The role of macrophage polarization and related key molecules in pulmonary inflammation and fibrosis induced by coal dust dynamic inhalation exposure in Sprague-Dawley rats.

Coal dust is the main occupational hazard factor during coal mining operations. This study aimed to investigate the role of macrophage polarization and its molecular regulatory network in lung inflammation and fibrosis in Sprague-Dawley rats caused by coal dust exposure. Based on the key exposure parameters (exposure route, dose and duration) of the real working environment of coal miners, the dynamic inhalation exposure method was employed, and a control group and three coal dust groups (4, 10 and 25 mg/m3) were set up. Lung function was measured after 30, 60 and 90 days of coal dust exposure. Meanwhile, the serum, lung tissue and bronchoalveolar lavage fluid were collected after anesthesia for downstream experiments (histopathological analysis, RT-qPCR, ELISA, etc.). The results showed that coal dust exposure caused stunted growth, increased lung organ coefficient and decreased lung function in rats. The expression level of the M1 macrophage marker iNOS was significantly upregulated in the early stage of exposure and was accompanied by higher expression of the inflammatory cytokines TNF-α, IL-1ß, IL-6 and the chemokines IL-8, CCL2 and CCL5, with the most significant trend of CCL5 mRNA in lung tissues. Expression of the M2 macrophage marker Arg1 was significantly upregulated in the mid to late stages of coal dust exposure and was accompanied by higher expression of the anti-inflammatory cytokines IL-10 and TGF-ß. In conclusion, macrophage polarization and its molecular regulatory network (especially CCL5) play an important role in lung inflammation and fibrosis in SD rats exposed to coal dust by dynamic inhalation.

Rotenone-induced cell apoptosis via endoplasmic reticulum stress and PERK-eIF2α-CHOP signalling pathways in TM3 cells.

Rotenone (ROT), a widely used natural pesticide, has an uncertain effect on reproductive toxicity. In this study, we used 20 mice distributed randomly into four groups, with each group receiving ROT doses of 0, 2, 4, and 8 mg/kg/day for 28 days. The results demonstrated that ROT induced significant testicular damage, including impaired spermatogenesis, inhibition of testosterone synthesis, and apoptosis of Leydig cells. Additionally, ROT disrupted the normal ultrastructure of the endoplasmic reticulum (ER) in testicular tissue, leading to ER stress in Leydig cells. To further explore whether ROT-induced apoptosis in Leydig cells is related to ER stress, the mouse Leydig cell line (TM3 cells) was treated with ROT at 0, 250, 500, and 1000 nM. ROT inhibited TM3 cell viability, induced cytotoxicity, and reduced testosterone content in the culture supernatants. Furthermore, ROT treatment triggered apoptosis in TM3 cells by activating ER stress and the PERK-eIF2α-CHOP signalling pathway. Pre-treatment of TM3 cells exposed to ROT with the ER stress inhibitor 4-phenylbutyric acid (4-PBA) alleviated these effects, decreasing apoptosis and preserving testosterone levels. Further intervention with the PERK inhibitor GSK2606414 reduced ROT-induced apoptosis and testosterone reduction by inhibiting PERK activity. In summary, ROT-induced male reproductive toxicity is specifically driven by apoptosis, with the PERK-eIF2α-CHOP signalling pathway activated by ER stress playing a crucial role in the apoptosis of Leydig cells triggered by ROT.

The role of stimulator of interferon genes-mediated AMPK/mTOR/P70S6K autophagy pathway in cyfluthrin-induced testicular injury.

Cyfluthrin is widely used in the field of sanitary pest control by its wide insecticidal spectrum, high efficiency and low toxicity, low residue, and good biodegradability. But, as a double-edged sword, a large amount of cyfluthrin remains are still in the environment. The residual cyfluthrin is absorbed into the food chain through vegetation and then poses a risk to soil organisms and human health. Several studies have suggested that cyfluthrin is one of the main factors causing testicular damage, but the mechanism remains unclear. In this study, we established in vivo and in vitro models of testicular injury in rats and GC-2 cells exposed to cyfluthrin to explore whether stimulator of interferon genes (STING) gene mediates the regulation of AMPK/mTOR/p70S6K autophagy pathway, which lays a foundation for further study of the mechanism of testicular injury induced by cyfluthrin. The results showed that the activity of super oxide dismutase in testis decreased and the activity of malonic dialdehyde increased with the increase of concentration in vivo and in vitro. At the same time, the levels of mitochondrial damage and inflammation in the testis also increased, which further activated autophagy. In this process, the increased level of inflammation is related to the increased expression of STING gene, and AMPK/mTOR/p70S6K autophagy pathway is also involved. To sum up, cyfluthrin has certain reproductive toxicity, and long-term exposure can induce testicular cell damage. STING gene can participate in cyfluthrin-induced testicular injury through AMPK/mTOR/P70S6K autophagy pathway.

