Objective To investigate the effect of phlorizin on the apoptosis and oxidative stress of rat cardiomyocytes H9C2 induced by hypoxia/reoxygenation(H/R)and its possible mechanism.Methods H9C2 cells were cultured in vitro.H/R model was established after pretreatment with different doses(16,32,64 μmol/L)of phlorizin or transfection with anti-miR-125a-5p,anti-miR-NC,miR-125a-5p mimics and negative controls.Proliferation was detected by CCK-8,and apoptosis was detected by flow cytometry.The protein expression levels of B lymphoblastoma-2 associated X protein(Bax)and B lymphocytoma-2(Bcl-2)were detected by Western blot assay.The release of lactate dehydrogenase(LDH)and the activity of superoxide dismutase(SOD)were detected by colorimetric method.Real-time fluorescence quantitative PCR(qRT-PCR)was used to detect the expression of miR-125a-5p.Results Compared with the H/R group,inhibition rate,apoptosis rate,Bax protein expression,LDH content and miR-125a-5p expression were decreased after low,medium and high doses of phlorizin treatment(P＜0.05),and SOD activity,Bcl-2 protein expression were increased(P＜0.05).After inhibiting the expression of miR-125a-5p,the inhibition rate,apoptosis rate,Bax protein expression and LDH content of H9C2 cells induced by H/R were decreased(P＜0.05),and SOD activity,Bcl-2 protein expression were increased(P＜0.05).Overexpression of miR-125a-5p reversed the effect of phloridin on H/R-induced proliferation,apoptosis and oxidative stress of H9C2 cells.Conclusion Phlorizin may reduce H/R-induced apoptosis and oxidative stress in H9C2 cells by decreasing the expression of miR-125a-5p.

Objective:To study the effects of progesterone on the morphology, proliferation, and secretion of cytokines of human decidual stromal cells (DSCs) in late pregnancy, and to explore the mechanism of progesterone in preventing spontaneous preterm birth.Methods:Human decidual stromal cells in late pregnancy were cultured and treated with different concentrations of progesterone (in the experimental groups, 10 -6 mol/L, 10 -5 mol/L and 10 -4 mol/L progesterone was added to the culture medium respectively, and no progesterone was added to the culture medium of control group). The morphology of DSCs was observed under the microscope, the cell length/width ratio was measured, the proliferation was detected by methyl thiazolyl tetrazolium (MTT) method, and the expressions of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) mRNA were detected by RT-qPCR. Results:The length/width ratios of DSCs in progesterone 10 -4 mol/L (5.87±0.19) and 10 -5 mol/L (5.98±0.27) groups were lower than that in control group (6.42±0.19), the differences were statistically significant ( P<0.001, P=0.002). The length/width ratio in the 10 -4 mol/L group was lower than that in the 10 -6 mol/L group (6.28±0.32, P=0.005). The proliferation of DSCs in the 10 -5 mol/L (0.70±0.04) and 10 -4 mol/L (0.78±0.04) groups was higher than that in control group (0.59±0.05; P=0.027, P=0.002), and proliferation of DSCs in 10 -4 mol/L group was higher than that in 10 -6 mol/L group (0.61±0.01, P=0.004). The expression of TNF-α mRNA in each progesterone group was lower than that in control group (all P<0.001) and the expression of TNF-α mRNA in the 10 -5 mol/L and 10 -4 mol/L groups was lower than that in the 10 -6 mol/L group (all P<0.001) . The expressions of IL-6 mRNA decreased gradually in control group, 10 -6 mol/L, 10 -5 mol/L and 10 -4 mol/L groups, the differences were statistically significant (all P<0.001). Conclusion:Progesterone can make the decidual stromal cells wider, promote proliferation, and decrease the expressions of TNF-α and IL-6 mRNA, which may play an important role in the mechanism of progesterone preventing spontaneous preterm birth.

