疗前(P<0.05),且维生素D组低于对照组(P<0.05)。结论骨质疏松症患者应用高剂量维生素D补充剂治疗可增加BMD,降低血清PⅠNP、β-CTX水平,有助于延缓骨吸收,减少骨量丢失。展开更多
目的研究天山雪莲愈伤组织提取物(extract from callus of Saussureainvolucrate,ESI)对人成骨肉瘤细胞MG-63增殖及分化的影响,探讨ESI抗骨质疏松的作用及机制。方法以MG-63为研究对象,采用MTT法和乳酸脱氢酶(LDH)法检测ESI对成骨细胞...目的研究天山雪莲愈伤组织提取物(extract from callus of Saussureainvolucrate,ESI)对人成骨肉瘤细胞MG-63增殖及分化的影响,探讨ESI抗骨质疏松的作用及机制。方法以MG-63为研究对象,采用MTT法和乳酸脱氢酶(LDH)法检测ESI对成骨细胞增殖的影响,相关试剂盒检测碱性磷酸酶(ALP)活性和羟脯氨酸(Hyp)水平,茜素红染色法观察对矿化骨结节形成的影响;实时荧光定量PCR(RT-PCR)检测骨保护素(OPG)和核因子-κB活化因子受体配体(RANKL)基因表达水平;Western blotting法检测OPG/RANKL蛋白水平;检测p38特异性抑制剂SB203580对ESI作用于成骨细胞增殖、分化、矿化以及OPG/RANKL表达的影响。结果 ESI低于125μg/mL对成骨细胞无细胞毒性,31.25、62.5μg/mL对成骨细胞生长有促进作用;ESI显著提高ALP活性、Hyp水平以及矿化骨结节形成;显著上调MG-63细胞OPG mR NA水平,下调RANKLmR NA水平,上调OPG/RANKL蛋白水平;SB203580显著抑制ESI对成骨细胞增殖、ALP活性、矿化结节形成的促进作用以及对胶原蛋白积累量和OPG/RANKL值的提高作用。结论 ESI能够促进成骨细胞增殖、分化和矿化,其机制可能与调节OPG和RANKL基因表达有关,并且可能通过p38丝裂原活化蛋白激酶(MAPK)通路进行信号转导。展开更多
文摘目的:研究链脲佐菌素(streptozocin, STZ)所致Ⅰ型糖尿病大鼠肠系膜淋巴管收缩性情况,以及肠管血流灌注情况。方法:将健康SPF级12周龄成年Wistar大鼠16只,体重为190~220 g,随机分为正常组和Ⅰ型糖尿病组,腹腔注射STZ制备Ⅰ型糖尿病大鼠模型。一周后,利用激光散点动态血流监测系统(PeriCam PSI)观察大鼠肠管血流灌注量,利用动态可视化微循环研究系统(Gene&Ⅰ)观察大鼠肠系膜淋巴管收缩性,测量肠组织湿干比用以明确水肿情况。结果:糖尿病组大鼠的肠管血液灌注量相比正常组大鼠的肠管血液灌注量有着明显的提高(243.21±9.19 vs 199.33±10.33,P<0.05),同时其肠组织湿干比也有明显提高(5.10±0.09 vs 4.43±0.08,P<0.05),Ⅰ型糖尿病大鼠肠系膜淋巴管的收缩性无显著性变化(P>0.05),IndexⅠ收缩分数、IndexⅡ总收缩活性指数和L.D-Index肠系膜淋巴管动力学指数无统计学差异。结论:STZ诱导Ⅰ型糖尿病一周后会导致大鼠的肠道发生组织水肿,肠管血液灌注量增加,而对肠系膜淋巴管收缩性影响不大。
文摘AIM： To study the effect of oxymatrine-baicalin combination （OB） against HBV replication in 2.2.15 cells and α smooth muscle actin （ α SMA） expression, type I, collagen synthesis in HSC-T6 cells. METHODS： The 2.2.15 cells and HSC-T6 cells were cultured and treated respectively. HBsAg and HBeAg in the culture supernatants were detected by ELISA and HBV DNA levels were determined by fluorescence quantitative PCR. Total RNA was extracted from HSC-T6 cells and reverse transcribed into cDNA. The cDNAs were amplified by PCR and the quantities were expressed in proportion to β actin. The total cellular proteins extracted from HSC-T6 cells were separated by electrophoresis. Resolved proteins were electrophoretically transferred to nitrocellulose membrane. Protein bands were revealed and the quantities were corrected by β actin. RESULTS： In the 2.2.15 cell culture system, the inhibitory rate against secretion of HBsAg and HBeAg in the OB group was significantly stronger than that in the oxymatrine group （HBsAg, P = 0.043; HBeAg, P = 0.026; respectively）; HBV DNA level in the OB group was significantly lower than that in the oxymatrine group （P = 0.041）. In HSC-T6 cells the mRNA and protein expression levels of α SMA in the OB group were significantly lower as compared with those in the oxymatrine group （mRNA, P = 0.013; protein, P = 0.042; respectively）; The mRNA and protein expression levels of type I collagen in the OB group were significantly lower as compared with those in the oxymatrine group （mRNA, P 〈 0.01; protein, P 〈 0.01; respectively）.CONCLUSION： OB combination has a better effect against HBV replication in 2.2.15 cells and is more effective against α SMA expression and type I collagen synthesis in HSC-T6 cells than oxymatrine in vitro.
