目的:研究镍铬合金修复体对口腔牙龈组织的影响。方法:本文运用免疫组化染色SP(Streptavidin-peroxidase)法检测COX-2(cyclooxygenase-2)、HSP60(heat shock protein 60)、HSP70(heat shock protein 70)在镍铬合金修复体患者牙龈组织和...目的:研究镍铬合金修复体对口腔牙龈组织的影响。方法:本文运用免疫组化染色SP(Streptavidin-peroxidase)法检测COX-2(cyclooxygenase-2)、HSP60(heat shock protein 60)、HSP70(heat shock protein 70)在镍铬合金修复体患者牙龈组织和正常牙龈组织中的表达情况。经患者同意,从临床采集镍铬合金修复体患者牙龈30例作为实验组,采集口内无任何修复体患者的正常牙龈26例,将实验组中同一患者的牙龈组织分成3份,用免疫组织化学技术分别作COX-2、HSP60、HSP70的检测。每种指标检测30例,对照组同实验组。结果进行统计学分析。结果:HSP60和HSP70在镍铬合金修复体患者牙龈组织中表达明显高于对照组正常牙龈组织(P<0.05)。COX-2在实验组中的表达亦高于对照组(P<0.05)。结论:镍铬合金修复体在口腔中游离出的金属离子对牙龈组织具有致敏性和致炎性,但是否具有致癌性还有待研究。展开更多
Aim： To examine the possible effect of heat treatment on expression of heat shock proteins （Hsps） 105, 70, and 60 in primary monkey Sertoli cells and to evaluate the possible signal pathways. Methods： Western blot...Aim： To examine the possible effect of heat treatment on expression of heat shock proteins （Hsps） 105, 70, and 60 in primary monkey Sertoli cells and to evaluate the possible signal pathways. Methods： Western blot analysis, realtime polymerase chain reaction （PCR）, and confocal immunohistochemistry were used to analyze mRNA and protein levels of the Hsps in response to 43~C treatment of Sertoli cells isolated from pubertal monkey testes. Results： Staining with Hoechst 33342 indicated Sertoli cells did not undergo apoptosis after heat treatment. Hspl05 was expressed in cytoplasm of untreated Sertoli cells. Both Hspl05 mRNA and protein levels were increased approximately 20-fold compared to those of the untreated controls at 12 h after heat treatment. Untreated Sertoli cells did not express Hsp70, but heat stress induced its expression in the cell cytoplasm. The time-course of changes in Hsp70 was similar to that of Hsp105. In contrast to Hsp105 and Hsp70, the change in Hsp60 expression was much less obvious. The protein level between 12 h and 48 h after heat treatment was only approximately 1.5-fold that of the untreated control. Extracellular regulated kinase （ERK） 1/2 inhibitor （U0126） or phosphoinositide kinase-3 （PI3K） inhibitor （LY294002） could partially block the response of Hspl05 and Hsp70 induced by heat treatment. Conclusion： These results indicate that the heat-induced expression of the three types of Hsp in monkey Sertoli cells might be regulated by ERK and/or PI3K signal pathways, but the profile of their expression is different, suggesting that they might have different regulatory functions in Sertoli cells.展开更多
目的:观察电针足三里对应激性胃溃疡大鼠胃黏膜损伤的影响,分析其与热休克蛋白(HSPs)基因表达的关系,探讨电针足三里促进胃黏膜损伤修复的分子生物学机制。方法:将3月龄SD大鼠随机分为正常组、模型组和电针组。采用冷-束缚法制作应激性...目的:观察电针足三里对应激性胃溃疡大鼠胃黏膜损伤的影响,分析其与热休克蛋白(HSPs)基因表达的关系,探讨电针足三里促进胃黏膜损伤修复的分子生物学机制。方法:将3月龄SD大鼠随机分为正常组、模型组和电针组。采用冷-束缚法制作应激性胃溃疡模型。造模后次日起电针组每天电针足三里20min,连续3d;模型组只进行与电针组一样的固定处理;正常组不做任何处理。采用HE染色法观察胃组织病理形态、Guth法检测胃黏膜损伤指数(UI)、逆转录聚合酶链反应(RT-PCR)法检测胃组织HSP60、HSP70 m RNA表达。结果:与正常组比较,模型组大鼠胃黏膜可见明显溃疡灶,UI显著升高(P<0.01),HSP60、HSP70 m RNA表达均降低,其中HSP70 m RNA降低尤为明显(P<0.05);电针组大鼠较模型组大鼠胃组织病理变化有所改善,胃黏膜UI显著降低(P<0.05),HSP60、HSP70 m RNA表达均显著升高(P<0.05,P<0.01)。结论:电针足三里可以上调应激性胃溃疡大鼠胃组织HSP60、HSP70 m RNA表达,促进应激性胃黏膜损伤的修复。胃组织HSP60、HSP70 m RNA的表达增强可能是电针足三里促进胃黏膜损伤修复的分子机制之一。展开更多
Molecular chaperones are a family of proteins that were first noticed to exist about 45 years ago from their increased transcription under heat shock conditions.As a result,the regulation of their encoding genes has b...Molecular chaperones are a family of proteins that were first noticed to exist about 45 years ago from their increased transcription under heat shock conditions.As a result,the regulation of their encoding genes has been subject to extensive studies.Recent studies revealed that the biological activities of molecular chaperones can also be effectively modulated at the protein level.The ways of modulation so far elucidated include allosteric effect,covalent modification,protein-protein interaction,and con-formational alteration induced by such macro-environmental conditions as temperature and pH.These latter aspects were reviewed here.Emphasized here is the importance of such immediate structural alterations that lead to an immediate activity increase,providing the immediate protection needed for the cells to survive the stress conditions.展开更多
