Eco-friendly regeneration of lignin with acidic deep eutectic solvent for adsorption of pollutant dyes for water cleanup.

In this study, a simple and eco-friendly method was used to treat alkaline lignin with an acidic deep eutectic solvent (DES) to obtain regenerated lignin for the efficient adsorption of pollutant dyes from aqueous environment. Based on the yield and adsorption capacity of the sorbent for these dyes, conditions such as the type and concentration of DES component, solid-to-liquid ratio, reaction time, and temperature were optimized. By characterizing and comparing alkali lignin with regenerated lignin, a series of reactions were demonstrated to occur during the DES treatment process. The performance and mechanism of methylene blue and rhodamine B adsorption on regenerated lignin were studied systematically, and the maximum adsorbed amounts were 348.29 and 551.05 mg/g at 323 K, respectively. This study provides a new strategy for the green preparation of functionalized lignin and its use in the water pollutant treatment.

Exosome-transmitted ANGPTL1 suppresses angiogenesis in glioblastoma by inhibiting the VEGFA/VEGFR2/Akt/eNOS pathway.

OBJECTIVE: Glioblastoma (GBM) is a highly vascularized malignancy that relies on new vessel generation, and thus targeting angiogenesis has been a promising anti-GBM approach. ANGPTL1 is well-known for its anti-angiogenic property; nevertheless, its role in GBM is yet to be explored. Recently, the crucial role of exosomes (Exos) as intercellular communication mediators has gained prominence in GBM therapy. This work aimed to explore the role of exosomal ANGPTL1 in GBM angiogenesis and its mechanisms. METHODS: Bioinformatic analysis was performed to evaluate ANGPTL expression in GBM. Human GBM cell lines (U87 and U251) and a xenograft mouse model were employed. Exos were isolated from oe-NC- and oe-ANGPTL-transfected bone mesenchymal stem cells and identified. Cell proliferation, migration, and apoptosis were detected. Immunofluorescence, qRT-PCR, western blotting, co-immunoprecipitation, and immunohistochemistry were used to determine the molecular mechanisms underlying exosomal ANGPTL1 against GBM angiogenesis. Besides, tube generation and transmission electron microscope assays were conducted to assess GBM angiogenesis. RESULTS: Low ANGPTL1 expression was observed in GBM tumor tissues and cells. Functionally, e-ANGPTL-Exos inhibited GBM malignant progression and angiogenesis in vitro and in vivo. Mechanically, e-ANGPTL-Exos reduced VEGFA expression and blocked the VEGFR2/Akt/eNOS pathway in GBM cells and tumor tissues. Co-immunoprecipitation revealed a link between ANGPTL1 and VEGFA in GBM cells. Notably, oe-VEGFA abolished the suppressive functions of e-ANGPTL-Exos in GBM progression and angiogenesis and the VEGFR2/Akt/eNOS axis. The VEGFR2 inhibitor, vandetanib, eliminated the promotive effects of oe-VEGFA on GBM angiogenesis with suppressed VEGFR2/Akt/eNOS pathway. CONCLUSIONS: Exosomal ANGPTL1 suppressed GBM angiogenesis by inhibiting the VEGFA/VEGFR2/Akt/eNOS axis.

Transketolase drives the development of aortic dissection by impairing mitochondrial bioenergetics.

AIM: Aortic dissection (AD) is a disease with rapid onset but with no effective therapeutic drugs yet. Previous studies have suggested that glucose metabolism plays a critical role in the progression of AD. Transketolase (TKT) is an essential bridge between glycolysis and the pentose phosphate pathway. However, its role in the development of AD has not yet been elucidated. In this study, we aimed to explore the role of TKT in AD. METHODS: We collected AD patients' aortic tissues and used high-throughput proteome sequencing to analyze the main factors influencing AD development. We generated an AD model using BAPN in combination with angiotensin II (Ang II) and pharmacological inhibitors to reduce TKT expression. The effects of TKT and its downstream mediators on AD were elucidated using human aortic vascular smooth muscle cells (HAVSMCs). RESULTS: We found that glucose metabolism plays an important role in the development of AD and that TKT is upregulated in patients with AD. Western blot and immunohistochemistry confirmed that TKT expression was upregulated in mice with AD. Reduced TKT expression attenuated AD incidence and mortality, maintained the structural integrity of the aorta, aligned elastic fibers, and reduced collagen deposition. Mechanistically, TKT was positively associated with impaired mitochondrial bioenergetics by upregulating AKT/MDM2 expression, ultimately contributing to NDUFS1 downregulation. CONCLUSION: Our results provide new insights into the role of TKT in mitochondrial bioenergetics and AD progression. These findings provide new intervention options for the treatment of AD.

Effect of melatonin on oxidative stress indicators in animal models of fibrosis: A systematic review and meta-analysis.

