Myocardial infarction (MI) is the leading cause of cardiovascular disease-related death worldwide. Nonetheless, existing therapeutic approaches for MI are hampered by issues such as reliance on pharmacological agents and suboptimal patient adherence. Caffeic acid (CA) is a bioactive polyphenolic compound with important anti-inflammatory, anti-bacterial and anti-oxidant functions. Still, its specific role and mechanism in treating cardiovascular disease remain to be further studied. In recent years, a large number of studies have shown that the kelch-like ECH-associated protein 1/nuclear factor erythroid 2 related factor 2 (Keap1/Nrf2) pathway is a key factor in the occurrence and development of cardiovascular diseases. In this study, H₂O₂-induced oxidative stress model of H9c2 cells and left anterior descending branch (LAD) conjunctival induced acute myocardial infarction reperfusion (AMI/R) model were used to evaluate the protective effect of CA on the heart. The interaction between CA and Keap1 was analyzed by CA-labeled fluorescence probe, target fishing, isothermal titration calorimetry (ITC), protein crystallography and surface plasmon resonance (SPR). Our results suggested that CA binds Keap1 and degrades Keap1 in a p62-dependent manner, further promoting nuclear transcription of Nrf2 and thus effectively reducing oxidative stress. In addition, based on the three-dimensional eutectic structure, it was confirmed that CA directly targets Keap1 protein by interacting with residues M550 and N532, inducing conformation changes in Keap1 protein. We also found that the CA analog chlorogenic acid (GCA) can bind Keap1. In conclusion, this study elucidates a novel molecular mechanism and structural basis for the protective effects of CA against oxidative damage via the Keap1-Nrf2 pathway.

Objective:To investigate the effect of pelvic floor muscle exercise (PFMT) combined with transcutaneous electrical nerve stimulation (TENS) on urinary incontinence after radical prostatectomy.Methods:A total of 120 patients with urinary incontinence after radical prostatectomy in Shuguang Hospital, Shanghai University of Traditional Chinese Medicine from July 2020 to June 2021 were retrospective selected and divided into control group and observation groupthe according to different treatment method, 60 cases in each group. The control group was treated with PFMT, and the observation group was treated with PFMT combined with TENS. Urodynamic indexes of 72 h urine pad usage, maximum urine flow rate, maximum cystometric capacity, maximum urethral closure pressure, abdominal leakage point pressure, ICI-Q-SF score and the clinical efficacy were compared between the two groups. Measurement data were expressed as mean ± standard deviation ( ± s), and t-test was used for comparison between groups; Chi-square test was used for comparison of enumeration data between groups. Results:After treatment, the 72 h urine urine pad usage in the observation group [(1.95±1.13) pieces] was lower than that in the control group [(6.28±2.47) pieces], and the difference was statistically significant ( P<0.05). After treatment, the maximum flow rate [(13.92±2.53) mL/s], maximum cystometric capacity [(338.72±19.22) mL], maximum urethral closure pressure [(69.75±5.04) cmH 2O], abdominal leakage point pressure [(90.56±5.26) cmH 2O] in observation group after treatment were better than those in control group [(11.48±2.18) mL/s, (325.81±18.63) mL, (65.29±4.78) cmH 2O, (83.58±5.29) cmH 2O], the difference were statistically significant ( P<0.05). After treatment, the ICI-Q-SF score of the observation group [(5.97±1.82) points] was lower than that of the control group [(10.95±2.64) points], and the difference was statistically significant ( P<0.05); the clinical effective rate of observation group (93.33%) was higher than that of control group (78.33%), and the difference was statistically significant ( P<0.05). Conclusion:PFMT combined with TENS is better than PFMT alone in the treatment of postoperative urinary incontinence after radical prostatectomy.

