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Objective To evaluate the effect of hydrogen on autophagy during inflammatory responses following lung injury in burned mice.Methods Ninety-six clean-grade healthy male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 4 groups (n=24 each) using a random number table:sham operation group (SH group),H2 group (H2 group),burn group (B group) and burn plus H2 group (B+H2 group).Forty percent of the total body surface was shaved with 80 g/L sodium sulfide and then exposed to a 92 ℃ scald device for 18 s in B and B+H2 groups.Forty percent of the total body surface was shaved with 80 g/L sodium sulfide and then exposed to a scald device of skin temperature for 18 s in SH and H2 groups.Mice inhaled 2％ H2 for 1 h starting from 1 and 6 h after burn in H2 and B+H2 groups.The animals were sacrificed at 24 h after burn and lungs were removed for determination of wet/dry weight ratio (W/D rario),expression of autophagy-related microtubule-associated protein 1 light chain 3 (LC3) (by Western blot),activity of myeloperoxidase (MPO),and contents of interleukin-6 (IL-6) and high mobility group box 1 (HMGBI) (by enzyme-linked immunosorbent assay).The ratio of LC3-Ⅱ to LC3-Ⅰ expression (LC3-Ⅱ/LC3-Ⅰ) was calculated.The bronchoalveolar lavage fluid (BALF) was collected at 24 h after burn to detect the concentrations of IL-6 and HMGB1 and to count neutrophil.Results Compared with group SH,the W/D ratio,levels of LC3-Ⅱ/LC3-Ⅰ,MPO,IL-6 and HMGB1,concentrations of IL-6 and HMGB1 in BALF and neutrophil count were significantly increased at 24 h after scald in B and B+H2 groups (P＜0.05).Compared with group B,the W/D ratio,levels of LC3-Ⅱ/LC3-Ⅰ,MPO,IL-6 and HMGB1,concentrations of IL-6 and HMGBl in BALF and neutrophil count were significantly decreased at 24 h after scald in group B+H2 (P＜0.05).Conclusion Hydrogen can alleviate the lung injury in burned mice,and the mechanism is related to enhancing autophagy.
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Objective@#To investigate the effects of hydrogen on the lung damage of mice at early stage of severe burn.@*Methods@#One hundred and sixty ICR mice were divided into sham injury, hydrogen, pure burn, and burn+ hydrogen groups according to the random number table, with 40 mice in each group. Mice in pure burn group and burn+ hydrogen group were inflicted with 40% total body surface area full-thickness scald (hereafter referred to as burn) on the back, while mice in sham injury group and hydrogen group were sham injured. Mice in hydrogen group and burn+ hydrogen group inhaled 2% hydrogen for 1 h at post injury hour (PIH) 1 and 6, respectively, while mice in sham injury group and pure burn group inhaled air for 1 h. At PIH 24, lung tissue of six mice in each group was harvested, and then pathological changes of lung tissue were observed by HE staining and the lung tissue injury pathological score was calculated. Inferior vena cava blood and lung tissue of other eight mice in each group were obtained, and then content of high mobility group box 1 (HMGB1) and interleukin-6 (IL-6) in serum and lung tissue was determined by enzyme-linked immunosorbent assay. Activity of superoxide dismutase (SOD) in serum and lung tissue was detected by spectrophotometry. After arterial blood of other six mice in each group was collected for detection of arterial partial pressure of oxygen (PaO2), the wet and dry weight of lung tissue were weighted to calculate lung wet to dry weight ratio. The survival rates of the other twenty mice in each group during post injury days 7 were calculated. Data were processed with one-way analysis of variance, LSD test and log-rank test.@*Results@#(1) At PIH 24, lung tissue of mice in sham injury group and hydrogen group showed no abnormality. Mice in pure burn group were with pulmonary interstitial edema, serious rupture of alveolar capillary wall, and infiltration of a large number of inflammatory cells. Mice in burn+ hydrogen group were with mild pulmonary interstitial edema, alveolar capillary congestion accompanied by slight rupture and bleeding, and the number of infiltration of inflammatory cells was smaller than that in pure burn group. The lung tissue injury pathological scores of mice in sham injury group, hydrogen group, pure burn group, and burn+ hydrogen group were (0.7±0.5), (0.8±0.5), (6.1±1.0), and (2.8±0.8) points, respectively. The lung tissue injury pathological score of mice in pure burn group was significantly higher than that in sham injury group (P<0.001). The lung tissue injury pathological score of mice in burn+ hydrogen group was significantly lower than that in pure burn group (P<0.001). (2) At PIH 24, the content of HMGB1 and IL-6 in serum and lung tissue of mice in hydrogen group was close to that in sham injury group (with P values above 0.05). The content of HMGB1 and IL-6 in serum and lung tissue of mice in pure burn group was significantly higher than that in sham injury group (with P values below 0.001). The content of HMGB1 and IL-6 in serum and lung tissue of mice in burn+ hydrogen group was significantly lower than that in pure burn group (with P values below 0.001). (3) At PIH 24, the activity of SOD in serum and lung tissue of mice in hydrogen group was close to that in sham injury group (with P values above 0.05). The activity of SOD in serum and lung tissue of mice in pure burn group was significantly lower than that in sham injury group (with P values below 0.001). The activity of SOD in serum and lung tissue of mice in burn+ hydrogen group was significantly higher than that in pure burn group (with P values below 0.001). (4) At PIH 24, there was no statistically significant difference in PaO2 among the mice in four groups (F=0.04, P>0.05). (5) At PIH 24, the ratios of lung wet to dry weight of mice in sham injury, hydrogen, pure burn, and burn+ hydrogen groups were 3.52±0.22, 3.61±0.24, 7.24±0.32, and 5.21±0.41, respectively. The ratio of lung wet to dry weight of mice in pure burn group was significantly higher than that in sham injury group (P<0.001). The ratio of lung wet to dry weight of mice in burn+ hydrogen group was significantly lower than that in pure burn group (P<0.001). (6) The survival rates of mice in sham injury group and hydrogen group during post injury days 7 were 100%. Compared with those in sham injury group, survival rates of mice in pure burn group from post injury days 3 to 7 were significantly decreased (with P values below 0.05). Compared with those in pure burn group, survival rates of mice in burn+ hydrogen group from post injury days 5 to 7 were significantly increased (with P values below 0.05).@*Conclusions@#Hydrogen can significantly alleviate the infiltration of inflammatory cells and improve the pathological lesions of lung tissue of mice with severe burn. It has the effects of reducing inflammatory reaction and inhibiting oxidative stress, further showing the protective effect on the lung of burn mice.
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Objective To explore the impact of dexamethasone on inflammatory response of thyrocytes.Methods Primary thyrocytes were extracted from thyroid tissue of patients with Graves' disease.The cells were stimulated with interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α),and cultured in dexamethasone.Thyrocytes were divided into 4 groups:control group,dexamethasone group,TNF-α + IFN-γ group,and dexamethasone+TNF-α+IFN-γ group.Interferon-γ-induced protein 10 (CXCL10) and CCL2 in supernatant of cell cultured in 4 groups were detected by enzyme-linked immunosorbent assay.Cell protein in 4 groups was extracted and GSK-3β,P50,and P100 protein were detected by Western blotting.Results MTT assay demonstrated that 10-5 mmol/L concentration of dexamethasone was optimal for cell culture.The CXCL10 level in TNF-α+IFN-γ group was higher than that in the control group and dexamethasone group (P＜0.01),but no difference was found between dexamethasone+TNF-α+IFN-γgroup and TNF-α+IFN-γgroup(P＞0.05).The CCL2 level in TNF-α+IFN-γ group was higher than that in control group and dexamethasone group(P＜0.01).There was a significant lowering of CCL2 level in dexamethasone + TNF-α + IFN-γgroup compared with TNF-α + IFN-γ group (P ＜ 0.05).The expression of GSK-3β and P100 protein was increased in TNF-α + IFN-γgroup compared with control group.The expression of GSK-3β and P100 protein was lower in dexamethasone+TNF-α + IFN-γ group than that in TNF-α + IFN-γ group.Conclusion TNF-α + IFN-γ could stimulate the secretion of CXCL10 and CCL2 in thyrocytes and thus activate the inflammatory response.Dexamethasone could reduce CCL2 secretion.Dexamethasone had little effect on CXCL10.Dexamethasone could reduce GSK-3β and P100 expressions,and inhibit the activation of NF-κB signaling pathway and thus the inflammatory response.
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ObjectiveTo study the associations of Val66Met functional polymorphism in brain-derived neurotrophic factor (BDNF)with creativity and personality traits in a healthy college student population.MethodThe creativity performance and personality traits of the 830 healthy college students (272 males and 558females) were assessed with Williams Creativity Scale (CAP) and adult Eysenek Personality Questionnaire (EPQ),then study was performed on the association Val66Met in BDNF with creativity and personality traits.ResultsThe results indicated that Val66Met was significantly associated with the curiosity of CAP (F=0.519,P=0.036).The numbers of Val allele showed a positive correlation to the performance of curiosity.Val66Val genotype individuals had the best performance (31.924 ± 4.010 ) while the Met66Met ones showed the worst performante(30.889 ± 3.478).However,the association of Val66Met with the personality traits of EPQ was uot significant in the study (P＞ 0.05).Furthermore,there was no a significant effect of the interaction between the genetic variant and Extraversion/Introversion on the curiosity of CAP (P =0.747 ).ConclusionThe present study suggests that Val66Met in BDNF contributes to creativity,but not to personality traits in the population.