摘要:目的: 探討動脈硬化閉塞癥(ASO)和靜脈血栓形成(VT)患者同型半胱氨酸(Hcy)變化。 方法 :通過循環酶法對34例非動脈硬化閉塞癥(ASO)和靜脈血栓形成(VT)患者(對照組),30例動脈硬化閉塞癥(ASO)患者和26例靜脈血栓形成(VT)患者血液中Hcy進行測定。 結果 :循環酶法測定HCY的批內平均變異系數為2．23％,批間平均變異系數為1．59％。34例對照組,〖WTBX〗t =1135,〖WTBX〗P =0266gt;005;動脈硬化閉塞癥(ASO)組Hcy含量明顯高于對照組(〖WTBX〗P lt;O．05),靜脈血栓形成(VT)組Hcy含量高于對照組(〖WTBX〗P lt;0．O5)。 結論 :高同型半胱氨酸血癥可能是動脈硬化閉塞癥(ASO)和靜脈血栓形成(VT)及復發的致病因素。可將同型半胱氨酸作為動脈硬化閉塞癥(ASO)和靜脈血栓形成(VT)及復發的重要指標。Abstract: Objective: TO syudy the changes of the Homocysteine about Atherosclerosis obliterans and Venous thrombosis patients. Methods : To measure the Hcy in the blood of 34 healthy cases both non ASO and non VT(the comparison group),30 cases of ASO patients and 26 cases of VT patients respectively by enzymatic cycling assay。〖WTHZ〗Results :The average variation coefficient of Hcy within the groups was 223% and among the groups was 159% measured by enzymatic cycling assay.In the 34 cases of comparison group,t=1135,P=0266gt;005,The content of Hcy in the blood of ASO patients group were significantly higher than the comparision group (Plt;005),and the content of Hcy in the blood of VT patients group were also higher than the comparison group (Plt;005). Conclusion : Hyper Hcy may be the pathogenic diathesis to form or to recrudesce ASO and VT.So we can treat Hcy as the significant index to form or to recrudesce ASO and VT.
ObjectiveTo explore the concentration of the plasma homocysteine (Hcy) and the relationship with TOAST subtypes in patients with acute cerebral infarction.
MethodsA total of 120 patients with acute cerebral infarction (ACI) treated from April 2012 to April 2013 were enrolled into the ACI group.They were classified with Korean TOAST classification as five subtypes:atherothrombosis (AT) type,small artery disease (SAD) type,cardioembolism (CE) type,stroke of other disease (SOD) type,and stroke of undetermined etiology (SUE) type.The plasma Hcy concentrations in each group and in 60 heathy people who were selected into the control group were measured.Furthermore,the relationship between plasma Hcy concentration and their subtypes were analyzed.
ResultsThe plasma Hcy level in ACI group was significant higher than that in the control group (P<0.01).The levels of plasma Hcy were much higher in patients with AT,SAD,SOD,and CE than those in the control groups (P<0.01).In different subtypes,AT and SAD subtypes had higher homocysteine concentration than SUD and CE subtypes did.The concentration of Hcy in AT and SAD group had no significant difference.
ConclusionACI is related to hyperhomocysteinemia.The plasma Hcy level varies with different TOAST subtypes of ACI,specially elevating in the subtypes of AT and SAD,which may indicate that hyperhomocysteinemia may increase stroke risk through proatherogenic effect and endothelial dysfunction.
Objective To evaluate the association between coronary heart disease (CHD) and plasma homocysteine level, and to provide additional information for prevention and management of CHD. Methods We searched CBM, CNKI, WanFang, and VIP databases. Case-control studies about the association between CHD and plasma homocysteine level published in China were identified. Meta-analysis was performed using RevMan 4.2 software. Results The result of meta-analysis showed the plasma homocysteine level in the CHD group was higher than that of the control group (WMD=4.88, 95%CI 4.40 to 5.35, Plt;0.000 01), and the loss of safety coefficient was 1 339. Conclusion High plasma homocysteine level is associated with increasing morbidity of CHD.
Objective To investigate the promoting effect of S-adenosyl-homocysteine hydrolase (AHCY) on the proliferation of lung cancer cells and its regulatory mechanism on the expression of methionine adenosyltransferase 1A (MAT1A). Methods Wayne plot analysis was performed on four lung cancer data chips, including GSE103512, GSE18842, GSE20189, and GSE102286, to screen for differentially expressed key genes. Protein immunoprecipitation assay was used to detect the interaction between AHCY and MAT1A. pAdTrack-CMV-NC+pCV702-NC (NC), pAdTrack-CMV, and pAdTrack-CMV+pCV702 were transfected into A549 and PC9 cells, respectively. The cell proliferation, apoptosis, the mitochondrial membrane potential, the ROS levels in cells, the total RNA methylation levels in cells, and the expression of AHCY and MAT1A in cells were detected, sequentially. Results The statistical analysis identified AHCY and MAT1A were the key differentially expressed genes across the four datasets. Co-immunoprecipitation experiments confirmed a direct interaction between AHCY and MAT1A in lung cancer (P<0.05). Upregulation of the expression of AHCY could significantly increase the proliferation of A549 and PC9 cells, decrease the cell apoptosis, increase the mitochondrial membrane potential, alleviate the intracellular reactive oxygen species levels, and decrease the total RNA methylation levels, while MAT1A overexpression partially reversed the promoting effects of AHCY on lung cancer cells. All differences were statistically significant (all P<0.05). Conclusions The expression of AHCY is significantly increased in lung cancer, while the expression of MAT1A is significantly decreased in lung cancer. High expression of AHCY can promote the cancer cell proliferation and affect total RNA methylation, while downregulate the expression of MAT1A in lung cancer cells.
