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Objective To analyze the clinical effect of Tongxinluo capsule in the treatment of female patients with microvascular angina .Methods 122 female patients with microvascular angina pectoris were selected ,and they were randomly divided into conventional group and observation group ,61 cases in each group .On the basis of the two groups in the same treatment ,including antiplatelet ,lipid,the observation group was given Tongxinluo capsule orally , treatment for 3 months.The therapeutic effect was compared between the two groups .Results The total effective rate of the observation group was 93.44％,which of the conventional group was 80.33％,the difference between the two groups was statistically significant (χ2 =4.603,P=4.603).The total effective rate of exercise electrocardiogram ( ECG ) improvement in the observation group was 91.80％, which of the conventional group was 75.41％, the difference between the two groups was statistically significant (χ2 =4.552,P=0.048).Conclusion Tongxinluo capsule in the treatment of female patients with microvascular angina pectoris has good clinical curative effect ,it can obviously improve the clinical symptoms ,promote disease recover ,which is worthy of popularizing .
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Objective: To analyze the relationship between inflammatory factors and relevant risk factors in patients of essential hypertension (EH) combining acute coronary syndrome (ACS) with its clinical significance. Methods: Our research included 3 groups: EH group, n=79 patients with standard criteria, EH+ACS group, n=85 and Control group, n=48 normal subjects. Blood levels of lipoprotein-associated phospholipase A2 (Lp-PLA2), tryptase (TPS) and relevant clinical, biochemical parameters were measured; risk factors for cardiovascular disease were examined and the relationship between above parameters, risk factors and ACS occurrence in EH patients was studied by Logistic regression analysis. Results: The OR values were all greater than 1 in fibrinogen (Fbg), high-sensitivity C-reactive protein (hs-CRP), TPS, atherosclerotic plaque, Lp-PLA2 and EH grading. Fbg was the most significant independent risk factor (OR=22.242, 95% CI 6.458-76.609, P<0.0001), the standardized partial regression coefficient b'as absolute value (b') was 1.079 which was the highestone in above 6 variables with the strongest impact for ACS occurrence in EH patients. Conclusion: Fbg, hs-CRP, TPS, atherosclerotic plaque and EH grading were the independent risk factors for ACS occurrence in EH patients; Fbg was the highest risk factor for ACS occurrence with the strongest impact, which provided a new direction for ACS prevention and treatment.
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Over-expression of CD151 was found to be associated with metastasis and poor prognosis of prostatic carcinoma. This study was designed to examine the mechanism by which CD151 promotes the proliferation and migration of prostatic cancer cells. The pAAV-CD151, pAAV-GFP and pAAV-CD151-AAA mutant plasmids were constructed and used to transiently transfect PC3 cells (a prostatic carcinoma 3 cell line) by the mediation of Fugene HD. Then, the cells were assigned to control group, pAAV-GFP group, pAAV-CD151 group, and pAAV-CD151-AAA group respectively. Cell proliferation was evaluated by using the 3-[4,5-dimet-hylthiazol-2-yl]-2,5, diphenyltetrazolium bromide (MTT) method. Cell migration assay was performed by using Boyden chambers. The formation of CD151-integrin α3/α6 complex was determined by the method of co-immunoprecipitation. The protein expression levels of CD151 and extracellular signal-regulated kinase (ERK) were measured by Western blotting. The results showed that transfection of pAAV-CD151 or pAAV-CD151-AAA mutant increased the expression of CD151 protein in PC3 cells. Co-immunoprecipitation showed that more CD151-integrin α3/α6 complex was formed in the pAAV-CD151 group than in the control group, the pAAV-GFP group and the pAAV-CD151-AAA mutant group. Furthermore, the proliferative and migrating capacity of PC3 cells was substantially increased in the pAAV-CD151 group but inhibited in the pAAV-CD151-AAA mutant group. CD151 transfection increased the expression of phospho-ERK. Taken together, it was concluded that CD151 promotes the proliferation and migration of PC3 cells through the formation of CD151-integrin complex and the activation of phosphorylated ERK.
Assuntos
Humanos , Masculino , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Integrina alfa3 , Metabolismo , Integrina alfa6 , Metabolismo , Neoplasias da Próstata , Metabolismo , Patologia , Tetraspanina 24 , MetabolismoRESUMO
Over-expression of CD151 was found to be associated with metastasis and poor prognosis of prostatic carcinoma. This study was designed to examine the mechanism by which CD151 promotes the proliferation and migration of prostatic cancer cells. The pAAV-CD151, pAAV-GFP and pAAV-CD151-AAA mutant plasmids were constructed and used to transiently transfect PC3 cells (a prostatic carcinoma 3 cell line) by the mediation of Fugene HD. Then, the cells were assigned to control group, pAAV-GFP group, pAAV-CD151 group, and pAAV-CD151-AAA group respectively. Cell proliferation was evaluated by using the 3-[4,5-dimet-hylthiazol-2-yl]-2,5, diphenyltetrazolium bromide (MTT) method. Cell migration assay was performed by using Boyden chambers. The formation of CD151-integrin α3/α6 complex was determined by the method of co-immunoprecipitation. The protein expression levels of CD151 and extracellular signal-regulated kinase (ERK) were measured by Western blotting. The results showed that transfection of pAAV-CD151 or pAAV-CD151-AAA mutant increased the expression of CD151 protein in PC3 cells. Co-immunoprecipitation showed that more CD151-integrin α3/α6 complex was formed in the pAAV-CD151 group than in the control group, the pAAV-GFP group and the pAAV-CD151-AAA mutant group. Furthermore, the proliferative and migrating capacity of PC3 cells was substantially increased in the pAAV-CD151 group but inhibited in the pAAV-CD151-AAA mutant group. CD151 transfection increased the expression of phospho-ERK. Taken together, it was concluded that CD151 promotes the proliferation and migration of PC3 cells through the formation of CD151-integrin complex and the activation of phosphorylated ERK.