SKAP1 Is a Novel Biomarker and Therapeutic Target for Gastric Cancer: Evidence from Expression, Functional, and Bioinformatic Analyses.

Gastric cancer (GC) is the third leading cause of cancer-related death worldwide. Due to the lack of early symptoms, GC is often diagnosed at an advanced stage when treatment options are limited. There is an urgent need to identify biomarkers for early detection, prognosis evaluation, and targeted treatment of GC. Studies have shown that Src kinase-associated phosphoprotein 1 (SKAP1) promotes cell proliferation and invasion and is associated with poor prognosis in colorectal cancer, malignant fibrous histiocytoma, and breast cancer. However, the role and mechanism of SKAP1 in GC are unclear. Here, analyses of multiple databases and experiments revealed that SKAP1 expression was higher in GC than in adjacent normal tissues. The Cancer Genome Atlas data showed that high SKAP1 expression was associated with poor GC prognosis. SKAP1 expression was higher in GC than in normal gastric epithelial cells. SKAP1 silencing reduced the proliferation, migration and invasion of the GC cell lines MKN45 and HGC27. Rescue experiments suggest that SKAP1 may promote GC progression by activating JAK1/PI3K/AKT signaling and regulating GC cell proliferation, invasion, migration, and other functions. Bioinformatics analysis revealed that SKAP1 was associated with immune cell infiltration and checkpoint expression in GC. High SKAP1 expression was associated with poorer immunotherapy outcomes, suggesting its potential as a predictive biomarker of GC immunotherapy efficacy. In summary, SKAP1 is overexpressed in GC, where it promotes cell proliferation, invasion and migration and is associated with poor prognosis and poor immunotherapy outcomes. SKAP1 may represent a biomarker and therapeutic target in GC and regulates cellular functions through JAK1/PI3K/AKT signaling.

Mechanism of 2,4-Dichlorophenoxyacetic acid-induced damage to rat testis via Fas/FasL pathway and the protective effect of Lycium barbarum polysaccharides.

The herbicide 2,4-Dichlorophenoxyacetic acid (2,4-D) is widely used to control broadleaved weeds and has been associated with male infertility. We studied the molecular mechanisms of 2,4-D induced male reproductive system damage and the protective effects of Lycium barbarum polysaccharides (LBP) using Sprague Dawley rats and TM4 cells. Treatment with 2,4-D caused architectural and functional changes in the testis, including collapsed and atrophied seminiferous tubules with reduced number of spermatozoa, scarce sperm in the epididymal duct, low levels of serum testosterone, decreased superoxide dismutase and glutathione peroxidase activity, high malondialdehyde content, and increased apoptosis in the testis and epididymis. The expression of Fas, FasL, FADD, Pro-caspase-8, Cleaved-Caspase-8, Pro-Caspase-3, and Cleaved-Caspase-3 were significantly increased in the testicular tissue of 2,4-D-treated rats. The proliferative activity of TM4 cells decreased with an increase in dose and time of 2,4-D exposure, along with enhanced Fas/Fas ligand expression and a decreased concentration of inhibin B in TM4 cell culture medium. Depletion of Fas by specific shRNA transfection reversed the effects of 2,4-D in TM4 cells, further confirming the involvement of death receptor pathway in 2,4-D-mediated apoptosis of sertoli cells. Treatment with LBP also reversed the effects of 2,4-D in testicular cells, resulting in improved cell architecture along with enhanced proliferative capacity. Moreover, in response to LBP treatment of Sertoli cells, the content of inhibin B increased, the level of reactive oxygen species and malondialdehyde decreased, the activities of superoxide dismutase and glutathione peroxidase increased, and the rate of apoptosis as well as the expression of Fas/Fas ligand signaling pathway proteins decreased.