Objective:To investigate the effects of tumor protein translation control antisense RNA1 (TPT1-AS1) on the radiosensitivity, cell proliferation, migration and invasion of hepatocellular carcinoma cells by targeting microRNA-30c-5p (miR-30c-5p).Methods:Thirty-four cases of liver cancer tissues and adjacent normal tissues were derived from liver cancer patients who were admitted to Shanxi Provincial People′s Hospital from March 2016 to March 2018. Liver cancer HepG2 cell was transfected with negative control siRNA (si-NC group), si-TPT1-AS1 (si-TPT1-AS1 group), pcDNA3.1 (pcDNA3.1 group), pcDNA3.1-TPT1-AS1 (pcDNA3.1-TPT1-AS1 group), si-TPT1-AS1 and anti-miR-NC (si-TPT1-AS1+ anti-miR-NC group), si-TPT1-AS1 and anti-miR-30c-5p (si-TPT1-AS1+ anti-miR-30c-5p group), respectively. Real-time quantitative reverse transcription polymerase chain reaction (qPCR) was used to detect the transcription levels of TPT1-AS1 and miR-30c-5p in normal tissues adjacent to cancer and liver cancer tissues, the clone formation test was used to test the radiosensitivity of HepG2 cells, and the Methyl Thiazolyl Tetrazolium (MTT) test was used to test the proliferation of HepG2 cells. Cell cycle distribution was detected by flow cytometry, Transwell array was used to detect the migration and invasion ability of HepG2 cells, dual luciferase reporter array was used to verify the targeting relationship of TPT1-AS1 and miR-30c-5p, western blot was used to detect the expressions of proliferation, migration and invasion-related proteins.Results:The expression levels of TPT1-AS1 and miR-30c-5p in liver cancer tissues were 0.84±0.08 and 0.13±0.01, statistically different from 0.31±0.03 and 0.50±0.05 in normal tissues adjacent to cancer ( P<0.05). When the cells were treated with 2, 4, 6, 8 Gy irradiation, the cell survival scores of the si-TPT1-AS1 group were 0.280±0.040, 0.069±0.011, 0.020±0.003 and 0.005±0.001, respectively, lower than 0.648±0.070, 0.348±0.080, 0.130±0.020 and 0.060±0.009 of the si-NC group ( P<0.05), the radiosensitization ratio of the si-TPT1-AS1 group was 1.672. The number of cell migration and invasion in the si-TPT1-AS1 group were (50.00±4.36) and (44.00±4.03), respectively, which were lower than (109.00±8.68) and (94.00±7.49) in the si-NC group ( P<0.05), the cell absorbance ( A) values at 24, 48 and 72 hours were 0.28±0.03, 0.43±0.04 and 0.68±0.07, respectively, lower than 0.46±0.04, 0.87±0.08 and 1.35±0.13 of the si-NC group ( P<0.05), the protein expression levels of Cyclin D1, p21, E-cadherin and MMP-2 were 0.25±0.02, 0.65±0.06, 0.68±0.07 and 0.27±0.03, respectively, statistically different from 0.88±0.08, 0.17±0.02, 0.14±0.01 and 0.89±0.09 of si-NC group ( P<0.05), the proportions of S phase and G 2 phase in the si-TPT1-AS1 group were (17.82±1.03)% and (34.15±2.29)%, respectively, significantly different from (35.14±2.61)% and (16.84±1.21)% in the si-NC group ( P<0.05). The luciferase activity of cells in the WT-TPT1-AS1+ miR-30c-5p group was 0.26±0.02, lower than 0.92±0.09 in the WT-TPT1-AS1+ miR-NC group ( P<0.05). The cell survival scores in the si-TPT1-AS1+ anti-miR-30c-5p group were 0.450±0.081, 0.200+ 0.045, 0.070±0.010, 0.026±0.004 after treatment with 2, 4, 6, 8 Gy irradiation, higher than 0.285±0.043, 0.075±0.014, 0.028±0.004, 0.006±0.001 of si-TPT1-AS1+ anti-miR-NC group ( P<0.05). The radiosensitization ratio of the si-TPT1-AS1+ anti-miR-30c-5p group was 0.694. The number of migration and invasion in the si-TPT1-AS1+ anti-miR-30c-5p group were 79.00±6.65 and 68.00±6.33, higher than (52.00±4.41) and (46.00±4.06) of si-TPT1-AS1+ anti-miR-NC Group ( P<0.05), the A values at 24, 48 and 72 hours were 0.37±0.03, 0.64±0.06 and 0.96±0.09, respectively, higher than 0.26±0.03, 0.41±0.04, and 0.65±0.06 of si-TPT1-AS1+ anti-miR-NC group ( P<0.05), the expression levels of Cyclin D1, p21, E-cadherin and MMP-2 protein were 0.57±0.06, 0.43±0.04, 0.43±0.04 and 0.64±0.06, statistically different from 0.24±0.02, 0.66±0.06, 0.65±0.06 and 0.28±0.03 of the si-TPT1-AS1+ anti-miR-NC group ( P<0.05). Conclusions:The expression of TPT1-AS1 up-regulates in the liver cancer tissues. TPT1-AS1 may down-regulate miR-30c-5p expression, reduce the radiosensitivity of liver cancer cells, and promote the proliferation, migration and invasion of liver cancer cells.

