Unraveling the mechanism of quercetin alleviating BHPF-induced apoptosis in Epithelioma papulosum cyprini cells: SIRT3-mediated mitophagy.

Fluorene-9-bisphenol (BHPF), as an alternative to bisphenol A, is now increasingly used in plastic products. The accumulation of BHPF in the water environment has posed potential safety risks to aquatic organisms. Unfortunately, the toxicity of BHPF on the physiological metabolism of aquatic animals remains unclear, especially on the molecular mechanisms of BHPF kidney toxicity and antagonizing BHPF toxicity. Quercetin (QCT), a naturally occurring flavonoid, has been reported to mitigate the toxic effects on aquatic organisms induced by a variety of environmental contaminants. It is unclear whether QCT can be a candidate for mitigating BHPF toxicity. In this study, we investigated the protective effect of QCT on BHPF-induced apoptosis and elucidated the possible mechanism of the protective effect mediated by QCT. We treated epithelioma papulosum cyprini cells (EPCs) with 20 µM of BHPF and/or 20 µM of QCT, and the results showed that BHPF significantly increased the release of reactive oxygen species (ROS) from EPCs, decreased the expression of SIRT3, and initiated endogenous apoptosis. Molecular docking provides evidence for the interaction of QCT and SIRT3. Our intervention with Honokiol (HKL) showed that QCT or HKL treatment significantly attenuated BHPF-induced mitochondrial dysfunction and mitochondrial apoptosis (mtApoptosis) in EPCs, and activated mitophagy, restoring autophagy flux. To further investigate the specific mechanism of the protective effect of QCT, we intervened with Cyclosporin A (CsA), and our results suggest that QCT activation of SIRT3-promoted regulation of mitophagy may be a therapeutic strategy to attenuate the toxic effects of BHPF on EPCs. In conclusion, our findings suggest that BHPF induces oxidative damage and mtApoptosis in EPCs and that QCT activates mitophagy and improves autophagic flux through activation of SIRT3, thereby alleviating apoptosis mediated by mitochondrial dysfunction in EPCs. Our study provides a theoretical basis for reassessing the safety of BHPF for aquatic organisms and reveals a novel detoxification mechanism against the toxic effects of BHPF.

Dendrobine regulates STAT3 to attenuate mitochondrial dysfunction and senescence in vascular endothelial cells triggered by oxidized low-density lipoprotein.

Our previous studies have highlighted the potential therapeutic efficacy of dendrobine, an alkaloid, in atherosclerosis (AS), nevertheless, the underlying mechanism remains unclear. This study employs a combination of network pharmacology and in vitro experiments to explore the regulatory pathways involved. Through network pharmacology, the biological function for intersection targets between dendrobine and AS were identified. Molecular docking was conducted to investigate the interaction between the dominant target and dendrobine. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to mimic AS, and the effects of dendrobine on cell viability, lipid deposition, mitochondrial function, and cellular senescence were evaluated. Subsequently, cells were treated with the mitophagy inhibitor Mdivi-1 and the STAT3 agonist colivelin to assess the role of mitophagy and STAT3 signaling in dendrobine regulation. Intersection targets were associated with biological processes, including reactive oxygen species production. Dendrobine attenuated the effects of ox-LDL treatment on HUVECs, mitigating changes in cell activity, lipid deposition, mitochondrial function, and cellular senescence. Both Mdivi-1 and colivelin treatments resulted in decreased cell viability and increased cellular senescence, with colivelin suppressing mitophagy. Cotreatment with Mdivi-1 and colivelin further aggravated cellular senescence and inhibited FoxO signaling. Together, this study indicated that dendrobine regulated the STAT3/FoxO signaling pathway, alleviating mitochondrial dysfunction and cellular senescence. This study contributes valuable insights to the potential clinical application of dendrobine.

Raman signal optimization based on residual network adaptive focusing.

Due to its high sensitivity and specificity, Micro-Raman spectroscopy has emerged as a vital technique for molecular recognition and identification. As a weakly scattered signal, ensuring the accurate focus of the sample is essential for acquiring high quality Raman spectral signal and its analysis, especially in some complex microenvironments such as intracellular settings. Traditional autofocus methods are often time consuming or necessitate additional hardware, limiting real-time sample observation and device compatibility. Here, we propose an adaptive focusing method based on residual network to realize rapid and accurate focusing on Micro-Raman measurements. Using only a bright field image of the sample acquired on any image plane, we can predict the defocus distance with a residual network trained by Resnet50, in which the focus position is determined by combining the gradient and discrete cosine transform. Further, detailed regional division of the bright field map used for characterizing the height variation of actual sample surface is performed. As a result, a focus prediction map with 1µm accuracy is obtained from a bright field image in 120 ms. Based on this method, we successfully realize Raman signal optimization and the necessary correction of spectral information. This adaptive focusing method based on residual network is beneficial to further enhance the sensitivity and accuracy of Micro-Raman spectroscopy technology, which is of great significance in promoting the wide application of Raman spectroscopy.