Effects of 2,4-dichlorophenoxyacetic acid on the expression of NLRP3 inflammasome and autophagy-related proteins as well as the protective effect of Lycium barbarum polysaccharide in neonatal rats.

The pesticide 2,4-dichlorophenoxyacetic acid (2,4-D) has neurotoxic effects, but its mechanism is not clear. In this study, a 2,4-D (75 mg/kg. b.w) exposure model was established in SD rats with colostrum. Lipopolysaccharide (1 mg/kg b.w) was used as the positive control, and Lycium barbarum polysaccharide (LBP, 50 mg/kg b.w) was used as an intervention factor to explore the neurotoxic effect of 2,4-D and the neuroprotective effect of LBP. Our research results show that 2,4-D causes a decrease in the number of hippocampal CA3 pyramidal cells and pyknosis in nuclei with a triangular or irregular shape and that rats show signs of anxiety or depression. In rat serum, superoxide dismutase, and glutathione peroxidase activity decreased, while malondialdehyde content increased. Protein and mRNA levels of TNFα, IL-6, IL-1ß, IL-18, NLRP3, ASC, caspase-1, IL-1ß, IL-18, and p62 increased, while those of LC3-II/LC3-I and Beclin-1 decreased in hippocampal tissues. In conclusion, 2,4-D increased the oxidative stress level, induced neuroinflammatory response, and decreased the autophagy level in experimental rats. LBP may have upregulated the autophagy level in the body by inhibiting the activation of the NLRP3 inflammasome, thus playing a neuroprotective role.

Inhibition of connective tissue growth factor attenuates paraquat-induced lung fibrosis in a human MRC-5 cell line.

Chronic exposure to Paraquat (PQ) may result in progressive pulmonary fibrosis and subsequent chronic obstructive pulmonary malfunction. Connective tissue growth factor (CTGF) has been proposed as a key determinant in the development of lung fibrosis. We investigated thus whether knock down of CTGF can prevent human lung fibroblasts (MRC-5) activation and proliferation with the subsequent inhibition of PQ-induced fibrosis. MRC-5 was transfected with CTGF-siRNAs and exposed to different concentrations of PQ. The siRNA-silencing efficacy was evaluated using western blotting analyses, qRT-PCR and flow cytometry. Next, the viability and migration of MRC-5 was determined. MMP-2, MMP-9, and TIMP-1 accumulation were quantified to evaluate the lung fibrosis exposure to PQ. Over expression of CTGF mRNA was observed in human MRC-5 cell as early as 6 h following PQ stimulation. CTGF gene expression in MRC-5 cells was substantially reduced by RNAi, which significantly suppressed the expression of the lung fibrosis markers such as tissue inhibitor of metalloproteinase-2 (TIMP-2), Matrix metalloproteinase-2 (MMP-2) and Matrix metalloproteinase-9 (MMP-9) that were stimulated by PQ. Inhibition of CTGF expression suppressed impeded the proliferation and migration ability of MRC-5 cells and resulted in cell-extracellular matrix (ECM) protein accumulation in cells. Our results suggest that CTGF promoted the development of PQ-induced lung fibrosis in collaboration with transforming growth factor ß1 (TGFß1). Furthermore, the observed arresting effects of CTGF knock down during this process suggested that CTGF is the potential target site for preventing PQ-induced pulmonary fibrosis. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1620-1626, 2016.

MAPK pathway mediates epithelial-mesenchymal transition induced by paraquat in alveolar epithelial cells.

Epithelial-mesenchymal transition (EMT) is believed to be involved in lung fibrosis process induced by paraquat (PQ); however, the molecular mechanism of this process has not been clearly established. The present study investigated the potential involvement of EMT after PQ poisoning. The expressions of EMT markers, such as E-cadherin and α-smooth muscle actin (α-SMA), at multiple time points after exposure to different concentrations of PQ were evaluated by western blot analysis. Following PQ treatment, EMT induction was observed under microscopy. Related fibrosis genes, including Matrix metalloproteinase 2 (MMP-2), Matrix metalloproteinase 9 (MMP-9), collagens type I (COL I), and type III (COL III), were also evaluated by measuring their mRNA levels using RT-PCR analysis. Signaling pathways were analyzed using selective pharmacological inhibitors for MAPK. Cell migration ability was evaluated by scratch wound and Transwell assays. The data showed that PQ-induced epithelial RLE-6NT cells to develop mesenchymal cell characteristics, as indicated by a significant decrease in the epithelial marker E-cadherin and a significant increase in the extracellular matrix (ECM) marker α-smooth muscle actin in a dose and time-dependent manner. Moreover, PQ-treated RLE-6NT cells had an EMT-like phenotype with elevated expression of MMP-2, MMP-9, and COL I and COL III and enhanced migration ability. Signal pathway analysis revealed that PQ-induced EMT led to ERK-1 and Smad2 phosphorylation through activation of the MAPK pathway. The results of the current study indicate that PQ-induced pulmonary fibrosis occurs via EMT, which is mediated by the MAPK pathway. This implies that the MAPK pathway is a promising therapeutic target in alveolar epithelial cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1407-1414, 2016.

