Multi-functional integrated design of a copper foam-based cathode for high-performance lithium-oxygen batteries.

Lithium-oxygen batteries (LOBs) with extraordinarily high energy density are some of the most captivating energy storage devices. Designing an efficient catalyst system that can minimize the energy barriers and address the oxidant intermediate and side-product issues is the major challenge regarding LOBs. Herein, we have developed a new type of integrated cathode of Cu foam-supported hierarchical nanowires decorated with highly catalytic Au nanoparticles which achieves a good combination of a gas diffusion electrode and a catalyst electrode, contributing to the synchronous multiphase transport of ions, oxygen, and electrons as well as improving the cathode reaction kinetics effectively. Benefiting from such a unique hierarchical architecture, the integrated cathode delivered superior electrochemical performance, including a high discharge capacity of up to 11.5 mA h cm-2 and a small overpotential of 0.49 V at 0.1 mA cm-2, a favorable energy efficiency of 84.3% and exceptional cycling stability with nearly 1200 h at 0.1 mA cm-2 under a fixed capacity of 0.25 mA h cm-2. Furthermore, density functional theory (DFT) calculations further reveal the intrinsic direct catalytic ability to form/decompose Li2O2 during the ORR/OER process. As a consequence, this work provides an insightful investigation on the structural engineering of catalysts and holds great potential for advanced integrated cathode design for LOBs.

Ameliorative Effect of Macadamia Nut Protein Peptides on Acetaminophen-Induced Acute Liver Injury in Mice.

This study aims to examine the ameliorative effect of macadamia nut protein peptides (MPP) on acetaminophen (APAP)-induced liver injury (AILI) in mice, and develop a new strategy for identifying hepatoprotective functional foods. The molecular weight distribution and amino acid composition of MPP were first studied. Forty mice were then randomized into four groups: control group (CON), APAP model group, APAP+MPP low-dose group (APAP+L-MPP), and APAP+MPP high-dose group (APAP+H-MPP). The APAP+L-MPP (320 mg/kg per day) and APAP+H-MPP (640 mg/kg per day) groups received continuous MPP gavage for 2 weeks. A 12 h of APAP (200 mg/kg) gavage resulted in liver damage. Pathological alterations, antioxidant index levels, expression of toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB), and associated inflammatory factors were determined for each treatment group. The results revealed that the total amino acid content of MPP was 39.58 g/100 g, with Glu, Arg, Asp, Leu, Tyr, and Gly being the major amino acids. The molecular weight range of 0-1000 Da accounted for 73.54%, and 0-500 Da accounted for 62.84% of MPP. MPP ameliorated the pathological morphology and reduced the serum levels of alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase of AILI in mice. MPP significantly increased the activities of superoxide dismutase and glutathione peroxidase in the liver compared with the APAP group. MPP inhibited the expression of TLR4, NF-κB, interleukin-1ß (IL-1ß), and tumor necrosis factor-α (TNF-α) genes in AILI mice. MPP also inhibited the expression levels of inflammatory factors (TNF-α and IL-6). Our study concludes that MPP alleviates AILI in mice by enhancing antioxidant capacity and inhibiting TLR4/NF-κB pathway-related gene activation.

In Situ 1D Carbon Chain-Mail Catalyst Assembly for Stable Lithium-Sulfur Full Batteries.

The main obstacles for the commercial application of Lithium-Sulfur (Li-S) full batteries are the large volume change during charging/discharging process, the shuttle effect of lithium polysulfide (LiPS), sluggish redox kinetics, and the indisciplinable dendritic Li growth. Especially the overused of metal Li leads to the low utilization of active Li, which seriously drags down the actual energy density of Li-S batteries. Herein, an efficient design of dual-functional CoSe electrocatalyst encapsulated in carbon chain-mail (CoSe@CCM) is employed as the host both for the cathode and anode regulation simultaneously. The carbon chain-mail constituted by carbon encapsulated layer cross-linking with carbon nanofibers protects CoSe from the corrosion of chemical reaction environment, ensuring the high activity of CoSe during the long-term cycles. The Li-S full battery using this carbon chain-mail catalyst with a lower negative/positive electrode capacity ratio (N/P < 2) displays a high areal capacity of 9.68 mAh cm-2 over 150 cycles at a higher sulfur loading of 10.67 mg cm-2 . Additionally, a pouch cell is stable for 80 cycles at a sulfur loading of 77.6 mg, showing the practicality feasibility of this design.

