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Study on Molecular Mechanism of Liver Yang Ascending Syndrome in Hypertension

Study on Molecular Mechanism of Liver Yang Ascending Syndrome in Hypertension
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摘要 Objective: To investigate the molecular mechanism of Liver Yang Ascending Syndrome (LYAS) in hypertension. Methods: The plasma norepinephrine (NE), epinephrine (E) contents in patients with LYAS or Liver and Kidney Yin Deficiency Syndrome (LKYDS) of hypertension and normal controls were determined by high performance liquid chromatography-electrochemical detector (HPLC-ECD). The polymorphism of tyrosine hydroxylase (TH) gene in the three groups were analysed by Southern Blot assay. The polymorphism of TH and monoamine oxidation A(MAO-A), monoamine oxidation B(MAO-B) gene microsatellite in these groups were analysed by polymerase chain reaction (PCR)-SSCP. At the same time, the LYAS model was established by administering Aconitum preparation (AP) to spontaneous hypertension rats (SHR). The adrenal gland medulla of the experimental animal was examined for their TH expression at the protein level after ABC immuno-histochemical staining with the TH monoclonal antibody (McAb). The adrenal TH gene mRNA expression was demonstrated by in situ hybridization with the synthetized TH oligonucleic acid probe. The results of immuno-histochemistry and in situ hybridization were analyzed with the image analysis system (IAS). Results: The plasma NE and E contents in patients with LYAS were more obviously increased than those in LKYDS and normal controls. The TH gene amplified and the type A1 TH microsatellite D11S4046 was markedly higher in the LYAS group than those in the other groups. The TH mRNA protein expression in the adrenal tissue of the AP induced LYAS model in SHR elevated. Conclusion: The LYAS of hypertension has the characters as amplified TH gene and increased TH mRNA and protein expression, which suggested that the overexpression of TH is probably the mechanism of LYAS in hypertension. Objective: To investigate the molecular mechanism of Liver Yang Ascending Syndrome (LYAS) in hypertension. Methods: The plasma norepinephrine (NE), epinephrine (E) contents in patients with LYAS or Liver and Kidney Yin Deficiency Syndrome (LKYDS) of hypertension and normal controls were determined by high performance liquid chromatography-electrochemical detector (HPLC-ECD). The polymorphism of tyrosine hydroxylase (TH) gene in the three groups were analysed by Southern Blot assay. The polymorphism of TH and monoamine oxidation A(MAO-A), monoamine oxidation B(MAO-B) gene microsatellite in these groups were analysed by polymerase chain reaction (PCR)-SSCP. At the same time, the LYAS model was established by administering Aconitum preparation (AP) to spontaneous hypertension rats (SHR). The adrenal gland medulla of the experimental animal was examined for their TH expression at the protein level after ABC immuno-histochemical staining with the TH monoclonal antibody (McAb). The adrenal TH gene mRNA expression was demonstrated by in situ hybridization with the synthetized TH oligonucleic acid probe. The results of immuno-histochemistry and in situ hybridization were analyzed with the image analysis system (IAS). Results: The plasma NE and E contents in patients with LYAS were more obviously increased than those in LKYDS and normal controls. The TH gene amplified and the type A1 TH microsatellite D11S4046 was markedly higher in the LYAS group than those in the other groups. The TH mRNA protein expression in the adrenal tissue of the AP induced LYAS model in SHR elevated. Conclusion: The LYAS of hypertension has the characters as amplified TH gene and increased TH mRNA and protein expression, which suggested that the overexpression of TH is probably the mechanism of LYAS in hypertension.
出处 《Chinese Journal of Integrative Medicine》 SCIE CAS 2000年第4期244-249,共6页 中国结合医学杂志(英文版)
基金 ThisstudywasfundedbyNationalNaturalSciencesFounda tionofChina
关键词 HYPERTENSION Liver Yang Ascending Syndrome Liver and Kidney Yin Deficiency Syndrome tyrosine hydroxylase molecular mechanism hypertension, Liver Yang Ascending Syndrome, Liver and Kidney Yin Deficiency Syndrome, tyrosine hydroxylase, molecular mechanism
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