Rotenone activates the LKB1-AMPK-ULK1 signaling pathway to induce autophagy and apoptosis in rat thoracic aortic endothelial cells.

BACKGROUND: The specific mechanism by which rotenone impacts thoracic aortic autophagy and apoptosis is unknown. We aimed to investigate the regulatory effects of rotenone on autophagy and apoptosis in rat thoracic aortic endothelial cells (RTAEC) via activation of the LKB1-AMPK-ULK1 signaling pathway and to elucidate the molecular mechanisms of rotenone on autophagy and apoptosis in vascular endothelial cells. METHODS: In vivo, 60 male SD rats were randomly selected and divided into 5 groups: control (Con), DMSO, 1, 2, and 4 mg/kg groups, respectively. After 28 days of treatment, histopathological and ultrastructural changes in each group were observed using HE and transmission electron microscopy; Autophagy, apoptosis, and LKB1-AMPK-ULK1 pathway-related proteins were detected by Western blot; Apoptosis levels in the thoracic aorta were detected by TUNEL. In vitro, RTAEC were cultured and divided into control (Con), DMSO, 20, 100, 500, and 1000 nM groups. After 24 h of intervention, autophagy, apoptosis, and LKB1-AMPK-ULK1 pathway-related factors were detected by Western blot and qRT-PCR; Flow cytometry to detect apoptosis levels; Autophagy was inhibited with 3-MA and CQ to detect apoptosis levels, and changes in autophagy, apoptosis, and downstream factors were detected by the AMPK inhibitor CC intervention. RESULTS: Gavage in SD rats for 28 days, some degree of damage was observed in the thoracic aorta and heart of the rotenone group, as well as the appearance of autophagic vesicles was observed in the thoracic aorta. TUNEL analysis revealed higher apoptosis in the rotenone group's thoracic aorta; RTAEC cultured in vitro, after 24 h of rotenone intervention, showed increased ROS production and significantly decreased ATP production. The flow cytometry data suggested an increase in the number of apoptotic RTAEC. The thoracic aorta and RTAEC in the rotenone group displayed elevated levels of autophagy and apoptosis, and the LKB1-AMPK-ULK1 pathway proteins were activated and expressed at higher levels. Apoptosis and autophagy were both suppressed by the autophagy inhibitors 3-MA and CQ. The AMPK inhibitor CC reduced autophagy and apoptosis in RTAEC and suppressed the production of the AMPK downstream factors ULK1 and P-ULK1. CONCLUSIONS: Rotenone may promote autophagy in the thoracic aorta and RTAEC by activating the LKB1-AMPK-ULK1 signaling pathway, thereby inducing apoptosis.

Association between Indoor Environment, Blood Trace Elements, and Immune Globulin among Workers from Vegetables Plastic Greenhouses in Yinchuan, China.

Background: To study the association between indoor environment (MiE), blood trace elements (BTE), and immune globulin (PRO) among workers from vegetables plastic greenhouse, and to assess the mediate effects on MiE and PRO by BTE. Methods: Overall, 168 practitioner and corresponding sheds were included from cross-sectional study in 2016. BTE and PRO were determined by physical test and MiE data from field and laboratory measurement. The association was assessed using canonical correlation analysis. The direct and indirect effects between MiE, PRO and BTE were conducted by structural equation model. 5000 times bootstrap methods were performed to estimate coefficient and 95% confidence interval. Results: MiE was moderately correlated with BTE (canonical coefficient = 0.439), and BTE was strongly correlated with PRO (canonical coefficient = 0.514 and 0.481). No statistical evidence was found for the overall impact of MiE on PRO, and BTE as an intermediary affecting its relevance was not confirmed. Only the path way of the BTE impact on PRO had a significant positive effect (P=0.012). Conclusion: BTE was positively associated with PRO, therefore, reducing exposure in greenhouse is a pathway to remain blood trace elements, and further effect the immune protein in human body.