Hydroxytyrosol mitigates Mycoplasma gallisepticum-induced pulmonary injury through downregulation of the NF-κB/NLRP3/IL-1ß signaling pathway in chicken.

In this study, the anti-inflammatory and antiapoptotic effects of hydroxytyrosol (HT) in Mycoplasma gallisepticum (MG)-infected chicken were investigated, and the underlying molecular mechanisms were explored. The results revealed severe ultrastructural pathological changes after MG infection in the lung tissue of chicken, including inflammatory cell infiltration, thickening of the lung chamber wall, visible cell swelling, mitochondrial cristae rupture, and ribosome shedding. MG possibly activated the nuclear factor κB (NF-κB)/nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)/interleukin (IL)-1ß signaling pathway in the lung. However, HT treatment significantly ameliorated MG-induced pathological damage of the lung. HT reduced the magnitude of pulmonary injury after MG infection by reducing apoptosis and releasing the proinflammatory factors. Compared with the MG-infected group, the HT-treated group exhibited significant inhibition of the expression of NF-κB/NLRP3/IL-1ß signaling-pathway-related genes; for example, the expressions of NF-κB, NLRP3, caspase-1, IL-1ß, IL-2, IL-6, IL-18, and TNF-α significantly decreased (P < 0.01 or <0.05). In conclusion, HT effectively inhibited MG-induced inflammatory response and apoptosis and protected the lung by blocking the activation of NF-κB/NLRP3/IL-1ß signaling pathway and reducing the damage caused by MG infection in chicken. This study revealed that HT may be a suitable and effective anti-inflammatory drug against MG infection in chicken.

Molecular mechanism of anti-inflammatory effects of the proteasome inhibitor MG-132 on Con A-induced acute liver injury in mice.

MG-132, an aldehyde-based peptide proteasome inhibitor (PI) that binds to the proteasome and reversibly inhibits proteasome activity, has been widely used in experimental research. However, it is not clear whether MG-132 has anti-inflammatory effects on liver injury. The molecular mechanism of the anti-inflammatory effect of the PI MG-132 on Con A-induced acute liver injury (ALI) mice was investigated by ELISA, HE, q RT-PCR, and IHC. The results showed that the serum activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and TNF-α and IL-6 contents of mice in the high and medium dose groups were reduced compared with those in the ALI group. The superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels in liver tissues were significantly increased, and the malondialdehyde (MDA) content was decreased. The pathological sections of mice in the ALI group showed typical ALI manifestations such as significant central venous stasis of liver tissues, cell swelling, and inflammatory cell infiltration. The pathological damage of liver tissues was relieved significantly in the three dose groups, especially in the high-dose group. The transcriptional level of TLR4/NF-κB pathway key factors mRNA was significantly reduced, and the expression of TLR4 and NF-κB P65 protein in liver tissues was significantly and positively correlated with the contents of TNF-α and IL-1ß (p < 0.01). Our findings suggest that MG-132 can alleviate the inflammatory response to Con A-induced ALI and exert a hepatoprotective effect, and its anti-inflammatory effect is related to the inhibition of TLR4/NF-κB signaling pathway activation.

Oleocanthal alleviated lipopolysaccharide-induced acute lung injury in chickens by inhibiting TLR4/NF-κB pathway activation.

This study aimed to investigate the ameliorative effect of oleocanthal (OC) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in chickens and its possible mechanisms. In total, 20 chickens were randomly divided into 4 groups: control (CON) group, LPS group, LPS + OC group, and OC group. LPS + OC and OC groups were intragastrically administered a 5 mg/kg·d OC dose for 7 d. On d 8, the LPS group and LPS + OC group were intratracheally administered 2 mg/kg LPS for 12 h. It was found that OC ameliorated the pathological morphology and significantly suppressed apoptosis after OC treatment in LPS-induced ALI chicken (P < 0.01). Antioxidant capacity was higher in the LPS + OC group compared with the LPS group (P < 0.01). OC downregulated the related genes and proteins expression of toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB) pathway in LPS group (P < 0.01). In conclusion, OC supplementation can alleviate LPS-induced ALI in chickens by suppressing apoptosis, enhancing lung antioxidant capacities and inhibiting TLR4/NF-κB pathway activation.