Objective:To study the effects of progesterone on the morphology, proliferation, and secretion of cytokines of human decidual stromal cells (DSCs) in late pregnancy, and to explore the mechanism of progesterone in preventing spontaneous preterm birth.Methods:Human decidual stromal cells in late pregnancy were cultured and treated with different concentrations of progesterone (in the experimental groups, 10 -6 mol/L, 10 -5 mol/L and 10 -4 mol/L progesterone was added to the culture medium respectively, and no progesterone was added to the culture medium of control group). The morphology of DSCs was observed under the microscope, the cell length/width ratio was measured, the proliferation was detected by methyl thiazolyl tetrazolium (MTT) method, and the expressions of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) mRNA were detected by RT-qPCR. Results:The length/width ratios of DSCs in progesterone 10 -4 mol/L (5.87±0.19) and 10 -5 mol/L (5.98±0.27) groups were lower than that in control group (6.42±0.19), the differences were statistically significant ( P<0.001, P=0.002). The length/width ratio in the 10 -4 mol/L group was lower than that in the 10 -6 mol/L group (6.28±0.32, P=0.005). The proliferation of DSCs in the 10 -5 mol/L (0.70±0.04) and 10 -4 mol/L (0.78±0.04) groups was higher than that in control group (0.59±0.05; P=0.027, P=0.002), and proliferation of DSCs in 10 -4 mol/L group was higher than that in 10 -6 mol/L group (0.61±0.01, P=0.004). The expression of TNF-α mRNA in each progesterone group was lower than that in control group (all P<0.001) and the expression of TNF-α mRNA in the 10 -5 mol/L and 10 -4 mol/L groups was lower than that in the 10 -6 mol/L group (all P<0.001) . The expressions of IL-6 mRNA decreased gradually in control group, 10 -6 mol/L, 10 -5 mol/L and 10 -4 mol/L groups, the differences were statistically significant (all P<0.001). Conclusion:Progesterone can make the decidual stromal cells wider, promote proliferation, and decrease the expressions of TNF-α and IL-6 mRNA, which may play an important role in the mechanism of progesterone preventing spontaneous preterm birth.

Herpes simplex virus type Ⅰ(HSV-1) is a common pathogen, and human is the only natural host of it.Following a period of lytic replication in epithelial cells, HSV-1 enters axon terminals of sensory neurons and then travels via retrograde transport to the sensory ganglia where latency can be established.Upon the stimulation of some stressors, the latent virus can reactivate, leading to recurrent diseases.Therefore, to clarify the mechanism of HSV-1 latent infection and stress-induced reactivation will offer new insights into the prevention, treatment and control of HSV-1 infection.In this review, we describes the mechanisms underlying HSV-1 latent infection and stress-induced reactivation.

The DNA copy-number variant (CNV) is a kind of segments of DNA ranging from 1 kb to 3 Mb that is present in a variable number of copies.CNVs widely distribute across the human genome,and dramatically increases genetic diversity.In recent years,researches have found that most CNVs are closely related to complex diseases.If a cancer gene is directly encompassed or overlapped by a CNV,it may lead to activation of oncogenes or inactivation of tumor suppressor genes,and finally results in tumorigenesis.CNVs can affect gene expression,phenotype differences and phenotypic adaptations by changing gene dosages and gene activities,and then sequentially lead to tumor or any other genetic dieases.Investigating CNVs is apparently helpful for studing chromosome recombination,genomic evolution,gene expression and the pathogenesis of multiple complex diseases especially tumor.