Lycium barbarum polysaccharides attenuate cardiovascular oxidative stress injury by enhancing the Keap1/Nrf2 signaling pathway in exhaustive exercise rats.

Moderate exercise is beneficial to physical and mental health. When the amount of exercise and exercise intensity exceeds a certain limit and reaches the state of exhaustion, oxidative stress levels in the body increase, which can lead to oxidative stress­associated damage. Lycium barbarum polysaccharide (LBP) is one of the primary active ingredients extracted from wolfberry. Following exhausting exercise in rats, LBP supplements decrease damage to the myocardium and blood vessels, indicating that LBP exerts a protective effect on the cardiovascular system. The Kelch­like ECH­associated protein 1 (Keap1)/NF­E2­related factor 2 (Nrf2) anti­oxidative stress signaling pathway improves total oxidizing ability; anti­apoptosis and other aspects serve a vital role. In the present study, LBP intervention was performed in vivo and in vitro to observe its effect on the Keap1/Nrf2 pathway and oxidative stress­associated indicators in order to clarify its protective mechanism. For the in vivo experiments, 60 male Sprague­Dawley rats were randomly divided into normal control and aerobic, exhaustive and exhaustive exercise + LBP (200 mg/kg/day) groups. For the in vitro experiments, a rat thoracic aortic endothelial cell (RTAEC) oxidative stress model was established using angiotensin II (AngII) and divided into blank control, LBP (3,200 µg/ml), AngII (1x10­4 mol/l) and AngII + LBP groups. For in vitro experiments, small interfering (si)RNA (50 nmol) was used to transfect RTAEC and induce gene silencing of Nrf2. ELISA, hematoxylin and eosin staining, TUNEL, immunofluorescence, western blotting, immunohistochemistry and reverse transcription­quantitative PCR were used to evaluate and verify the effect of LBP on oxidative stress indicators and the expression of Keap1/Nrf2 antioxidative stress signaling pathway. The in vivo experiments showed that LBP decreased the expression of serum malondialdehyde (MDA) and AngII, as well as apoptosis of blood vessels and cardiomyocytes and expression of TNF­α in rats following exhaustive exercise. Meanwhile, LBP enhanced expression of the Keap1/Nrf2 signaling pathway and downstream associated protein glutamyl­cysteine synthetase catalytic subunit (GCLC), quinone oxidoreductase 1 (NQO1) and glutamate­cysteine ligase modified subunit (GCLM) in the thoracic aorta and myocardium of rats following exhaustive exercise. In RTAEC in vitro, LBP decreased the expression of MDA and TNF­α in the supernatant, promoted the nuclear translocation of Nrf2 and increased expression levels of GCLC, NQO1 and GCLM. Following siNrf2 transfection into endothelial cells, the anti­inflammatory and antioxidant stress effects of LBP were decreased. LBP was found to enhance the expression of the Keap1/Nrf2 antioxidant stress signaling pathway in endothelial cells, decreasing oxidative stress and the inflammatory response. Moreover, LBP improved the antioxidant stress ability of endothelial cells and alleviated injury of myocardial vascular tissue, thereby protecting the cardiovascular system.

Role of EGFR/ErbB2 and PI3K/AKT/e-NOS in Lycium barbarum polysaccharides Ameliorating Endothelial Dysfunction Induced by Oxidative Stress.

