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In the field of photocatalytic degradation, the separation and recycle technology of powdery g-C3N4 after usage has not been mature, which causes secondary pollution problems for large-scale industrial applications. In this paper, carbon-fiber/g-C3N4 nanosheet arrays were fabricated by chemical vapor deposition(CVD) under argon protection, and the optical, electrochemical and photocatalytic performance of carbon-fiber/g-C3N4 nanosheet arrays were studied. The results indicated that carbon-fiber/g-C3N4 nanosheet arrays generated photon-excited electrons and holes under visible light irradiation during photocatalytic process. The excellent electrical conductivity of carbon fiber could trap photon-excited electrons in conduction band of g-C3N4 nanosheet and creat holes in valence band of g-C3N4 nanosheet. 20.7%, 33.5% and 99.5% of 2, 4-dinitrophenol were degraded by photocatalysis, electrocatalysis and photoelectrocatalysis of carbon-fiber/g-C3N4 nanosheet arrays within 240 min. The external voltage further enhanced the separation of photo-generated electrons and holes, which made the photoelectrocatalysis of carbon-fiber/g-C3N4 nanosheet arrays exerted unexpected performance through synergistic interactions of photocatalysis and electrocatalysis. The assembly of powdery photocatalysts and carbon fibers textile might provide a general methodology in the design of separable and recyclable photocatalysts with broad applications in environment-related fields. The assembly strategy developed herein significantly reduced the separable and recyclable cost of powdery photocatalysts and offered valuables references for industrial application of photocatalysis and photoelectrocatalysis.

Objective: To observe and verify the changes of transcriptome in hyperoxia-induced acute lung injury (HALI), and to further clarify the changes of pathways in HALI., Methods: Twelve healthy male C57BL/6J mice were randomly divided into normoxia group and HALI group according to the random number table, with 6 mice in each group. The mice in the normoxia group were fed normally in the room, and the mice in the HALI group was exposed to 95% oxygen to reproduce the HALI animal model. After 72 hours of hyperoxia exposure, the lung tissues were taken for transcriptome sequencing, and then Kyoto Encyclopedia of Genes and Genomes database (KEGG) pathway enrichment analysis was performed. The pathological changes of lung tissue were observed under light microscope after hematoxylin-eosin (HE) staining. Real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were used to verify the key molecules in the signal pathways closely related to HALI identified by transcriptomics analysis., Results: Transcriptomic analysis showed that hyperoxia induced 537 differentially expressed genes in lung tissue of mice as compared with the normoxia group including 239 up-regulated genes and 298 down-regulated genes. Further KEGG pathway enrichment analysis identified 20 most significantly enriched pathway entries, and the top three pathways were ferroptosis signaling pathway, p53 signaling pathway and glutathione (GSH) metabolism signaling pathway. The related genes in the ferroptosis signaling pathway included the up-regulated gene heme oxygenase-1 (HO-1) and the down-regulated gene solute carrier family 7 member 11 (SLC7A11). The related genes in the p53 signaling pathway included the up-regulated gene tumor suppressor gene p53 and the down-regulated gene murine double minute 2 (MDM2). The related gene in the GSH metabolic signaling pathway was up-regulated gene glutaredoxin 1 (Grx1). The light microscope showed that the pulmonary alveolar structure of the normoxia group was normal. In the HALI group, the pulmonary alveolar septum widened and thickened, and the alveolar cavity shrank or disappeared. RT-RCR and Western blotting confirmed that compared with the normoxia group, the mRNA and protein expressions of HO-1 and p53 in lung tissue of the HALI group were significantly increased [HO-1 mRNA (2 -ΔΔCt ): 2.16±0.17 vs. 1.00±0.00, HO-1 protein (HO-1/β-actin): 1.05±0.01 vs. 0.79±0.01, p53 mRNA (2 -ΔΔCt ): 2.52±0.13 vs. 1.00±0.00, p53 protein (p53/β-actin): 1.12±0.02 vs. 0.58±0.03, all P < 0.05], and the mRNA and protein expressions of Grx1, MDM2, SLC7A11 were significantly decreased [Grx1 mRNA (2 -ΔΔCt ): 0.53±0.05 vs. 1.00±0.00, Grx1 protein (Grx1/β-actin): 0.54±0.03 vs. 0.93±0.01, MDM2 mRNA (2 -ΔΔCt ): 0.48±0.03 vs. 1.00±0.00, MDM2 protein (MDM2/β-actin): 0.57±0.02 vs. 1.05±0.01, SLC7A11 mRNA (2 -ΔΔCt ): 0.50±0.06 vs. 1.00±0.00, SLC7A11 protein (SLC7A11/β-actin): 0.72±0.03 vs. 0.98±0.01, all P < 0.05]., Conclusions: HALI is closely related to ferroptosis, p53 and GSH metabolism signaling pathways. Targeting the key targets in ferroptosis, p53 and GSH metabolism signaling pathways may be an important strategy for the prevention and treatment of HALI.

