Association between occupational noise exposure and the risk of cardiovascular diseases / 中华劳动卫生职业病杂志

Objective: To explore the association between occupational noise exposure and cardiovascular disease (CVD) risk in a large Chinese population. Methods: In December 2019, the study included 21412 retired participants from the Dongfeng-Tongji Cohort Study at baseline from September 2008 to June 2010, occupational noise exposure was evaluated through workplace noise level and/or the job titles. In a subsample of 8931 subjects, bilateral hearing loss was defined as a pure-tone mean of 25 dB or higher at 0.5, 1 , 2, and 4 kHz in both ears. Logistic regression models were used to explore the association of occupational noise exposure, bilateral hearing loss with 10-year CVD risk. Results: Compared with participants without occupational noise exposure, the 10-year CVD risk was significantly higher for noise exposure duration ≥20 years (OR=1.20, 95%CI:1.01-1.41 , P=0.001) after adjusting for potential confounders. In the sex-specific analysis, the association was only statistically significant in males (OR=2.34, 95%CI: 1.18-4.66, P<0.001) , but not in females (OR=1.15, 95%CI:0.97-1.37, P=0.153). In the subsample analyses, bilateral hearing loss, which was an indicator for exposure to loud noise, was also associated with a higher risk of 10-year CVD (OR= 1.17, 95% CI:1.05-1.44, P <0.001) , especially for participants who were males (OR =1.24, 95% CI:1.07-2.30, P<0.001) , aged equal and over 60 years old (OR=2.30, 95%CI: 1.84-2.88, P<0.001) , and exposed to occupational noise (OR=1.66, 95%CI: 1.02-2.70, P=0.001). Conclusion: Occupational noise exposure may be a risk factor for CVD.

Influence of hydrogen sulfide on zymogen activation of homocysteine-induced matrix metalloproteinase-2 in H9C2 cardiocytes

Objective To observe the influence of different concentrations of homocysteine (Hcy) and hydrogen sulfide (H

Influence of hydrogen sulfide on zymogen activation of homocysteine-induced matrix metalloproteinase-2 in H9C2 cardiocytes

OBJECTIVE@#To observe the influence of different concentrations of homocysteine (Hcy) and hydrogen sulfide (H2S) on the secretion and activation of matrix metalloproteinase-2 (MMP-2) in cardiocytes so as to search for new ways to fight against myocardial tissue fibrosis.@*METHODS@#Cardiocytes H9C2 was cultured in vitro and different concentrations of Hcy and H2S were added for 6-h and 24-h cultivation. MTT cell proliferation assay was applied to test the activation change of cardiocytes H9C2 after affecting by different concentrations of Hcy and H2S. ELISA and MTT were employed to detect the expression and enzymatic activity of MMP-2.@*RESULTS@#The H9C2 cell inhibition of activity was more significant with 1000 μmol/L of Hcy as compared with other concentrations (P  0.05). Hcy with concentrations of 10, 50 and 100 μmol/L could increase the quantity of MMP-2 secreted by cardiocytes H9C2, and the interaction strength was concentration-dependent (P < 0.05). After interacting with 100 μmol/L of Hcy for 6 h, the zymogen activation effect of MMP-2 was stronger than that of the 2.5-25 μmol/L group (P < 0.05). After interacting with Hcy and H2S (1.0 mmol/L) for 6 h and 24 h, the activation effect of MMP-2 was stronger than those interacted with 10, 25, 50 and 100 μmol/L of Hcy (P < 0.05).@*CONCLUSIONS@#Hcy can increase the production of MMP-2 secreted by H9C2 cell and improve its zymogen activation. Besides, the interaction strength is concentration-dependent; while H2S can up-regulate the activation of MMP-2 and co-promote the activation of MMP-2 with Hcy as well.

Testosterone alleviates tumor necrosis factor-alpha-mediated tissue factor pathway inhibitor downregulation via suppression of nuclear factor-kappa B in endothelial cells / 亚洲男科学杂志(英文版)

We have observed earlier that testosterone at physiological concentrations can stimulate tissue factor pathway inhibitor (TFPI) gene expression through the androgen receptor in endothelial cells. This study further investigated the impact of testosterone on TFPI levels in response to inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). Cultured human umbilical vein endothelial cells were incubated in the presence or absence of testosterone or TNF-alpha. TFPI protein and mRNA levels were assessed by enzyme-linked immunosorbent assay and quantitative real-time reverse transcription polymerase chain reaction. To study the cellular mechanism of testosterone's action, nuclear factor-kappa B (NF-kappaB) translocation was confirmed by electrophoretic mobility shift assays. We found that after NF-kappaB was activated by TNF-alpha, TFPI protein levels declined significantly by 37.3% compared with controls (P < 0.001), and the mRNA levels of TFPI also decreased greatly (P < 0.001). A concentration of 30 nmol L(-1) testosterone increased the secretion of TFPI compared with the TNF-alpha-treated group. NF-kappaB DNA-binding activity was significantly suppressed by testosterone (P < 0.05). This suggests that physiological testosterone concentrations may exert their antithrombotic effects on TFPI expression during inflammation by downregulating NF-kappaB activity.

Effects of testosterone on extracellular signal-regulated kinase 1/2 phosphorylation in human umbilical vein endothelial cells / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the effects of testosterone on extracellular signal-regulated kinase l/2 ( ERK1/2) phosphorylation in human umbilical vein endothelial cells (HUVEC).</p><p><b>METHODS</b>Activations of ERK1/2 stimulated by physiological testosterone were detected by Western blotting in cultured HUVEC.</p><p><b>RESULTS</b>A rapid phosphorylation expression of ERK1/2 was observed by treatment of the HUVECs with 3 x 10(-8) mol/L testosterone, especially at 30 minutes. This phosphorylation was greatly inhibited by incubation with androgen receptor antagonist flutamide for 3 hours previously.</p><p><b>CONCLUSION</b>Testosterone at physiological concentrations induces the mitogen-activated protein kinase (MAPK, ERK1/2 and MEK1/2) phosphorylation within a short time, and flutamide could impair the process.</p>

Testosterone's effect on tPA and PAI-1 mRNA levels of HUVEC / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the effect of testosterone with varied concentrations on the tPA and PAI-1 mRNA levels of Human umbilical vein endothelial cells (HUVEC).</p><p><b>METHODS</b>HUVEC within 2 - 3 passages were cultured with testosterone (3, 30, 3 x 10(3), 3 x 10(4) nmol/L) , and the control confluent cells were cultured in the same medium without steroid for 48 hours. RT-PCR was carried out to detect tPA and PAI-1 mRNA levels.</p><p><b>RESULTS</b>tPA mRNA level increased, while PAI-1 mRNA levels decreased significantly, at the testosterone concentrations ranging from 3 to 3 x 10(3) nmol/L (P < 0.05). Both tPA and PAI-1 mRNA level decreased obviously of 3 x 10(4) nmol/L group.</p><p><b>CONCLUSION</b>The results indicated that testosterone could stimulate tPA gene expression, while decreased PAI-1 mRNA level of HUVEC, which suggested that testosterone might have beneficial effects on preventing male's thrombotic diseases.</p>