Lycium barbarum polysaccharides (LBP) are the major ingredients of wolfberry. In this study, we investigated the role of LBP in endothelial dysfunction induced by oxidative stress and the underlying mechanisms using thoracic aortic endothelial cells of rat (RAECs) as a model. We found that Ang II inhibits cell viability of RAECs with 10-6mol/L of Ang II treatment for 24h most potential (P<0.05), the level of reactive oxygen species (ROS) is increased by Ang II treatment (P<0.01), and the expression of Occludin and Zonula occludens-1 (ZO-1) is decreased by Ang II treatment (P<0.05). However, preincubation of cells with LBP could inhibit the changes caused by Ang II, LBP increased cell viability (P<0.05), decreased the level of ROS (P<0.01), and up-regulated the expression of Occludin (P<0.05) and ZO-1. In addition, Ang II treatment increased the expression of EGFR and p-EGFR (Try1172) and which can be inhibited by LBP. On the contrary, expression of ErbB2, p-ErbB2 (Try1248), PI3K, p-e-NOS (Ser1177) (P<0.05), and p-AKT (Ser473) (P<0.05) was inhibited by Ang II treatment and which can be increased by LBP. Treatment of the cells with inhibitors showed that the regulation of p-e-NOS and p-AKT expression by Ang II and LBP can be blocked by PI3K inhibitor wortmannin but not EGFR and ErbB2 inhibitor AC480. Taken together, our results suggested that LBP plays a critical role in maintaining the integrality of blood vessel endothelium through reduced production of ROS via regulating the activity of EGFR, ErbB2, PI3K/AKT/e-NOS, and which may offer a novel therapeutic option in the management of endothelial dysfunction.

Association between pesticide exposure intensity and self-rated health among greenhouse vegetable farmers in Ningxia, China.

BACKGROUND: Self-rated health (SRH) has been shown to be a stronger comprehensive predictor of health status than the clinical record. Although an association between specific pesticide exposures and health conditions has been reported in different populations, data on the relationship between pesticides exposure intensity (PEI) and SRH in greenhouse farmers is scarce. The aim of the current study was to evaluate this association among vegetable greenhouse farmers in Yinchuan City, western China. METHODS: Three consecutive cross-sectional studies were conducted in the years 2015, 2016 and 2017. Face-to-face interviews by trained investigators, using questionnaires, were performed. PEI was calculated by a validated method and then categorized into high, middle and low groups. SRH was measured via a single ten-point scale question and then divided into excellent (score >5) and poor SRH (score ≤5). A multivariable logistic regression model was used to evaluate the association. Meanwhile, the dose-response and interaction effects were estimated. RESULTS: A steady association between high PEI and poor SRH (OR: 1.55, 95% CI: 1.05-2.28 in the full model) was identified. Although high PEI was significantly associated with poor SRH in males and the Han ethnicity group, no significant association was found with poor SRH in females or those of Hui ethnicity. Interaction effects of education level and frequency of breakfast with PEI were determined (Pinteraction = 0.04 and 0.02, respectively); synergistic enhanced effects for poor SRH were observed. CONCLUSION: These findings indicate that high PEI might be associated with poor SRH among vegetable greenhouse farmers. A lower education level and never eating breakfast contributed to an increased likelihood of poor SRH in those with high PEI. The local government should be making great efforts to promote healthy behaviors and improve protection awareness.

[Effects of Lycium barbarum on the behavior, body weight and TNF-alpha level of rat treated with binding].

OBJECTIVE: To explore the effects of Lycium barbarum (L) on the behavior and body weight and TNF-alpha level of rat treated with binding. METHODS: Rats were randomly divided into 6 groups: control group,binding group, 2.5% L group, 5.0% L group, 2.5% L plus binding group, 5.0% L plus binding group. Lycium barbarums were pressed into juice, then rats were fed with the drinking water contening juice. Rats were bound to restrict for 21 days. RESULTS: (1) The increases of serum-cortisol level and the decreases of body weight and the increases of TNF-alpha level of rats of binding group in comparision with control groups (P < 0.05) (2) Rats body weight gain, movement and TNF-alpha level in both of 2.5% L plus binding group and 5.0% L plus binding group were more higher than those in binding group (P < 0.05). Serum-cortisol level of these two groups were more lower and had statistical significance in comparison with those of binding groups (P < 0.05). CONCLUSION: Binding could suppress body weight gain and markedly reduce the activity and TNF-alpha level of rat. Lycium barbarum could be a good adjustment on the behavior, body weight and TNF-alpha.

[Study on the status and the relationship between job burnout and work ability in hospital staff in Yinchuan City].

