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Study on molecular mechanism of liver yang ascending syndrome in hypertension
  
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KeyWord:hypertension, Liver Yang Ascending Syndrome, Liver and Kidney Yin Deficiency Syndrome, tyrosine hydroxylase, molecular mechanism
Author NameAffiliation
Yiqiang Jin Institute of Integrated Traditional Chinese and Western Medicine, The Affiliated Xiangya Hospital, Hunan Medical University, 410008, Changsha 
Suiyu Hu Institute of Integrated Traditional Chinese and Western Medicine, The Affiliated Xiangya Hospital, Hunan Medical University, 410008, Changsha 
Donghong Yan Institute of Integrated Traditional Chinese and Western Medicine, The Affiliated Xiangya Hospital, Hunan Medical University, 410008, Changsha 
Aiping Liu Institute of Integrated Traditional Chinese and Western Medicine, The Affiliated Xiangya Hospital, Hunan Medical University, 410008, Changsha 
Faqing Tang Institute of Integrated Traditional Chinese and Western Medicine, The Affiliated Xiangya Hospital, Hunan Medical University, 410008, Changsha 
Chun Xiao Institute of Integrated Traditional Chinese and Western Medicine, The Affiliated Xiangya Hospital, Hunan Medical University, 410008, Changsha 
Binlai Chen Institute of Integrated Traditional Chinese and Western Medicine, The Affiliated Xiangya Hospital, Hunan Medical University, 410008, Changsha 
Yonghua Wang Institute of Integrated Traditional Chinese and Western Medicine, The Affiliated Xiangya Hospital, Hunan Medical University, 410008, Changsha 
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Abstract:
      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 A 1 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.
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