BACKGROUND AND OBJECTIVE: Imbalance of oxidative stress has been detected in a range of fibrotic diseases. Melatonin as an indoleamine hormone plays an important role in regulating the circadian rhythm of human, while in recent years, its antioxidant effect has also attracted increasing attention. This study aimed to perform a systematic review and meta-analysis to comprehensively evaluate the antioxidant effect of melatonin in animal models of fibrosis. METHODS: The PubMed, Cochrane Library, EMBASE, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang database, China Science and Technology Journal Database (VIP), and SinoMed databases were searched from inception to March 1st, 2022 to retrieve eligible studies that evaluated the effect of melatonin supplementation on the levels of malondialdehyde (MDA), lipid peroxidation (LPO), nitric oxide (NO), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), and catalase (CAT) in animal models of fibrosis. RESULTS: A total of 64 studies were included in this meta-analysis. The results showed that melatonin supplementation significantly reduced the levels of oxidative indicators including MDA (P < 0.00001), LPO (P < 0.00001) and NO (P < 0.0001), and elevated the levels of antioxidant indicators including GSH (P < 0.00001), GPx (P < 0.00001) and SOD (P < 0.00001) in fibrotic diseases. CONCLUSIONS: Our research findings showed that melatonin supplementation could significantly reduce the levels of oxidative indicators including MDA, LPO and NO and elevate the levels of antioxidant indicators including GSH, GPx and SOD so as to correct oxidative stress in animal models of fibrosis. However, no significant changes were observed in CAT level. More clinical studies are needed to further confirm the beneficial role of melatonin in fibrotic diseases.

Silencing of lncRNA CHRM3-AS2 Expression Exerts Anti-Tumour Effects Against Glioma via Targeting microRNA-370-5p/KLF4.

Objectives: Long non-coding RNAs (lncRNAs) are key regulators involved in the progression of glioma, and many functional lncRNAs are yet to be identified. This study aimed to explore the function of CHRM3-AS2, a rarely reported lncRNA, in glioma, as well as the underlying mechanisms involving miR-370-5p/KLF4. Methods: Differentially expressed RNAs (DERs) were screened from two gene expression profiles of glioblastoma (GBM). Fluorescence in situ hybridisation was performed to determine the subcellular localisation of CHRM3-AS2. Cell viability, colony formation, apoptosis, migration, and invasion were evaluated using cell counting kit-8, colony counts, flow cytometry, wound healing, and Transwell assays, respectively. mRNA and protein expression of specific genes were measured using quantitative real-time polymerase chain reaction and western blotting, respectively. Dual luciferase reporter gene, RNA immunoprecipitation, and RNA pull-down assays were performed to identify the target relationships. A mouse xenograft model was established for in vivo validation. Results: CHRM3-AS2 was screened as a prognosis-associated DER in GBM. CHRM3-AS2 expression was up-regulated in glioma cells, and CHRM3-AS2 was localised in the cytoplasm. Silencing of CHRM3-AS2 expression inhibited cell viability, colony formation, migration, and invasion and promoted apoptosis of U251 and SHG-44 cells. In addition, CHRM3-AS2 targeted miR-370-5p/KLF4 in glioma cells. The anti-tumour effect of CHRM3-AS2 silencing was weakened by miR-370-5p silencing or KLF4 overexpression. In vivo, silencing of CHRM3-AS2 expression inhibited tumour growth and Ki67 expression in mice. Overexpression of KLF4 also weakened the anti-tumour effect of CHRM3-AS2 silencing in mice. Conclusions: Silencing of CHRM3-AS2 expression inhibited the malignant progression of glioma by regulating miR-370-5p/KLF4 expression.

Effects of biochar addition on the anaerobic digestion of carbohydrate-rich, protein-rich, and lipid-rich substrates.

Although biochar addition into the anaerobic digestion of food waste (FW) is an efficient means to enhance methane production, the effects of biochar on various FW components remain unclear. Laboratory batch experiments were conducted to investigate the impact of sewage sludge-derived biochar (SSB) supplementation on the anaerobic digestion (AD) of major FW components, including carbohydrate-rich, protein-rich, and lipid-rich substrates. The lag phase of AD with the carbohydrate-rich substrate was 48.6% shorter when SSB was added, and the cumulative methane yield was 4.74 times higher compared to AD without biochar. SSB supplementation also increased the rate of methane production from the lipid-rich substrate. However, the effect of SSB addition on AD of the protein-rich substrate was minor. Analysis of the microbial communities revealed that methanogen growth was enhanced during AD of the carbohydrate-rich and lipid-rich substrates, but not the protein-rich substrate, following SSB supplementation. Also, the most dominant methanogenic genus varied with the substrates. SSB addition promoted the growth of hydrolytic and fermentative bacteria, particularly phylum Bacteroidetes.Implications: Biochar supplementation has been studied to overcome the shortcomings of anaerobic digestion (AD). However, the effects of biochar on different substrates remain unclear. This study compared carbohydrate-rich, protein-rich, and lipid-rich substrates in anaerobic digestion with sewage sludge-derived biochar (SSB). SSB supplementation improved methane generation from all but the protein-rich substrate. The study results imply that the effect of SSB addition on AD varied with the substrate due to the substrates underwent different degradation processes with different microbial communities.

Insight into the capacity fading of layered lithium-rich oxides and its suppression via a film-forming electrolyte additive.

The capacity fading of layered lithium-rich oxide (Li1.2Mn0.54Ni0.13Co0.13O2, LLO) cathodes greatly hinders their practical application in next generation lithium ion batteries. It has been demonstrated in this work that the slow capacity fading of a LLO/Li cell within 120 cycles is mainly caused by electrolyte oxidation and LLO phase transformation with Ni dissolution. After 120 cycles, the dissolution of Mn becomes worse than that of Ni, leading to structural destruction of the generated spinel phase structure of LLO and fast capacity fading. Tripropyl borate (TPB) is proposed as a film-forming electrolyte additive, which shows a great capability to enhance the cycling stability of LLO/Li, with a capacity retention improvement from 21% to 78% after 250 cycles at 0.5C. Electrochemical and physical characterization demonstrated that the TPB-derived SEI film shows great capability to suppress electrolyte oxidation and the structural destruction of the generated spinel phase of LLO.