Coptisine prevents angiotensin II­induced endothelial cell injury and senescence via the lncRNA SNHG12/miR­603/NAMPT pathway.

Atherosclerosis (AS) is a major health problem and targeting the associated molecular pathways is critical for developing therapies. The present study investigated the effect of coptisine on human umbilical vein endothelial cells (HUVECs) in response to angiotensin II (Ang II) induction by focusing on cellular senescence, apoptosis and inflammation. HUVECs were treated with different Ang II concentrations and long non-coding RNA small nucleolar RNA host gene 12 (SNHG12), microRNA (miRNA/miR)-603 and nicotinamide phosphoribosyltransferase (NAMPT) expressions were assessed. Cell viability, nicotinamide adenine dinucleotide (NAD+) levels, senescence, apoptosis and inflammation were assessed. The interactions among SNHG12, miR-603 and NAMPT were investigated using dual-luciferase reporter gene assays and RNA pull-down experiments. Coptisine treatment increased SNHG12 expression and attenuated Ang II-induced adverse effects in HUVECs. SNHG12 silencing abrogated coptisine's protective effects, indicating that SNHG12 is a key mediator. SNHG12 targets miR-603, which then directly targets NAMPT, an age-related gene involved in NAD(+) regulation. Coptisine modulated the SNHG12/miR-603/NAMPT pathway and miR-603 inhibition enhanced the protective effects of coptisine. NAMPT overexpression reversed the negative effects of miR-603 and enhanced the protective effect of the miR-603 inhibitor. Finally, the protective mechanism of coptisine is linked to the regulation of NAD(+), sirtuin 3 (SIRT3) and p53. Coptisine treatment counteracted the AngII-induced increase in SIRT3 and p53 protein levels, whereas the miR-603 inhibitor potentiated the effect of coptisine. SNHG12 knockdown partially abolished these effects, which were reversed by NAMPT overexpression. In conclusion, the present study revealed a novel protective mechanism involving the SNHG12/miR-603/NAMPT pathway in HUVECs exposed to Ang II, highlighting the potential therapeutic application of coptisine in treating atherosclerosis. These results suggested that coptisine exerts its protective effects by modulating the SNHG12/miR-603/NAMPT axis, which ultimately affects the regulation of NAD(+), SIRT3 and p53. Future studies should explore the potential of the SNHG12/miR-603/NAMPT pathway as a target for developing novel AS therapies.

Tracking intracellular nuclear targeted-chemotherapy of chidamide-loaded Prussian blue nanocarriers by SERS mapping.

The novel histone deacetylase drug chidamide (CHI) has been proven to regulate gene expression associated with oncogenesis via epigenetic mechanisms. However, huge side effects such as non-targeting, poor intracellular accumulation and low nuclear entry efficiency severely restrict its therapeutic efficacy. Dual-targeted nanodrug delivery systems have been proposed as the solution. Herein, we developed a CHI-loaded drug delivery nanosystem based on Prussian blue (PB) nanocarrier, which combines surface-enhanced Raman scattering (SERS) tracking function with cancer cell/nuclear-targeted chemotherapy capability. With the property of background-free SERS mapping, PB nanocarriers can serve as tracking agents to localize intracellular CHI. The incorporation of targeted molecules specifically enhances the cancer cell/nuclear internalization and chemotherapeutic effects of CHI-loaded PB nanocarriers. In vitro cytotoxicity assay clearly shows that the constructed CHI-loaded PB nanocarriers have significant inhibitory on Jurkat cell proliferation. Furthermore, SERS spectral analysis of Jurkat cells incubated with the CHI-loaded PB nanocarriers reveals obvious features of cellular apoptosis: DNA skeleton fragmentation, chromatin depolymerization, histone acetylation, and nucleosome conformation change. Importantly, this CHI-loaded PB nanocarrier will provide a new insight for lymphoblastic leukemia targeted chemotherapy.

Association of lactate detection with in-hospital mortality in critically ill patients with acute myocardial infarction: a retrospective cohort study.