Objective:To investigate the effects of tumor protein translation control antisense RNA1 (TPT1-AS1) on the radiosensitivity, cell proliferation, migration and invasion of hepatocellular carcinoma cells by targeting microRNA-30c-5p (miR-30c-5p).Methods:Thirty-four cases of liver cancer tissues and adjacent normal tissues were derived from liver cancer patients who were admitted to Shanxi Provincial People′s Hospital from March 2016 to March 2018. Liver cancer HepG2 cell was transfected with negative control siRNA (si-NC group), si-TPT1-AS1 (si-TPT1-AS1 group), pcDNA3.1 (pcDNA3.1 group), pcDNA3.1-TPT1-AS1 (pcDNA3.1-TPT1-AS1 group), si-TPT1-AS1 and anti-miR-NC (si-TPT1-AS1+ anti-miR-NC group), si-TPT1-AS1 and anti-miR-30c-5p (si-TPT1-AS1+ anti-miR-30c-5p group), respectively. Real-time quantitative reverse transcription polymerase chain reaction (qPCR) was used to detect the transcription levels of TPT1-AS1 and miR-30c-5p in normal tissues adjacent to cancer and liver cancer tissues, the clone formation test was used to test the radiosensitivity of HepG2 cells, and the Methyl Thiazolyl Tetrazolium (MTT) test was used to test the proliferation of HepG2 cells. Cell cycle distribution was detected by flow cytometry, Transwell array was used to detect the migration and invasion ability of HepG2 cells, dual luciferase reporter array was used to verify the targeting relationship of TPT1-AS1 and miR-30c-5p, western blot was used to detect the expressions of proliferation, migration and invasion-related proteins.Results:The expression levels of TPT1-AS1 and miR-30c-5p in liver cancer tissues were 0.84±0.08 and 0.13±0.01, statistically different from 0.31±0.03 and 0.50±0.05 in normal tissues adjacent to cancer ( P<0.05). When the cells were treated with 2, 4, 6, 8 Gy irradiation, the cell survival scores of the si-TPT1-AS1 group were 0.280±0.040, 0.069±0.011, 0.020±0.003 and 0.005±0.001, respectively, lower than 0.648±0.070, 0.348±0.080, 0.130±0.020 and 0.060±0.009 of the si-NC group ( P<0.05), the radiosensitization ratio of the si-TPT1-AS1 group was 1.672. The number of cell migration and invasion in the si-TPT1-AS1 group were (50.00±4.36) and (44.00±4.03), respectively, which were lower than (109.00±8.68) and (94.00±7.49) in the si-NC group ( P<0.05), the cell absorbance ( A) values at 24, 48 and 72 hours were 0.28±0.03, 0.43±0.04 and 0.68±0.07, respectively, lower than 0.46±0.04, 0.87±0.08 and 1.35±0.13 of the si-NC group ( P<0.05), the protein expression levels of Cyclin D1, p21, E-cadherin and MMP-2 were 0.25±0.02, 0.65±0.06, 0.68±0.07 and 0.27±0.03, respectively, statistically different from 0.88±0.08, 0.17±0.02, 0.14±0.01 and 0.89±0.09 of si-NC group ( P<0.05), the proportions of S phase and G 2 phase in the si-TPT1-AS1 group were (17.82±1.03)% and (34.15±2.29)%, respectively, significantly different from (35.14±2.61)% and (16.84±1.21)% in the si-NC group ( P<0.05). The luciferase activity of cells in the WT-TPT1-AS1+ miR-30c-5p group was 0.26±0.02, lower than 0.92±0.09 in the WT-TPT1-AS1+ miR-NC group ( P<0.05). The cell survival scores in the si-TPT1-AS1+ anti-miR-30c-5p group were 0.450±0.081, 0.200+ 0.045, 0.070±0.010, 0.026±0.004 after treatment with 2, 4, 6, 8 Gy irradiation, higher than 0.285±0.043, 0.075±0.014, 0.028±0.004, 0.006±0.001 of si-TPT1-AS1+ anti-miR-NC group ( P<0.05). The radiosensitization