Ellagic acid Alleviates hepatic ischemia-reperfusion injury in C57 mice via the Caspase-1-GSDMD pathway.

BACKGROUND: Ellagic acid (EA) has improving function against oxidative damage and inflammatory reaction in many disorders. Hepatic ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in the veterinary clinic. In the present study, the protective effects of EA pretreatment against hepatic IRI-induced injury and the underlying mechanisms were investigated. RESULTS: We found that pyroptosis is involved in hepatic IRI, which is manifested in increasing the expression of pyroptosis-related genes and promoting the expression of active caspase-1, thereby cleaving GSDMD-N to cause pyroptosis, and caspase-1-/- mice were used to verify this conclusion. In addition, we found that EA protects against hepatic IRI by inhibiting pyroptosis, including reducing the activity of caspase-1 and its expression in the liver, inhibiting the lysis of GSDMD-N, and reducing the levels of IL-18 and IL-1ß. CONCLUSIONS: The present results have demonstrated that prophylactic administration of EA ameliorated hepatic IRI by inhibiting pyroptosis induced in hepatic ischemia-reperfusion in vivo through the caspase-1-GSDMD axis, providing a potential therapeutic option prevent hepatic IRI in pets.

Hydroxytyrosol alleviates dextran sodium sulfate-induced colitis by inhibiting NLRP3 inflammasome activation and modulating gut microbiota in vivo.

OBJECTIVE: An increase in the global prevalence of inflammatory bowel disease has been reported in recent years. Although its pathogenesis has not been fully elucidated, inflammatory bowel disease is highly correlated with intestinal oxidative stress, immune disorders, overexpression of proinflammatory factors, and imbalance of gut microbiota. Hydroxytyrosol (HT), extracted from olive oil and leaves, exhibits significant antioxidant and antiinflammatory activities. METHODS: Therefore, this study sought to evaluate whether the antiinflammatory effect of HT on dextran sodium sulfate (DSS)-induced ulcerative colitis in mice is regulated by targeting the NLRP3 inflammasome and gut microbiota. RESULTS: Colon pathologic morphology and apoptosis were found to be ameliorated in the DSS + HT group compared to the DSS group. Antioxidant capacity was higher in the DSS + HT group than in the DSS group (P < 0.01). HT suppressed expression levels of NLRP3, caspase-1, and ASC mRNA and downregulated interleukin-18 and interleukin-1ß levels in the DSS group (P < 0.01). Furthermore, HT exerted a shift from pathogens to probiotics, and increased the levels of short-chain fatty acids (P < 0.01) in the DSS group. CONCLUSION: In summary, HT supplementation exerts antiinflammatory effects in DSS-induced ulcerative colitis by enhancing colonic antioxidant capacities, inhibiting NLRP3 inflammasome activation, and modulating gut microbiota in vivo.

Immunomodulatory and antioxidant effects of hydroxytyrosol in cyclophosphamide-induced immunosuppressed broilers.

As an important olive component, hydroxytyrosol (HT) has good medicinal and health effects. However, its importance in alleviating immune suppression in broilers has not been established. Therefore, we aimed at evaluating the immunomodulatory and antioxidant effects of HT in immune suppressed broilers. Immune suppressed broiler models were established via intraperitoneal injection of 80 mg/kg cyclophosphamide (Cy). Thirty two Cobb 500 male broilers were randomly allocated into 4 groups of 8 each. Broilers in the model (Cy) and HT treatment (Cy+HT) groups were intraperitoneally administered with Cy (80 mg/kg BW) once a day for 3 d. From the 4th d, broilers in the Cy+HT and HT groups were treated with 0.5 mL of 200 mg/L HT solution, once a day, for 7 d. The Cy and Con groups were orally administered with normal saline. On the 14th and 28th d, serum and duodenal samples were obtained for testing. It was found that HT increased villi height (VH)/crypt depth (CD) ratio in the duodenum and suppressed serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels. Moreover, it elevated the expressions of CD4+ and CD8+ T lymphocytes. HT upregulated the mRNA expression levels of interleukin-2 (IL-2), interleukin-4 (IL-4), and interleukin-10 (IL-10), enhanced the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and downregulated malondialdehyde (MDA) levels in Cy-induced immune-suppressed broilers. In conclusion, HT can alleviate immune-suppression as well as enhance immunity and antioxidant activities in the local mucosa of small intestines in broilers. Therefore, it can be used as an immune stimulant. More studies should be performed to confirm our findings and to elucidate on the mechanisms of HT.

