Pathological pain or clinical pain is caused by tissue and nerve injuries,and is usually chronic and mainly divided into inflammatory pain and neuropathic pain. Pathological pain is typically characterized by hyperalg...Pathological pain or clinical pain is caused by tissue and nerve injuries,and is usually chronic and mainly divided into inflammatory pain and neuropathic pain. Pathological pain is typically characterized by hyperalgesia (increased responsiveness to noxious stimuli) and allodynia (painful responses to normally innocuous stimuli). The mitogen-activated proteins kinases (MAPKs) are a family of evolutionally conserved molecules that play a critical role in cell signaling,consisting of extracellular signal regulated kinase (ERK),p38,and c-Jun N-terminal kinase (JNK),which play an important role in neural plasticity of pathological pain. Inhibition of MAPKs alleviates inflammatory pain and neuropathic pain in different animal models. It is very important to study the inhibition of MAPKs as a therapeutic approach to treat pathological pain.展开更多
Mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal kinases (JNKs) and p38 MAPK, play an important role in transducting environmental stimuli to the t...Mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal kinases (JNKs) and p38 MAPK, play an important role in transducting environmental stimuli to the transcriptional machinery in the nucleus in mammalian cells by virtue of their ability to phosphorylate and regulate the activity of various transcription factors. It was recently found that the changes in activity of MAPKs occurred during ischemia/reperfusion, but the biological significance of the changes was still controversial.展开更多
Myocardial hypertrophy is an independent risk factor for cardiac events. Mitogen-activated protein kinases (MAPK), including extracellular signal-regulated kinases, C-jun N-terminal kinases and P38-MAPK, are the commo...Myocardial hypertrophy is an independent risk factor for cardiac events. Mitogen-activated protein kinases (MAPK), including extracellular signal-regulated kinases, C-jun N-terminal kinases and P38-MAPK, are the common intracellular pathway of transducing hypertrophic signs. All three MAPK subfamilies play an important role in development of myocardial hypertrophy.展开更多
目的:研究在支气管哮喘豚鼠肺组织中丝裂原活化蛋白激酶(MAPK)信号通路对γ-谷氨酰半胱氨酸合酶(γ-GCS)的影响。方法:成年雄性豚鼠20只随机分成哮喘组和对照组,每组10只,以腹腔内注射联合雾化吸入卵蛋白复制哮喘模型。测支气管肺泡灌洗...目的:研究在支气管哮喘豚鼠肺组织中丝裂原活化蛋白激酶(MAPK)信号通路对γ-谷氨酰半胱氨酸合酶(γ-GCS)的影响。方法:成年雄性豚鼠20只随机分成哮喘组和对照组,每组10只,以腹腔内注射联合雾化吸入卵蛋白复制哮喘模型。测支气管肺泡灌洗液(BALF)细胞总数并进行分类计数;原位杂交和RT-PCR测肺组织中γ-GCS-h mRNA表达;免疫组化测γ-GCS、磷酸化细胞外激活蛋白激酶(p-ERK)、磷酸化c-Jun氨基末端激酶(p-JNK)和磷酸化p38(p-p38)在肺组织中的表达;W estern b lotting测p-ERK、p-JNK和p-p38在肺组织中的表达;双酶法测γ-GCS的活性。结果:(1)哮喘组BALF中细胞总数、嗜酸性粒细胞明显多于对照组(P<0.01)。(2)免疫组化显示肺组织中p-ERK、p-p38、p-JNK和γ-GCS蛋白质表达哮喘组明显高于对照组(P<0.01);W estern b lotting亦显示肺组织中p-ERK、p-JNK和p-p38蛋白质表达哮喘组均明显高于对照组。(3)原位杂交和RT-PCR显示在肺组织中γ-GCS-h mRNA表达哮喘组明显高于对照组(P<0.01)。(4)γ-GCS活性哮喘组明显高于对照组(P<0.01)。(5)直线相关性分析显示:在肺组织中p-ERK、p-p38与γ-GCS-hmRNA、γ-GCS蛋白质呈显著正相关,p-JNK与γ-GCS-h mRNA、γ-GCS蛋白质无明显相关性。结论:支气管哮喘豚鼠肺中p-ERK、p-p38、p-JNK和γ-GCS表达均增加;p-ERK和p-p38可能上调γ-GCS表达。展开更多