OBJECTIVE: To investigate the status of job burnout and work ability and to explore their relationship in hospitals employee. METHODS: Maslach burnout inventory (MBI) and work ability index (WAI) were used to measure burnout and work ability of 522 doctors and nurse in 10 hospitals in Yinchuan City. RESULTS: The results indicated that, there were remarkable differences between the doctors and nurses in the scores of MBI. The scores of DE and PA of the doctors were remarkable higher than those of nurses (P < 0.01 and P < 0.05). However, in different hospitals, the scores of EE of the doctors in national hospitals were significant higher than those of doctors in private hospitals. But the scores of PA and WAI of the doctors in national hospitals were remarkable lower than those of doctors in private hospitals. In all, the Pearson correlation showed that there are significantly negative correlations between job burnout and work ability (r = - 0.113- - 0.494, P < 0.01). The multianalysis indicated that the variables of influence work ability included the factors of EE, PA, status of sleeping, ages and type of job. CONCLUSION: There are higher job burnout in hospital staff, even so, status of work ability can be improved with enhancing personal resource and achievement, adjusting job burnout and improving the status of sleeping maladjustment.

[Relationship between occupational stress and blood glucose, blood lipid, blood pressure of video display terminal operators].

OBJECTIVE: To explore the relationship between occupational stress and blood glucose, Blood lipid and blood pressure. METHODS: 108 video display terminals(VDT) operators who had the working experience were recruited to the study. The occupational stress indicator (OSI), the lever of blood glucose, cholesterol, triglyceride, lipoprotein of high density and lipoprotein of low density in serum were measured by using GOD-PAP, CHOD-PAP, GPO-PAP and PVS. The subjects were classified into three groups according to the score of occupational stress. RESULTS: The contents of blood glucose of low, middle and high level of stress groups were (3.39 +/- 1.24), (3.59 +/- 1.26), (2.54 +/- 0.94) mmol/L respectively (F = 7.324, P < 0.01), and with the increase of level of stress, the content of blood glucose decreased significantly (r = -0.376, P < 0.01). CONCLUSION: The level of blood glucose of VDT operators is affected by occupational stress, among video display terminals and it can be used as the index for estimating occupational stress.

Spontaneously hypertensive rats are sensitive to thoracic aorta damage induced by a hot and humid environment.

The purpose of this study was to investigate the effect of a hot and humid environment on thoracic aorta damage in spontaneously hypertensive rats (SHRs). Wistar-Kyoto (WKY) rats were randomly divided into three groups (n=8 in each group): Control group (WKY-CN), heat exposure for 8 h group (WKY-8) and heat exposure for 24 h group (WKY-24). The CN group was exposed to room temperature (24°C); WKY-8 and WKY-24 group were exposed to heat (32°C) and 65% relative humidity for 8 and 24 h, respectively. Accordingly, SHRs were randomly divided into three groups (n=8 each group): SHR-CN, SHR-8 and SHR-24. After 7 days of heat exposure, the weight, food consumption and blood pressure of rats was measured. Noradrenaline (NA)-induced contraction of aorta rings was measured using an organ bath system, and vascular morphology was observed. Expression levels of apoptotic genes and proteins in the thoracic aorta were also measured. The experimental results indicated that, in the heat exposure environment, rat food intake was reduced. Rat weight was significantly increased in all groups except SHR-24 (all P<0.01 except SHR-8, P<0.05). Heat exposure significantly increased the blood pressure of rats in the WKY-24 (P<0.01 for systolic; P<0.05 for diastolic), SHR-8 and SHR-24 (all P<0.01) groups. This effect was more notable in SHR compared with WKY. NA-induced contraction of aorta rings significantly increased in the SHR-CN group, compared with the WKY-CN group (P<0.01). Heat exposure significantly elevated the NA-induced contraction in both 8 h groups compared with the CN groups (P<0.01). This effect was accompanied by structural damage to the thoracic aorta and increased expression of apoptotic genes and proteins. In conclusion, thoracic aorta damages in SHRs were more sensitive to heat exposure. The enhanced NA-induced contraction may have partly been due to increased apoptosis in the thoracic aorta.

Effect of dehydration heat exposure on thoracic aorta reactivity in rats.