OBJECTIVES: To assess the associations of lactate level or lactate clearance at different time points with in-hospital mortality in critically ill patients with acute myocardial infarction (AMI). DESIGN: A cohort study. SETTING: The Medical Information Mart for Intensive Care III database. PARTICIPANT: 490 AMI patients. INTERVENTION: None. PRIMARY AND SECONDARY OUTCOME MEASURES: In-hospital mortality of patients. RESULTS: In total, 120 (24.49%) patients died at the end of follow-up. After adjusting for confounders, increased risk of in-hospital mortality in patients with AMI was observed in those with high lactate level (24 hours) (HR=1.156, 95%CI: 1.002 to 1.333). Increased lactate clearance (24 hours) was correlated with a decreased risk of in-hospital mortality in patients with AMI (HR=0.995, 95% CI: 0.994 to 0.997). The area under the curves (AUCs) of lactate level (24 hours) and lactate clearance (24 hours) were 0.689 (95% CI: 0.655 to 0.723) and 0.672 (95% CI: 0.637 to 0.706), respectively. The AUC of lactate level (24 hours) and lactate clearance (24 hours) was higher than lactate level (baseline). CONCLUSIONS: Increased lactate level (24 hours) was associated with an elevated risk of in-hospital mortality in patients with AMI and increased lactate clearance (24 hours) was correlated with a decreased risk of in-hospital mortality in patients with AMI despite the age and genders.

Prevention of High-Fat-Diet-Induced Dyslipidemia by Lactobacillus plantarum LP104 through Mediating Bile Acid Enterohepatic Axis Circulation and Intestinal Flora.

This work aimed to investigate the alleviative mechanism of Lactobacillus plantarum LP104 (LP104) isolated from kimchi on high-fat-diet-induced dyslipidemia by targeting the intestinal flora and bile acid (BA) metabolism. Oral administration of LP104 over 8 weeks reduced body weight gain and body fat, as well as ameliorating serum and hepatic dyslipidemia in HFD-fed C57BL/6N mice significantly. LP104 intervention also increased the ileal tauro-α/ß-muricholic acid sodium salt (T-α-MCA or T-ß-MCA) and tauroursodeoxycholic acid (TUDCA) concentrations to suppress the enterohepatic farnesoid X receptor/fibroblast growth factor 15-fibroblast growth factor receptor 4 (FXR/FGF15-FGFR4) signaling pathway, which stimulated the hepatic cholic acid (CA) and chenodeoxycholic acid (CDCA) de novo synthesis through using cholesterol. Then, LP104 treatment accelerated BA excretion with the feces and cholesterol efflux to improve HFD-caused hyperlipidemia effectively. The 16S rRNA gene high-throughput sequencing revealed that LP104 promoted intestinal flora rebalance by increasing the abundances of Bacteroides, Akkermansia, Lactobacillus, and Clostridium and decreasing the abundance of Oscillospira and Coprococcus. Meanwhile, Spearman correlation analysis demonstrated that the differential flora were closely related to BA signaling molecules including CA, CDCA, T-α-MCA, T-ß-MCA, and TUDCA after LP104 intervention. These findings provided new evidence that LP104 had the potential to be used as a naturally functional food for the prevention of dyslipidemia.

A SERS-Based Dual-Parameter Monitoring Nanoprobe of ROS and PI3K/Akt during Ginsenoside Rg3-Induced Cell Apoptosis.

Both the reactive oxygen species (ROS) level and Phosphatidylinositol 3 Kinase (PI3K) protein content are two crucial parameters for characterizing states of cell apoptosis. Current methods measure these parameters with two different techniques, respectively, which usually lead to evaluation contingency. Ginsenoside Rg3 exhibits an excellent anticancer effect, which is enacted by the Phosphatidylinositol 3 Kinase/Protein Kinase B (PI3K/Akt) pathway involving ROS; however, the precise mechanism that induces cell apoptosis remains unknown. This is due to the lack of information on quantitative intracellular ROS and PI3K. Here, we used a surface-enhanced Raman scattering (SERS)-based boric acid nanoprobe to monitor the intracellular ROS level and phosphatidylinositol-3,4,5-triphosphate (PI(3,4,5)P3) content, which reflects the regulatory effect of the PI3K/Akt pathway. After treatment with ginsenoside Rg3, the PI3K/Akt content first increased and then decreased as the ROS level increased. Moreover, when the ROS level significantly increased, the mitochondrial membrane potential reduced, thus indicating the dynamic regulation effect of intracellular ROS level on the PI3K/Akt pathway. Importantly, in addition to avoiding evaluation contingency, which is caused by measuring the aforementioned parameters with two different techniques, this SERS-based dual-parameter monitoring nanoprobe provides an effective solution for simultaneous ROS level and PI3K content measurements during cell apoptosis. Furthermore, the intracellular ROS level was also able to have a dynamic regulatory effect on the PI3K/Akt pathway, which is essential for studying ROS/PI3K/Akt-pathway-related cell apoptosis and its activation mechanism.