Objective: To investigate the effect of hyperoxia on intestinal metabolomics in mice., Methods: Sixteen 8-week-old male C57BL/6 mice were randomly divided into hyperoxia group and control group, with 8 mice in each group. The hyperoxia group was exposed to 80% oxygen for 14 days. Mice were anesthetized and euthanized, and cecal contents were collected for untargeted metabolomics analysis by liquid chromatography-mass spectrometry (LC-MS) combined detection. Orthogonal partial least square discriminant analysis (OPLS-DA), volcano plot analysis, heat map analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to analyze the effects of hyperoxia on metabolism., Results: (1) OPLS-DA analysis showed that R 2 Y was 0.967 and Q 2 was 0.796, indicating that the model was reliable. (2) Volcano plot and heat map analysis showed significant statistical differences in the expression levels of metabolites between the two groups, with 541 up-regulated metabolites, 64 down-regulated metabolites, and 907 no differences, while the elevated 5-hydroxy-L-lysine was the most significant differential metabolite induced by high oxygen. (3) KEGG pathway enrichment analysis showed that porphyrin and chlorophyll metabolism (P = 0.005), lysine degradation (P = 0.047), and aromatic compound degradation (P = 0.024) were the targets affected by hyperoxia. (4) Differential analysis of metabolic products through KEGG enrichment pathway showed that hyperoxia had a significant impact on the metabolism of porphyrin and chlorophyll, lysine, and aromatic compounds such as benzene and o-cresol., Conclusions: Hyperoxia significantly induces intestinal metabolic disorders. Hyperoxia enhances the metabolism of porphyrins and chlorophyll, inhibits the degradation of lysine, and delays the degradation of aromatic compounds such as benzene and o-cresol.

Objective: To explore the effects of heme oxygenase-1 (HO-1) on the apoptosis, expression of caspase-3 and cytochrome-C (Cyt-C) on hydrogen peroxide (H(2)O(2)) oxidative damage in primary cultured rat's type II alveolar epithelium cell (AECII)., Methods: AECII from male Sprague-Dawley (SD) rats were separated and cultured. The cells were randomly divided into four groups: control group (A group, the cells were cultured with normal saline), H(2)O(2) group (B group, cultured with 0.5 mmol/L H(2)O(2)), HO-1 pretreatment group (C group, pretreatment with 0.2 μmol/L HO-1 for 2 hours followed by 0.5 mmol/L H(2)O(2)), HO-1 inhibition group [D group, pretreatment with 10 μmol/L zinc protoporphyrin IX (ZnppIX) for 2 hours followed by 0.5 mmol/L H(2)O(2)]. The cells in each group were cultured after different treatment. The cell apoptosis rate was determined by flow cytometry at 2, 6, 12 hours after the intervention. The protein expression of caspase-3 and Cyt-C were determined by Western Blot., Results: The cell apoptosis rate in each group was gradually increased with prolonged time of H(2)O(2) treatment. The apoptosis rate at different time points after treatment in B group was significantly higher than that in A group, while the rate in C group was significantly lower than that in B group [2 hours: (11.46 ± 1.47)% vs. (20.83 ± 1.55)%, 6 hours: (12.30 ± 1.37)% vs. (27.14 ± 1.53)%, 12 hours: (12.62 ± 1.39)% vs. (35.66 ± 0.74)%, all P<0.05]. There were no significant differences in apoptotic rate at 2, 6, 12 hours between D group [(24.33 ± 1.36)%, (31.67 ± 1.24)%, (36.93 ± 2.40)%] and B group. The protein expression of caspase-3 and Cyt-C was gradually increased with prolonged time of H(2)O(2) treatment. The protein expression of caspase-3 and Cyt-C at different time points in B group was significantly higher than that in A group. The protein expression of caspase-3 (gray scale) in C group was significantly lower than that in B group (2 hours: 0.250 ± 0.039 vs. 0.650 ± 0.072, 6 hours: 0.470 ± 0.080 vs. 0.960 ± 0.118, 12 hours: 0.680 ± 0.099 vs. 1.830 ± 0.220, all P<0.05), and the Cyt-C protein expression (gray scale) was also significantly lowered in C group (2 hours: 0.250 ± 0.074 vs. 0.390 ± 0.069, 6 hours: 0.340 ± 0.043 vs. 0.670 ± 0.120, 12 hours: 0.470 ± 0.072 vs. 1.360 ± 0.112, all P<0.05). There were no significant differences in protein expression of caspase-3 and Cyt-C between D group (caspase-3: 0.720 ± 0.052, 1.060 ± 0.109, 1.880 ± 0.159; Cyt-C: 0.500 ± 0.110, 0.860 ± 0.050, 1.480 ± 0.140) and B group., Conclusions: HO-1 preconditioning reduced the apoptotic rate of the AECII oxidative damaged by H(2)O(2) at different time points (2-12 hours) and decreased the expression of caspase-3 and Cyt-C. The mitochondrial apoptosis pathway participated in the protection mechanism of HO-1 in oxidative damage AECII.