Walnut oil alleviates LPS-induced intestinal epithelial cells injury by inhibiting TLR4/MyD88/NF-κB pathway activation.

In this study, we investigated the protective effects of walnut oil (WO) on mouse intestinal epithelial cells using used MODE-K cells as a model and explored the underlying mechanisms. Our data suggested that WO attenuated lipopolysaccharide (LPS)-induced pathological changes and inhibited the rate of LPS-induced apoptosis in MODE-K cells. Furthermore, WO down-regulated LPS-induced gene and protein expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), nuclear factor-κB (NF-κB), tumor necrosis factor-α, and interleukin-6. In conclusion, this study shows that WO exerts an anti-inflammatory effect on LPS-induced MODE-K cells injury by inhibiting the TLR4/MyD88/NF-κB pathway activation. Based on our data, a prominent functional food candidate can be provided for inflammatory bowel disease treatment. PRACTICAL APPLICATIONS: Walnut oil (WO) has excellent anti-inflammatory properties and is widely used in traditional dietary supplements. However, whether WO causes anti-lipopolysaccharide (LPS)-induced intestinal injury remains unclear. In this study, we investigated the protective effects of WO on mouse intestinal epithelial cells using MODE-K cells as a model and explored their potential mechanisms. Our data showed that WO ameliorated the pathological morphology, inhibited the apoptosis of LPS-induced MODE-K cell injury, decreased the release of pro-inflammatory cytokines, and down-regulated the related genes and proteins expression of the LPS-TLR4/MyD88/NF-κB inflammatory pathway. The results of this study would enhance the utilization of WO in the prevention of gastrointestinal diseases in animals and humans inflammatory bowel disease as well as in functional foods formulations.

In Situ Electrochemical Intercalation-Induced Phase Transition to Enhance Catalytic Performance for Lithium-Sulfur Battery.

Accelerating the conversion of polysulfide to inhibit shutting effect is a promising approach to improve the performance of lithium-sulfur batteries. Herein, the hollow titanium nitride (TiN)/1T-MoS2 heterostructure nanospheres are designed with efficient electrocatalysis properties serving as a sulfur host, which is formed by in situ electrochemical intercalation from TiN/2H-MoS2 . Metallic, few-layered 1T-MoS2 nanosheets with abundant active sites decorated on TiN nanospheres enable fast electron transfer, high adsorption ability toward polysulfides, and favorable catalytic activity contributing to the conversion kinetics of polysulfides. Benefiting from the synergistic effects of these favorable features, the as-developed hollow TiN/1T-MoS2 nanospheres with advanced architecture design can achieve a high discharge capacity of 1273 mAh g-1 at 0.1 C, good rate performance with a capacity retention of 689 mAh g-1 at 2 C, and long cycling stability with a low-capacity fading rate of 0.051% per cycle at 1 C for 800 cycles. Notably, the TiN/1T-MoS2 /S cathode with a high sulfur loading of up to 7 mg cm-2 can also deliver a high capacity of 875 mAh g-1 for 50 cycles at 0.1 C. This work promotes the prospect application for TiN/1T-MoS2 in lithium-sulfur batteries.

Walnut oil alleviates DSS-induced colitis in mice by inhibiting NLRP3 inflammasome activation and regulating gut microbiota.