文摘目的:研究镍铬合金修复体对口腔牙龈组织的影响。方法:本文运用免疫组化染色SP(Streptavidin-peroxidase)法检测COX-2(cyclooxygenase-2)、HSP60(heat shock protein 60)、HSP70(heat shock protein 70)在镍铬合金修复体患者牙龈组织和正常牙龈组织中的表达情况。经患者同意,从临床采集镍铬合金修复体患者牙龈30例作为实验组,采集口内无任何修复体患者的正常牙龈26例,将实验组中同一患者的牙龈组织分成3份,用免疫组织化学技术分别作COX-2、HSP60、HSP70的检测。每种指标检测30例,对照组同实验组。结果进行统计学分析。结果:HSP60和HSP70在镍铬合金修复体患者牙龈组织中表达明显高于对照组正常牙龈组织(P<0.05)。COX-2在实验组中的表达亦高于对照组(P<0.05)。结论:镍铬合金修复体在口腔中游离出的金属离子对牙龈组织具有致敏性和致炎性,但是否具有致癌性还有待研究。
基金Acknowledgment This study was supported by the ＂973＂ project （No. 2006CB504001）, the Major Research Plan （No. 2006CB944001）, the CAS Innovation Project （KSCA2- YW-R-55）, the National Natural Science Foundation of China （No. 3061800530230190 30600311）, and the Beijing Natural Science Foundation （No. 5073032）.
文摘Aim： To examine the possible effect of heat treatment on expression of heat shock proteins （Hsps） 105, 70, and 60 in primary monkey Sertoli cells and to evaluate the possible signal pathways. Methods： Western blot analysis, realtime polymerase chain reaction （PCR）, and confocal immunohistochemistry were used to analyze mRNA and protein levels of the Hsps in response to 43~C treatment of Sertoli cells isolated from pubertal monkey testes. Results： Staining with Hoechst 33342 indicated Sertoli cells did not undergo apoptosis after heat treatment. Hspl05 was expressed in cytoplasm of untreated Sertoli cells. Both Hspl05 mRNA and protein levels were increased approximately 20-fold compared to those of the untreated controls at 12 h after heat treatment. Untreated Sertoli cells did not express Hsp70, but heat stress induced its expression in the cell cytoplasm. The time-course of changes in Hsp70 was similar to that of Hsp105. In contrast to Hsp105 and Hsp70, the change in Hsp60 expression was much less obvious. The protein level between 12 h and 48 h after heat treatment was only approximately 1.5-fold that of the untreated control. Extracellular regulated kinase （ERK） 1/2 inhibitor （U0126） or phosphoinositide kinase-3 （PI3K） inhibitor （LY294002） could partially block the response of Hspl05 and Hsp70 induced by heat treatment. Conclusion： These results indicate that the heat-induced expression of the three types of Hsp in monkey Sertoli cells might be regulated by ERK and/or PI3K signal pathways, but the profile of their expression is different, suggesting that they might have different regulatory functions in Sertoli cells.
文摘目的:观察电针足三里对应激性胃溃疡大鼠胃黏膜损伤的影响,分析其与热休克蛋白(HSPs)基因表达的关系,探讨电针足三里促进胃黏膜损伤修复的分子生物学机制。方法:将3月龄SD大鼠随机分为正常组、模型组和电针组。采用冷-束缚法制作应激性胃溃疡模型。造模后次日起电针组每天电针足三里20min,连续3d;模型组只进行与电针组一样的固定处理;正常组不做任何处理。采用HE染色法观察胃组织病理形态、Guth法检测胃黏膜损伤指数(UI)、逆转录聚合酶链反应(RT-PCR)法检测胃组织HSP60、HSP70 m RNA表达。结果:与正常组比较,模型组大鼠胃黏膜可见明显溃疡灶,UI显著升高(P<0.01),HSP60、HSP70 m RNA表达均降低,其中HSP70 m RNA降低尤为明显(P<0.05);电针组大鼠较模型组大鼠胃组织病理变化有所改善,胃黏膜UI显著降低(P<0.05),HSP60、HSP70 m RNA表达均显著升高(P<0.05,P<0.01)。结论:电针足三里可以上调应激性胃溃疡大鼠胃组织HSP60、HSP70 m RNA表达,促进应激性胃黏膜损伤的修复。胃组织HSP60、HSP70 m RNA的表达增强可能是电针足三里促进胃黏膜损伤修复的分子机制之一。
基金Supported by National Natural Science Foundation of China(Grant Nos. 30570355 and 30670022)National Key Basic Research Foundation of China (Grant Nos. 2006CB806508 and 2006CB910300)
文摘Molecular chaperones are a family of proteins that were first noticed to exist about 45 years ago from their increased transcription under heat shock conditions.As a result,the regulation of their encoding genes has been subject to extensive studies.Recent studies revealed that the biological activities of molecular chaperones can also be effectively modulated at the protein level.The ways of modulation so far elucidated include allosteric effect,covalent modification,protein-protein interaction,and con-formational alteration induced by such macro-environmental conditions as temperature and pH.These latter aspects were reviewed here.Emphasized here is the importance of such immediate structural alterations that lead to an immediate activity increase,providing the immediate protection needed for the cells to survive the stress conditions.