SERS-based error calibration of a TMB-H2O2 colorimetric system.

3,3',5,5'-tetramethylbenzidine (TMB)-H2O2 is widely used as an effective colorimetric system, in which the color reaction is implemented with peroxidase-catalyzed TMB oxidation by H2O2 that usually measured UV-vis absorption spectra or Raman spectra. However, its low accuracy significantly limits its application. Blue charge transfer complex (CTC), which is the product of TMB and H2O2 reaction and is used as the basis for partial colorimetric methods, usually causes colorimetric error owing to changes in the UV-vis absorption and Raman spectra during TMB oxidation under various environmental conditions (catalyst type, temperature, H2O2 concentration). Herein, we propose a surface-enhanced Raman spectrum (SERS)-based error calibration method to improve the accuracy of the TMB-H2O2 colorimetric system. It is found that under 633 nm laser excitation, TMB has three Raman peaks at 1189, 1335 and 1609 cm-1 in the single-electron oxidation phase, and these peaks disappear completely in the two-electron oxidation phase. By comparing these Raman peaks, we can conveniently obtain the actual process information during TMB oxidation. Using the proposed method, the accuracy of the TMB-H2O2 colorimetric system improved by more than 15%. Importantly, this SERS-based TMB-H2O2 error calibration method will open a new horizon for enzyme-linked immunosorbent assay (ELISA) and other biomedical applications.

The ameliorative effect of probiotics on diet-induced lipid metabolism disorders: A review.

High-fat diet induces lipid metabolism disorders that has become one of the grievous public health problems and imposes a serious economic and social burden worldwide. Safety probiotics isolated from nature are regarded as a novel supplementary strategy for preventing and improving diet-induced lipid metabolism disorders and related chronic diseases. The present review summarized the latest researches of probiotics in high fat diet induced lipid metabolism disorders to provide a critical perspective on the regulatory function of probiotics for future research. Furthermore, the screening criteria and general sources of probiotics with lipid-lowering ability also outlined to enlarge microbial species resource bank instantly, which promoted the development of functional foods with lipid-lowering strains from nature. After critically reviewing the lipid-lowering potential of probiotics both in vitro and in vivo and even in clinical data of humans, we provided a perspective that probiotics activated AMPK signaling pathway to regulate fat synthesis and decomposition, as well as affected positively the gut microbiota structure, intestinal barrier function and systemic inflammatory response, then these beneficial effects are amplified along Gut-liver axis, which regulated intestinal flora metabolites such as SCFAs and BAs by HMGCR/FXR/SHP signaling pathway to improve high fat diet induced lipid metabolism disorders effectively.

Ameliorative effect of Lactobacillus plantarum Lp2 against cyclophosphamide-induced liver injury in mice.

Cyclophosphamide (CTX) is a widely used anticancer drug that can cause liver injury, but there is no effective treatment available at present. The antioxidant properties of Lactobacillus plantarum Lp2 in vitro and its effect on CTX-induced liver injury in mice were investigated thoroughly. The order of antioxidant capacity of the fermentate of Lp2 was as followed: fermented supernatant > cell-free extract > intact cell. BALB/c mice were intraperitoneally injected with 80 mg/kg BW/d CTX for 3 days to build a liver injury model, then treated with Lp2 fermented supernatant (Lp2-s) and Lp2 culture broth (Lp2). After 10 days, the indicators of oxidative stress and liver injury were measured. Both Lp2-s and Lp2 restored the levels of T-SOD, CAT, GSH-Px, MDA, GSH, ALT, and AST. The western blotting results showed that Lp2-s and Lp2 ameliorated CTX-induced oxidative damage and hepatocyte apoptosis via inhibiting MAPKs pathway and strengthening Nrf2/HO-1/NQO1 antioxidant defense system, thus inhibiting the mitochondrial-mediated apoptosis pathway. Therefore, both Lp2-s and Lp2 had similar protective effects on CTX-induced liver injury.