Ulcerative colitis (UC) has become a global disease and closely related to changes in intestinal oxidative stress, inflammatory factors and gut microbiota. Furthermore, the NLRP3 inflammasome activation is a key cause in the pathogenesis of dextran sulfate sodium (DSS)-induced colitis. Recent data showed the potential antioxidative and anti-inflammatory advantage of walnut oil, which widely used in traditional medicine and has become a dietary supplement for some patients. Therefore, we investigated whether walnut oil exerts an anti-inflammatory effect on DSS-induced colitis mice by targeting NLRP3 inflammasome and gut microbiota. Our data showed that walnut oil ameliorated the pathological morphology, decreased the reactive oxygen species (ROS) production and pro-inflammatory cytokines release, down-regulated the related gene proteins expression of NLRP3/ASC/Caspase-1 inflammatory pathway, inhibited apoptosis, shifted from more pathogens towards probiotics, and increased the levels of short-chain fatty acids (SCFAs) in DSS-induced damaging process. Collectively, our study concludes that walnut oil exerts anti-inflammatory effect on DSS-induced colitis in mice by inhibiting the NLRP3 inflammasome activation and modulating gut microbiota, and may be a prominent functional food candidate for UC treatment.

The protective effect of walnut oil on lipopolysaccharide-induced acute intestinal injury in mice.

Walnut oil (WO) is widely used in traditional medicine, and it has become a dietary supplement in many countries. We isolated walnut oil from Juglans sigillata and evaluated its protective effects on acute intestinal injury, and Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway in lipopolysaccharide (LPS)-induced mice was studied. The results showed that the LPS + WO group significantly decreased serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1ß levels and increased the jejunum superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels compared with the LPS group. Walnut oil ameliorated the pathological morphology of the LPS-induced acute jejunum injury and decreased jejunum cells apoptosis rate and TLR4/NF-κB protein expression. Furthermore, the expression of the TLR4/NF-κB pathway key gene mRNA significantly reduced after treatment with walnut oil. This study concludes that walnut oil can exert the protective effect on LPS-induced acute intestinal injury in mice by inhibiting the TLR4/NF-κB signaling pathway.

Effect of walnut (Juglans sigillata) oil on intestinal antioxidant, anti-inflammatory, immunity, and gut microbiota modulation in mice.

The study investigated the anti-oxidant, anti-inflammatory, immunity, and gut microbiota modulation in mice (n = 60; 15 mice/group) after intragastric administration of walnut oil (WO; three groups (low (LD), medium (MD), and high doses (HD): 2.5, 5, and 10 ml/kg, respectively) and normal control (NC, saline). WO significantly increased the median villous height/crypt depth (VH/CD) ratio, the activities of superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in intestinal mucosa. WO exerted the anti-inflammatory effects by decreasing the expression of tumor necrosis factor-α (TNF-α) in the duodenal mucosa. All groups shared 157 operational taxonomic units (OTUs; 97% similarity) representing nine phyla. The relative abundance in gut microbiota shifted from more pathogenic bacteria-Helicobacter (NC: 22% versus MD: 3%) toward probiotic-Lactobacillus (NC: 19% versus MD: 40%). The immune organ index (spleen) and contents of secretory immunoglobulin A (S-IgA) were increased from small intestine. In conclusion, WO decreased the oxidative stress, inflammation, and improved the immunity and beneficial gut microbiota in the mice. PRACTICAL APPLICATIONS: Walnut oil (WO) is widely used in traditional medicine around the world and is prescribed as beneficial food oil in agro-industry. However, the intestinal benefits of WO have not been explored extensively, and even its therapeutic mechanism still remains unknown in modern medicine. In this study, WO from Juglans sigillata was investigated for its preventive and protective effects on the intestinal mucosa in mice including anti-oxidant, anti-inflammatory, immunity, and gut microbiota modulation. WO decreased the oxidative stress, inflammation, and improved immunity and beneficial gut microbiota in the mice. WO has shown strong probiotic effect on the gut, and thus, can be considered as a potential candidate in food. The study outcome would enhance utilization of WO for the prevention of gastrointestinal diseases (e.g., Helicobacter, etc.) both in animals and human (inflammatory bowel diseases, IBD) and the formulation of functional foods.

Combination effects of ellagic acid with erlotinib in a Ba/F3 cell line expressing EGFR H773_V774 insH mutation.