文摘目的:研究NADPH氧化酶4(NOX-4)调控PI3K信号通路在转化生长因子β1(TGF-β1)诱导肺癌细胞表达Ⅰ型胶原蛋白(collagen Ⅰ)的作用及分子机制。方法:体外培养人肺癌A549细胞,予TGF-β1刺激后,观察NOX家族和collagen家族的mRNA和蛋白表达的变化,以及PI3K class I催化亚基的表达和PI3K信号通路活化的变化;NOX-4抑制剂二亚苯基碘鎓(DPI)预先处理肺癌细胞,观察TGF-β1刺激后collagen Ⅰ的mRNA和蛋白表达的变化以及PI3K class I催化亚基表达和PI3K信号通路活化。结果:TGF-β1可以诱导肺癌细胞中NOX-4和collagen Ⅰ的mRNA和蛋白表达升高,并诱导PI3K class I催化亚基中PIK3CD表达升高和PI3K信号通路的活化。NOX-4抑制剂DPI可以抑制TGF-β1诱导的collagen Ⅰ表达升高;抑制NOX-4并不影响TGF-β1诱导的PI3K催化亚基PIK3CD表达,但可以降低TGF-β1诱导PI3K信号通路的活化程度。结论:NOX-4经调控PI3K信号通路的活化参与了TGF-β1诱导肺癌细胞表达collagen Ⅰ的分子机制。TGF-β1/NOX-4/PI3K信号通路轴在肺癌细胞collagen Ⅰ的表达中发挥了调控作用。
文摘目的探讨高剂量维生素D补充剂治疗前、后骨质疏松症患者骨代谢标志物水平变化及意义。方法骨质疏松症患者100例,随机分为对照组和维生素D组各50例,对照组口服钙尔奇D 600mg/d;维生素D组在对照组基础上口服维生素D滴剂,1滴/d;2组均连续治疗6个月。分别于治疗前,治疗3、6个月时检测2组L_(2-4)、股骨颈及大转子骨密度(bone mineral density,BMD),采用电化学发光法检测血清Ⅰ型胶原羧基端肽β特殊序列(βisomer of C-terminal telopeptide of typeⅠcollagen,β-CTX)和Ⅰ型前胶原氨基端肽(procollagenⅠN-terminal peptide,PⅠNP)水平,并进行比较。结果维生素D组、对照组治疗前BMD在L_(2-4)[(0.683±0.006)、(0.681±0.007)g/cm^2]、股骨颈[(0.559±0.009)、(0.555±0.021)g/cm^2]、大转子[(0.421±0.011)、(0.418±0.011)g/cm^2]比较差异均无统计学意义(P>0.05);治疗6个月时维生素D组BMD在L_(2-4)、肢骨颈、大转子[(0.784±0.172)、(0.679±0.007)、(0.507±0.091)g/cm^2],对照组BMD在L_(2-4)、肢骨颈、大转子[(0.701±0.080)、(0.611±0.163)、(0.457±0.079)g/cm^2]均高于治疗前,且维生素D组高于对照组(P<0.05);2组治疗3个月时L_(2-4)、股骨颈、大转子BMD与治疗前比较差异均无统计学意义(P>0.05);维生素D组治疗前血清β-CTX[(0.74±0.05)μg/L]、PⅠNP[(42.10±3.50)μg/L]与对照组[(0.76±0.12)、(42.40±3.60)μg/L]比较差异无统计学意义(P>0.05);维生素D组及对照组治疗3个月β-CTX[(0.57±0.11)、(0.63±0.14)μg/L]、PⅠNP[(30.20±6.50)、(36.90±10.30)μg/L],治疗6个月β-CTX[(0.33±0.12)、(0.54±0.11)μg/L]、PⅠNP[(24.50±0.90)、(29.60±2.40)μg/L]均低于治疗前(P<0.05),且维生素D组低于对照组(P<0.05)。结论骨质疏松症患者应用高剂量维生素D补充剂治疗可增加BMD,降低血清PⅠNP、β-CTX水平,有助于延缓骨吸收,减少骨量丢失。