ratio of the si-TPT1-AS1+ anti-miR-30c-5p group was 0.694. The number of migration and invasion in the si-TPT1-AS1+ anti-miR-30c-5p group were 79.00±6.65 and 68.00±6.33, higher than (52.00±4.41) and (46.00±4.06) of si-TPT1-AS1+ anti-miR-NC Group ( P<0.05), the A values at 24, 48 and 72 hours were 0.37±0.03, 0.64±0.06 and 0.96±0.09, respectively, higher than 0.26±0.03, 0.41±0.04, and 0.65±0.06 of si-TPT1-AS1+ anti-miR-NC group ( P<0.05), the expression levels of Cyclin D1, p21, E-cadherin and MMP-2 protein were 0.57±0.06, 0.43±0.04, 0.43±0.04 and 0.64±0.06, statistically different from 0.24±0.02, 0.66±0.06, 0.65±0.06 and 0.28±0.03 of the si-TPT1-AS1+ anti-miR-NC group ( P<0.05). Conclusions:The expression of TPT1-AS1 up-regulates in the liver cancer tissues. TPT1-AS1 may down-regulate miR-30c-5p expression, reduce the radiosensitivity of liver cancer cells, and promote the proliferation, migration and invasion of liver cancer cells.

Objective: To investigate the distribution characteristics of pathogens and related risk factors in patients with cardiovascular disease complicated with pulmonary infection. Methods: From June 2015 to October 2017, 252 patients with cardiovascular disease who were treated in the People's Hospital of Shanxi Province were selected.The number of patients complicated with pulmonary infection in the treatment process was counted, the distribution characteristics of pathogens in patients with pulmonary infection was analyzed.The relationship between gender, age, time in bed, smoking history, invasive operation, chronic obstructive pulmonary disease(COPD) and pulmonary infection in patients with cardiovascular disease were analyzed.Logistic regression analysis was used to analyze the risk factors of pulmonary infection in patients with cardiovascular disease. Results: There were 32 cases of pulmonary infection in 252 patients with cardiovascular disease, the incidence rate of pulmonary infection was 12.70%.Forty-one strains of pathogens were isolated from the patients with pulmonary infection, among them, there was Gram negative bacteria with 27 strains, accounting for 65.85%, Gram positive bacteria with 10 strains, accounting for 24.39%, and 4 fungi with 4 strains, accounting for 9.76%.The incidence of pulmonary infection in patients with cardiovascular disease was not related to the gender of the patients(χ²=0.267, P>0.05). The incidence rates of pulmonary infection in patients with age≥60 years old, time in bed for more than 2 weeks, smoking history, invasive operation, COPD were significantly higher than those of age<60, time in bed for less than 2 weeks, no smoking history, no invasive operation, no COPD(χ²=7.076, 7.066, 4.764, 12.603, 7.805, all P<0.05). The logistic regression analysis showed that age≥60 years old, time in bed for more than 2 weeks, smoking history, invasive operation, COPD were independent risk factors of patients with cardiovascular disease complicated with pulmonary infection(OR=4.229, 3.397, 3.504, 4.82, 3.804, all P<0.05). Conclusion The main pathogens of pulmonary infection in patients with cardiovascular disease are Gram negative bacteria, followed by Gram positive bacteria, only a few fungi.Excessive age, excessively long time in bed, smoking history, invasive operation, COPD are risk factors for pulmonary infection in patients with cardiovascular disease.