BACKGROUND: Epidermal growth factor receptor H773_V774 insH (EGFR-insH) is an EGFR exon 20 insertion mutation in non-small cell lung cancer (NSCLC), which is naturally resistant to available EGFR tyrosine kinase inhibitors (TKIs) and lacks a patient-derived cell line. METHODS: A Ba/F3 cell line expressing EGFR-insH mutation (Ba/F3-insH cell line) was generated using an IL3-deprivation method. A cell proliferation assay was performed to screen natural compounds that exhibit a synergistic effect with erlotinib. Trypan blue staining was used to assess cell growth and crystal violate staining was recruited to evaluate clonogenic potential. Flow cytometry was used to detect EGFR expression and cell apoptosis. A xenograft model was created to evaluate the effect of ellagic acid (EA) with erlotinib on tumor growth. RESULTS: EA was identified to synergistically inhibit the proliferation of Ba/F3-insH cells with erlotinib. The growth and clonogenic potential of Ba/F3-insH cells were definitely constrained by EA with erlotinib, whereas, the apoptosis of Ba/F3-insH cells was dramatically promoted by the combination. In a xenograft model of the Ba/F3-insH cell line, the combination treatment also exhibited a synergistic reduction in tumor growth. CONCLUSIONS: In this study, we generated a Ba/F3 cell line expressing EGFR H773_V774 insH mutation and identified a synergistic treatment (EA with erlotinib) that markedly inhibited the viability of Ba/F3-insH cells in vitro and in vivo. KEY POINTS: Our results indicated that the combination of ellagic acid with erlotinib has synergistic effects against EGFR H773_V774 insH mutation.

Heterojunctions of p-BiOI Nanosheets/n-TiO2 Nanofibers: Preparation and Enhanced Visible-Light Photocatalytic Activity.

p-BiOI nanosheets/n-TiO2 nanofibers (p-BiOI/n-TiO2 NFs) have been facilely prepared via the electrospinning technique combining successive ionic layer adsorption and reaction (SILAR). Dense BiOI nanosheets with good crystalline and width about 500 nm were uniformly assembled on TiO2 nanofibers at room temperature. The amount of the heterojunctions and the specific surface area were well controlled by adjusting the SILAR cycles. Due to the synergistic effect of p-n heterojunctions and high specific surface area, the obtained p-BiOI/n-TiO2 NFs exhibited enhanced visible-light photocatalytic activity. Moreover, the p-BiOI/n-TiO2 NFs heterojunctions could be easily recycled without decreasing the photocatalytic activity owing to their one-dimensional nanofibrous structure. Based on the above, the heterojunctions of p-BiOI/n-TiO2 NFs may be promising visible-light-driven photocatalysts for converting solar energy to chemical energy in environment remediation.

In2S3/carbon nanofibers/Au ternary synergetic system: hierarchical assembly and enhanced visible-light photocatalytic activity.

In this paper, carbon nanofibers (CNFs) were successfully synthesized by electrospinning technique. Next, Au nanoparticles (NPs) were assembled on the electrospun CNFs through in situ reduction method. By using the obtained Au NPs modified CNFs (CNFs/Au) as hard template, the In2S3/CNFs/Au composites were synthesized through hydrothermal technique. The results showed that the super long one-dimensional (1D) CNFs (about 306 nm in average diameter) were well connected to form a nanofibrous network; and, the Au NPs with 18 nm in average diameter and In2S3 nanosheets with 5-10nm in thickness were uniformly grown onto the surface of CNFs. Photocatalytic studies revealed that the In2S3/CNFs/Au composites exhibited highest visible-light photocatalytic activities for the degradation of Rhodamine B (RB) compared with pure In2S3 and In2S3/CNFs. The enhanced photocatalytic activity might arise from the high separation efficiency of photogenerated electron-hole pairs based on the positive synergetic effect between In2S3, CNFs and Au components in this ternary photocatalytic system. Meanwhile, the In2S3/CNFs/Au composites with hierarchical structure possess a strong adsorption ability towards organic dyes, which also contributed to the enhancement of photocatalytic activity. Moreover, the In2S3/CNFs/Au composites could be recycled easily by sedimentation due to their nanofibrous network structure.