The aim of the present study was to investigate the effect of one week dehydration heat exposure on thoracic aorta reactivity in rats. Eighteen Male Sprague-Dawley rats were randomly divided into 3 groups (n=6 each group): Control group (CN), heat exposure group (HE), dehydration heat exposure group (DHE). The CN group was exposed to a room temperature of 24°C, while the HE and DHE groups were exposed to a heat temperature of 32°C. After 7 days of heat exposure, the heart rate and blood pressure of the rats were measured, and the noradrenaline (NA)-induced contraction on the aorta rings was measured by tension recording. The average contents of malondialdehyde (MDA) and superoxide dismutase (SOD) in serum were detected using ELISA. The expression of apoptotic genes in the thoracic aorta was measured using RT-PCR. Compared with CN, the heart rate in the HE and DHE groups had a tendency to become retarded, but there was no significant difference (P>0.05). In the HE group, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) of the rats were significantly higher than that of the CN (P<0.05). In the DHE group, the SBP of rats was significantly higher than that of the CN (P<0.05), while the SBP, DBP, and MAP of the rats were decreased compared to the rats in the HE group, although there was no statistical significance (P>0.05). In the HE and DHE groups, the NA-induced contraction on the rats thoracic aorta ring was larger than that of the CN (P<0.05), albeit there was no significant difference between the HE and DHE groups (P>0.05). The serum SOD content decreased in the HE and DHE groups, however, the reduction was significant only in the DHE group (P<0.05). The content of MDA in serum was significantly increased in the DHE group (P<0.05). The expression of BAX was significantly upregulated whereas Bcl2 expression was decreased in the DHE group (P<0.05). The results showed that a high temperature was harmful to the body, especially in the case of lack of food and water. Additionally, the heat exposure elevated blood pressure, and increased arterial reactivity, which were related to the elevated production of MDA, led to the impaired production of SOD, and an increase of cell apoptosis. These findings are useful to understand the influence of dehydrated heat exposure on the vascular function, and they provide certain theoretical and experimental guidance for protection under high temperature.

Effect of acute heat stress on adrenocorticotropic hormone, cortisol, interleukin-2, interleukin-12 and apoptosis gene expression in rats.

The aim of the present study was to investigate the effect of acute heat stress on the neuroendocrine and immunological function in rats. Male Sprague-Dawley rats were randomly divided into two groups and respectively exposed to heat (32°C) or to room temperature (24°C). After 7 days of heat exposure, the heat-stress rat model was established. The organ coefficients of the pituitary and adrenal glands were determined. The body temperature was measured by telemetry. The average contents of adrenocorticotropic hormone (ACTH), cortisol (Cor), interleukin-2 (IL-2) and IL-12 in serum were detected. The expression of apoptotic genes in the spleen was measured. The results showed that acute heat stress did not evidently affect the body temperature and body weight (P>0.05), but the exposure increased the organ coefficients of the pituitary and adrenal glands (P<0.05). Heat exposure significantly elevated the level of ACTH, Cor, IL-2 and IL-12 (P<0.05). The expression of caspase-3 and Bax were not changed significantly (P>0.05), while Bcl2 was reduced (P<0.05).

Effects of Lycium barbarum polysaccharides on oxidative stress in hyperlipidemic mice following chronic composite psychological stress intervention.

Chronic composite psychological stress intervention is the accumulation of factors which may induce psychological stress, including food deprivation, water deprivation and swimming in cold water. Approximately 40% of cases of atherosclerosis are associated with chronic composite psychological stress. The aim of the present study was to explore the effects of Lycium barbarum polysaccharides (LBP) on blood lipid levels and oxidative stress in hyperlipidemic mice, following chronic composite psychological stress. A hyperlipidemic mouse model was generated, and the mice were subjected to chronic composite psychological stress and treated with LBP for 30 days. After 30 days the triglyceride (TG) and total cholesterol (TC) levels were measured in the serum, and the mRNA expression levels of cholesterol 7α­hydroxylase (CYP7A1) were determined in the liver, in order to observe any changes to lipid metabolism. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured in the liver to evaluate the effects of LBP on oxidative stress. The blood serum levels of interleukin­6 (IL­6) and heat shock protein 70 (HSP­70) were measured to evaluate the extent of the aortic inflammatory response, and to determine the protective effects of LBP. The levels of TG, TC, MDA and IL­6 were significantly higher in the mice subjected to chronic composite psychological stress (HS), as compared with the mice treated with LBP alone (HL), or treated with LBP and subjected to stress (HLS). In addition, SOD and HSP­70 levels, and the mRNA expression levels of CYP7A1 were significantly lower in the HS group, as compared with that in the HL and HLS groups. These results suggest that chronic composite psychological stress may promote the occurrence and development of atherosclerosis, by inducing the aortic inflammatory response and lipid peroxidation. Furthermore, treatment with LBP significantly inhibited oxidative stress and the aortic inflammatory response.