目的:探讨寒热中药的成分与TRP家族中TRPV1和TRPM8通道蛋白mRNA表达的相关性。方法:原代培养DRG神经元,在体外观察中药单体对通道蛋白表达的影响,基因的表达量采用荧光定量PCR(real time PCR)法检测,数据分析采用2?ΔΔCT法。结果:热性...目的:探讨寒热中药的成分与TRP家族中TRPV1和TRPM8通道蛋白mRNA表达的相关性。方法:原代培养DRG神经元,在体外观察中药单体对通道蛋白表达的影响,基因的表达量采用荧光定量PCR(real time PCR)法检测,数据分析采用2?ΔΔCT法。结果:热性中药的成分(吴茱萸碱、桂皮醛)上调TRPV1的表达,下调TRPM8的表达,尤以寒负荷后更为明显;寒性中药的成分(黄芩苷、大黄素)上调TRPM8的表达,下调TRPV1的表达,尤以热负荷后更为明显。结论:对TRPV1与TR-PM8的表达调节可能与中药的寒热药性相关,这可能是寒热性中药临床上发挥寒热调节作用的机制之一。展开更多
Migraine is a common and debilitating headache disorder. Although its pathogenesis remains elusive,abnormal trigeminal and central nervous system activity is likely to play an important role. Transient receptor potent...Migraine is a common and debilitating headache disorder. Although its pathogenesis remains elusive,abnormal trigeminal and central nervous system activity is likely to play an important role. Transient receptor potential(TRP) channels, which transduce noxious stimuli into pain signals, are expressed in trigeminal ganglion neurons and brain regions closely associated with the pathophysiology of migraine. In the trigeminal ganglion,TRP channels co-localize with calcitonin gene-related peptide, a neuropeptide crucially implicated in migraine pathophysiology. Many preclinical and clinical data support the roles of TRP channels in migraine. In particular,activation of TRP cation channel V1 has been shown to regulate calcitonin gene-related peptide release from trigeminal nerves. Intriguingly, several effective antimigraine therapies, including botulinum neurotoxin type A, affect the functions of TRP cation channels. Here, we discuss currently available data regarding the roles of major TRP cation channels in the pathophysiology of migraine and the therapeutic applicability thereof.展开更多
文摘目的:探讨寒热中药的成分与TRP家族中TRPV1和TRPM8通道蛋白mRNA表达的相关性。方法:原代培养DRG神经元,在体外观察中药单体对通道蛋白表达的影响,基因的表达量采用荧光定量PCR(real time PCR)法检测,数据分析采用2?ΔΔCT法。结果:热性中药的成分(吴茱萸碱、桂皮醛)上调TRPV1的表达,下调TRPM8的表达,尤以寒负荷后更为明显;寒性中药的成分(黄芩苷、大黄素)上调TRPM8的表达,下调TRPV1的表达,尤以热负荷后更为明显。结论:对TRPV1与TR-PM8的表达调节可能与中药的寒热药性相关,这可能是寒热性中药临床上发挥寒热调节作用的机制之一。
基金supported by the Japan Society for the Promotion of Science KAKENHI(26460706 and 19K07849)a Japan-China Sasakawa Medical Fellowship(2017816)a State Scholarship Fund of the China Scholarship Council(201908500072)。
文摘Migraine is a common and debilitating headache disorder. Although its pathogenesis remains elusive,abnormal trigeminal and central nervous system activity is likely to play an important role. Transient receptor potential(TRP) channels, which transduce noxious stimuli into pain signals, are expressed in trigeminal ganglion neurons and brain regions closely associated with the pathophysiology of migraine. In the trigeminal ganglion,TRP channels co-localize with calcitonin gene-related peptide, a neuropeptide crucially implicated in migraine pathophysiology. Many preclinical and clinical data support the roles of TRP channels in migraine. In particular,activation of TRP cation channel V1 has been shown to regulate calcitonin gene-related peptide release from trigeminal nerves. Intriguingly, several effective antimigraine therapies, including botulinum neurotoxin type A, affect the functions of TRP cation channels. Here, we discuss currently available data regarding the roles of major TRP cation channels in the pathophysiology of migraine and the therapeutic applicability thereof.