Antioxidant Mechanism of Lactiplantibacillus plantarum KM1 Under H2O2 Stress by Proteomics Analysis.

Lactiplantibacillus plantarum KM1 was screened from natural fermented products, which had probiotic properties and antioxidant function. The survival rate of L. plantarum KM1 was 78.26% at 5 mM H2O2. In this study, the antioxidant mechanism of L. plantarum KM1 was deeply analyzed by using the proteomics method. The results demonstrated that a total of 112 differentially expressed proteins (DEPs) were screened, of which, 31 DEPs were upregulated and 81 were downregulated. The Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that DEPs participated in various metabolic pathways such as pyruvate metabolism, carbon metabolism, trichloroacetic acid cycle, amino acid metabolism, and microbial metabolism in diverse environments. These metabolic pathways were related to oxidative stress caused by H2O2 in L. plantarum KM1. Therefore, the antioxidant mechanism of L. plantarum KM1 under H2O2 stress provided a theoretical basis for its use as a potential natural antioxidant.

Dendrobine modulates autophagy to alleviate ox-LDL-induced oxidative stress and senescence in HUVECs.

Dendrobine has potential advantages in suppressing atherosclerosis (AS). FK506-binding protein 1A (FKBP1A) is implicated in the regulation of autophagy, inflammation, and apoptosis. To reveal the mechanism by which dendrobine inhibits AS by modulating autophagy, oxidative stress, apoptosis, and senescence. An in vitro AS cell model was induced by culturing human umbilical vein endothelial cells (HUVECs) with oxidized low-density lipoprotein (ox-LDL). The cells were treated with dendrobine alone or in combination with short hairpin RNA (shRNA) targeting FKBP1A or together with 3-methyladenine (3MA), an autophagy inhibitor. Inflammatory cytokines levels tumor necrosis factor-α, interleukin-6 (IL-6), and IL-1ß were analyzed and oxidative stress levels were detected by the analysis of reactive oxygen species, malondialdehyde, and superoxide dismutase levels, followed by the analysis of apoptosis levels through terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Cell senescence was evaluated by senescence-associated ß-galactosidase and light chain 3 (LC3) levels were detected by immunofluorescence (IF) staining. The targeting relationship of dendrobine and FKBP1A was predicted by SwissTarget, PyMol, Autodock, and Open Babel software. Dendrobine reduced the levels of proinflammation factors, oxidative stress levels, apoptosis levels, and senescence phenotype in ox-LDL-induced HUVECs. Besides, cell viability has an opposite change. Furthermore, there was an increase in LC3 IF tensity, and LC3-II/I and Beclin1 expressions, and a decrease in p62 expression. However, these effects of dendrobine could be markedly destroyed by shRNA silencing FKBP1A and 3MA. Dendrobine can suppress inflammatory responses, oxidative stress, apoptosis, and senescence via FKBP1A-involved autophagy ox-LDL-treated HUVECs.

Colorimetry /SERS dual-sensor of H2O2 constructed via TMB-Fe3O4@ AuNPs.

Hydrogen peroxide (H2O2) detection with high sensitivity plays an important role in biomedical research and food engineering. By combining colorimetry and surface enhanced Raman spectroscopy (SERS), we synthetize a novel H2O2 dual-sensor constructed via TMB-Fe3O4@AuNPs. In the presence of H2O2, the peroxide model enzyme might catalyze the oxidation of 3,3',5,5'- tetramethylbenzidine (TMB) as blue charge transfer complex (CTC) for colorimetry, and then facilitate the sensitivity improvement of SERS detection. The achieved results show that in colorimetry, the linear range is from 40 µM to 5.5 mM with the detection limit of 11.1 µM; in SERS detection, the linear range is from 2 nM to 1 µM with the detection limit of 0.275 nM. Clearly, this mutual reference strategy improves both the detection limit of colorimetry and the sensitivity of SERS detection. Moreover, this colorimetry/SERS dual-sensor constructed via TMB-Fe3O4@AuNPs is successfully applied to the H2O2 detection in plasma and milk, indicating the excellent performance and flexibility.

Au/Ag composite-based SERS nanoprobe of Cr3.

