摘要
OBjECTIVE:To compare the correlations between salivary alpha-amylase(sAA) activity and amylase,alpha 1(salivary) gene(AMY1) copy number or its gene expression between splenic asthenia and healthy children,and investigate the reasons of attenuated sAA activity ratio before and after citric acid stimulation in splenic asthenia children.METHODS:Saliva samples from 20 splenic asthenia children and 29 healthy children were collected before and after citric acid stimulation.AMY1 copy number,sAA activity,and total sAA and glycosylated sAA contents were determined,and their correlations were analyzed.RESULTS:Although splenic asthenia and healthy children had no differences in AMY1 copy number,splenic asthenia children had positive correlations between AMY1 copy number and sAA activity before or after citric acid stimulation.Splenic asthenia children had a higher sAA glycosylated proportion ratio and glycosylated sAA content ratio,while their total sAA content ratio and sAA activity ratio were lower compared with healthy children.The glycosylated sAA content ratio was higher than the total sAA content ratio in both groups.Splenic asthenia and healthy children had positive correlations between total sAA or glycosylated sAA content and sAA activity.However,the role played by glycosylated sAA content in sAA activity in healthy children increased after citric acid stimulation,while it decreased in splenic asthenia children.CONCLUSION:Genetic factors like AMY1 copy number variations,and more importantly,sAA glycosylation abnormalities leading to attenuated sAA activity after citric acid stimulation,which were the main reasons of the attenuated sAA activity ratio in splenic asthenia children compared with healthy children.
OBjECTIVE：To compare the correlations between salivary alpha-amylase（sAA） activity and amylase,alpha 1（salivary） gene（AMY1） copy number or its gene expression between splenic asthenia and healthy children,and investigate the reasons of attenuated sAA activity ratio before and after citric acid stimulation in splenic asthenia children.METHODS：Saliva samples from 20 splenic asthenia children and 29 healthy children were collected before and after citric acid stimulation.AMY1 copy number,sAA activity,and total sAA and glycosylated sAA contents were determined,and their correlations were analyzed.RESULTS：Although splenic asthenia and healthy children had no differences in AMY1 copy number,splenic asthenia children had positive correlations between AMY1 copy number and sAA activity before or after citric acid stimulation.Splenic asthenia children had a higher sAA glycosylated proportion ratio and glycosylated sAA content ratio,while their total sAA content ratio and sAA activity ratio were lower compared with healthy children.The glycosylated sAA content ratio was higher than the total sAA content ratio in both groups.Splenic asthenia and healthy children had positive correlations between total sAA or glycosylated sAA content and sAA activity.However,the role played by glycosylated sAA content in sAA activity in healthy children increased after citric acid stimulation,while it decreased in splenic asthenia children.CONCLUSION：Genetic factors like AMY1 copy number variations,and more importantly,sAA glycosylation abnormalities leading to attenuated sAA activity after citric acid stimulation,which were the main reasons of the attenuated sAA activity ratio in splenic asthenia children compared with healthy children.
基金
National Natural Science Foundation of China(the Mechanism Study of Salivary Alpha Amylase Activity Change in Pi-Deficiency Syndrome Patients Based on the AMY1 Copy Number Variations,N-Glycosylated Protein Level andβ-Adrenergic Receptor Activation,No.81102703)
Science and Technology Planning Project of Guangdong Province(miRNA as Material Basis for the New Hypothesis"Pi-Metabolism Relevance,"and Study on the Molecular Mechanisms of Treating Metabolic Disorders Through Pi,No.2013A032500005)
and Administration of Traditional Chinese Medicine of Guangdong Province in China(Study on the Relevance Between the Pi-Deficiency Syndrome and Gene Differential Expression Profile of Immunity and Metabolism in Type 2 Diabetic Mellitus,No.20123001)