基金Natural Science Foundation of Hebei Province (302494)Natural Science Foundation of Hebei Province ( C200500720 )Special Foundation for Doctor Education in University from Ministry of Education of China (20050089001)~~
文摘Pathological pain or clinical pain is caused by tissue and nerve injuries,and is usually chronic and mainly divided into inflammatory pain and neuropathic pain. Pathological pain is typically characterized by hyperalgesia (increased responsiveness to noxious stimuli) and allodynia (painful responses to normally innocuous stimuli). The mitogen-activated proteins kinases (MAPKs) are a family of evolutionally conserved molecules that play a critical role in cell signaling,consisting of extracellular signal regulated kinase (ERK),p38,and c-Jun N-terminal kinase (JNK),which play an important role in neural plasticity of pathological pain. Inhibition of MAPKs alleviates inflammatory pain and neuropathic pain in different animal models. It is very important to study the inhibition of MAPKs as a therapeutic approach to treat pathological pain.
文摘Mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs), c-Jun NH2-terminal kinases (JNKs) and p38 MAPK, play an important role in transducting environmental stimuli to the transcriptional machinery in the nucleus in mammalian cells by virtue of their ability to phosphorylate and regulate the activity of various transcription factors. It was recently found that the changes in activity of MAPKs occurred during ischemia/reperfusion, but the biological significance of the changes was still controversial.
文摘Myocardial hypertrophy is an independent risk factor for cardiac events. Mitogen-activated protein kinases (MAPK), including extracellular signal-regulated kinases, C-jun N-terminal kinases and P38-MAPK, are the common intracellular pathway of transducing hypertrophic signs. All three MAPK subfamilies play an important role in development of myocardial hypertrophy.
文摘目的:研究在支气管哮喘豚鼠肺组织中丝裂原活化蛋白激酶(MAPK)信号通路对γ-谷氨酰半胱氨酸合酶(γ-GCS)的影响。方法:成年雄性豚鼠20只随机分成哮喘组和对照组,每组10只,以腹腔内注射联合雾化吸入卵蛋白复制哮喘模型。测支气管肺泡灌洗液(BALF)细胞总数并进行分类计数;原位杂交和RT-PCR测肺组织中γ-GCS-h mRNA表达;免疫组化测γ-GCS、磷酸化细胞外激活蛋白激酶(p-ERK)、磷酸化c-Jun氨基末端激酶(p-JNK)和磷酸化p38(p-p38)在肺组织中的表达;W estern b lotting测p-ERK、p-JNK和p-p38在肺组织中的表达;双酶法测γ-GCS的活性。结果:(1)哮喘组BALF中细胞总数、嗜酸性粒细胞明显多于对照组(P<0.01)。(2)免疫组化显示肺组织中p-ERK、p-p38、p-JNK和γ-GCS蛋白质表达哮喘组明显高于对照组(P<0.01);W estern b lotting亦显示肺组织中p-ERK、p-JNK和p-p38蛋白质表达哮喘组均明显高于对照组。(3)原位杂交和RT-PCR显示在肺组织中γ-GCS-h mRNA表达哮喘组明显高于对照组(P<0.01)。(4)γ-GCS活性哮喘组明显高于对照组(P<0.01)。(5)直线相关性分析显示:在肺组织中p-ERK、p-p38与γ-GCS-hmRNA、γ-GCS蛋白质呈显著正相关,p-JNK与γ-GCS-h mRNA、γ-GCS蛋白质无明显相关性。结论:支气管哮喘豚鼠肺中p-ERK、p-p38、p-JNK和γ-GCS表达均增加;p-ERK和p-p38可能上调γ-GCS表达。