Objective To study the efficacy of trimctazidine combined with atorvastatin for primary hypertension with paroxysmal auricular fibrillation,and its effects on LAD and CRP. Methods 160 patients of pri-mary hypertension with paroxysmal auricular fibrillation were randomly divided into 4 groups. Forty patients were treated with amiodarone (control group),600 mg/d for the first week,400 mg/d for the second week and 200 mg/d later;40 patients were treated with atorvastatin (20 mg/d,3 times per day) in addition to amiodarone (the atorvasat-in group);40 patients were treated with trimetazidine (20 mg/d,3 times per day) in addition to armiodarone (the trimetazidine group);40 patients were treated with combination of trimetazidine and atorvastatin in addition to amiod-atone (the combination group),and the dose was the same as the above groups. The treatment was started within 24 hours of recovering from paroxysmal auricular fibrillation and lasted for 1 year. Results After 1 year there was 1 pa-the control group,and 62.5% (25/40) for the atorvasatin group,64.1% (25/39) for the trimetazidine group,and 84.6% (33/39) for the combination group. Compared to the control group,the effective rate of the 3 treatment groups were all significantly higher (X2=4.56、5.13、17.55,P<0.05). The effective rate of the combination group was significantly higher than that of the atorvasatin group and the trimetazidine group (X2=4.95、4.30,P<0.05),and there was no significant difference of effective rate between the atorvasatin group and the trimetazidine group(X2= >0.05). After treatment LAD was (40.96+1.81) mm in the control group,(38.65±1.90) mm in the atorvasatin group,(39.15±1.85)mm in the trimetazidine group,and (37.22±1.74) mm in the combination group. LAD of the 3 treatment groups were all significantly different from the control group(F=3.42,P<0.05). LAD of the combina-tion group was significantly smaller than that of the atorvasatin group and the trimetazidine group (P<0.05),and there was no significant difference of the LAD between the atorvasatin group and the trimetazidine group(P>0.05). There was no significant difference between the 4 groups on CRP before treatment (F=0.96,P>0.05). After treat-ment CRP was (8.85±1.45) mg/L in the control group,(5.96±1.26) mg/L in the atorvasatin group,(6.81± 1.37) mg/L in the trimetazidine group,and (3.75±1.15) mg/L in the combination group. CRP of the 3 treatment groups were all significantly different from the control group (F=3.63,P<0.05). CRP of the combination group was significantly lower than that of the atorvasatin group and the trimetazidine group (P<0.05),and there was no signif-icant difference of CRP between the atorvasatin group and the trimetazidine group (P>0.05). Conclusion The treatment with trmetazidine combined with atorvastatin could prevent recurrence of paroxysmal auricular fibrillation though anti-inflammatory and inhibiting the remodeling of left atrial.

Objective To investigate the effect of statins and angiotensin receptor blocker (ARB) on paroxysmal atrial fibrillation in patients with chronic congestive heart failure. Methods All of 145 patients with chronic congestive heart failure and paroxysmal atrial fibrillation were randomly divided into four groups, Ⅰ group (treated with amiodarone ), Ⅱ group( treated with amiodarone and valsartan), Ⅲ group( treated with amiodarone and pravastatin)and Ⅳ group (treated with amiodarone,valsattan and pravastatin). After 2- year follow-up, observed the changes of left atrium diameter (LAD), C-reactive protein (CRP) and maintenance rate of sinus rhythm before and after treatment. Results After treatment, the data of LAD of the four groups were (44.1 ± 2.1 ), (41.7 ± 2.8), (44.4 ± 3.1 ), (40.1 ± 2.5) mm respectively. The LAD data of beth Ⅰ group and Ⅲ group were significantly higher than those of Ⅱ group and Ⅳ group (P < 0.05), but there was no significant difference either between Ⅰ group and Ⅲ group, or between Ⅱ group and Ⅳ group. The levels of CRP of the four groups were (4.56 ± 0.24), (4.47 ± 0.45 ), (2.87 ± 0.53 ), (2.54 ± 0.42) mg/Lrespectively, and the levels of CRP of Ⅰ group and Ⅱ group were obviously higher than those of Ⅲ group and Ⅳ group(P< 0.05 ), but there was no significant difference either between Ⅰ group and Ⅱ group,or between group and Ⅳ group. Maintenance rate of sinus rhythm of the four groups was 57.9%,79.4%,77.1%,85.3% respectively,the maintenance rate of sinus rhythm of Ⅰ group was significantly lower than that of Ⅱ,Ⅲ and Ⅳ group (P<0.05). Conclusions Va]asrtan and pravastatin may reduce recurrence of paroxysmal atrial fibri]lation in patients with chronic congestive heart failure. Valsartan may inhibit dilatation of left atrium, and pravastatin may decrease the level of CRP in blood.