Objective To study the effects of acetylcholine combined with vincristine (VCR) on A549 cells, furthermore to study the influence that is due to affecting the expression of the two proteins bcl-2 and p53. Methods MTT assay was used to analyze growth inhibition effect of acetylcholine alone and combined with IC50VCR on A549 cells.The expression of bcl-2 and p53 was measured by immunohistological chemistry technique(IHC) and Western blot.Results The inhibition rates for A549 cells with 0.1,1 and 10 μmol/L acetylcholine were (0.050±0.032)％,(0.101±0.021)％,(0.169±0.015)％.The inhibition rates for tumor cells with 0.1,1 and 10 μmol/L acetylcholine joint 0.2 μg/ml VCR were (0.529±0.023)％,(0.545±0.011)％,(0.589±0.015)％,the difference was statistically significant compared with the VCR group (q'values were 1.09,1.37,1.83,P＜0.05).Acetylcholine alone exerted inhibitory effect on A549 cells in a concentration dependent manner and significanrtly enhanced its sensitivity to VCR (P＜0.05).acetylcholibne (0.1-10 μmol/L)combined with IC50VCR decrased the expression of bcl-2 and p53 (P＜0.05).Conclusion Acetylcholine alone and combined with VCR can inhibit the growth of A549 cells. Significant synergistic effect between acetylcholine and VCR is found in inducing cell apoptosis by changing the expression of bcl-2 and p53.

Objective To evaluate the effects and possible mechanism of endovascular irradiation using liquid 32 P-filled ballon catheter on restenosis after interventional therapy.Methods 54 Wistar rats were randomly divided into injured group, which received the balloon injury of thoracic aorta, and irradiated group, which received the balloon injury of thoracic aorta followed immediately by ionizing radiation using 20 Gy or 28 Gy liquid 32 p-filled balloon catheter. The expressions of proliferation cellular nuclear antigen(PCNA) in vascular cells and smooth muscle actin(?-SM actin) in the vascular adventitia were detected by immunohistochemical method, and were quantified by computer image analysis. The morphologic changes of thoracic aorta were analyzed by computer image analysis . Results ⑴14 days after injury, both the lumen area and external elastic lamina (EEL) area of thoracic aorta in the irradiated group were significantly larger than those in injuried group, but the neointima area was significantly smaller in the irradiated group. The above chanages were negative relation with the irradiation doses. ⑵At third day after injury, the cell proliferation activity in the adventitia and media of thoracic aorta in the irradiated group obviously decreased in dose dependent manner compared with the injured group. At the 7th day after injury,there was not significant difference in the cell proliferation in the adventitia and media of the vessels between the irradiated group and injury group. ⑶At 7th and 14th days after injury. The ?-SM actin expression level in the adventitia of thoracic aorta in the irradiated group was significantly lower than that in the injured group, which was negatively related with the irradiation dose.Conclusion To some extent, there was a correlation between the irradiation dose of using liquid 32 p-filled balloon catheter and the areas of lumen, EEL and neointima. The endovascular irradiation could contribute to inhibiting the neointima and improving the vascular remodeling by inhibiting vascular cell proliferation and adventititial ?-SM actin expression.