Quantitative characterization of Cr3+, an important element revealing human metabolism and biological environmental variation, is still difficult to achieve by conventional biochemical methods due to the lack of high-sensitivity, real-time techniques with rapid response detection. Using surface-enhanced Raman scattering (SERS), we construct an Au/Ag composite-based SERS nanoprobe for the quantitative characterization of Cr3+ content in solution, in which DL-mercaptosuccinic acid (DL-MSA) is employed for Raman signal enhancement, and 4-mercaptobenzoic acid (4-MBA) is chosen as the Raman reporter. The achieved result demonstrates obvious advantages of the synthesized Au/Ag composite-based SERS nanoprobe in sensitivity and response speed. Importantly, this Au/Ag composite-based SERS nanoprobe might provide a new strategy for dynamic monitoring of Cr3+ content in human metabolism.

Receptor-mediated photothermal/photodynamic synergistic anticancer nanodrugs with SERS tracing function.

Phototherapy, especially the photothermal therapy (PTT) and the photodynamic therapy (PDT), have become very promising in cancer treatment due to its low invasiveness and high efficacy. Both PTT and PDT involve the utilization of light energy, and their synergistic treatment should be a good solution for cancer treatment by ingenious design. The therapeutic effect of phototherapy is closely associated with the amount and location of anticancer-nanodrugs accumulated in tumor cells, and the receptor-mediated endocytosis should be an excellent candidate for enhancing anticancer-nanodrugs internalization. Surface enhanced Raman spectroscopy (SERS) imaging is suitable for tracing nanodrugs due to its high selectivity, sensitivity and reliability. In this paper, we hope to construct a receptor-mediated PTT/PDT synergistic anticancer nanodrugs and evaluate the corresponding efficacy through SERS tracing function. Here, the receptor-mediated PTT/PDT synergistic anticancer nanodrugs are prepared by the chemical modification of gold nanorods (GNRs), involving protoporphyrin IX (PpIX), 4-mecaptobenzoic acid (MBA), and folic acid (FA). The achieved results show that the receptor-mediated endocytosis can greatly facilitate the internalized amount and intracellular distribution of the nanodrugs, thus lead to the anti-cancer efficacy improvement. Importantly, this receptor-mediated PTT/PDT synergistic treatment with SERS tracing function will provide a simple and effective strategy for the design and application of anticancer phototherapy nanodrugs.

Rapid iodine capture from radioactive wastewater by green and low-cost biomass waste derived porous silicon-carbon composite.

The effective and safe capture and storage of radioactive iodine (129I or 131I) are of significant importance during nuclear waste storage and nuclear energy generation. Herein, a porous silicon-carbon (pSi-C) composite derived from paper mill sludge (PMS) is synthesized and used for rapid iodine capture. The influences of the activator type, the impregnation ratio of the paper mill sludge to the activator, carbonization temperature, and carbonization time on the properties of the pSi-C composite are investigated. The pSi-C composite produced in the presence of ZnCl2 as the activator and at an impregnation ratio of 1 : 1, a carbonization temperature of 550 °C, and a carbonization time of 90 min has a surface area of 762.13 m2 g-1. The as-synthesized pSi-C composite exhibits promising iodine capture performance in terms of superior iodine adsorption capacity (q t ) of around 250 mg g-1 and rapid equilibrium adsorption with in 15 min. The devised method is environmentally friendly and inexpensive and can easily be employed for the large-scale production of porous silicon-activated carbon composites with excellent iodine capture and storage from iodine-contaminated water.

Activity of microporous lignin-derived carbon-based solid catalysts used in biodiesel production.

Lignin is utilized as a carbon precursor to produce microporous lignin-derived carbon-based solid acid (MLC-S) ZnCl2 activation and sulfonation with concentrated sulfuric acid. The effects of reaction conditions, namely the ratio of methanol to oleic acid, carbonization temperature, and catalyst dosage, on the efficiency of the esterification of oleic acid with methanol are investigated. As a carbon-based solid acid, the MLC-S offers high catalytic activity in the esterification, which is a crucial reaction in the synthesis of biodiesel. Compared with nonactivated lignin-derived carbon-based solid acid (LC-S), the highly porous structure of the MLC-S makes its active sites more accessible and ensures its excellent catalytic performance. Under the optimal conditions, the esterification of oleic acid with methanol reaches a conversion of 92.3%. Moreover, after recycling the MLC-S for five times, the extent of the esterification reaction is still as high as 72.9%. Obviously, the synthesized MLC-S has considerable potential for the esterification of oleic acid with methanol and thus for biodiesel production.

In situ exploring Chidamide, a histone deacetylase inhibitor, induces molecular changes of leukemic T-lymphocyte apoptosis using Raman spectroscopy.

Though it has been demonstrated that Chidamide (CS055/HBI-8000), a novel benzamide class of histone deacetylase (HDAC) subtype-selectively inhibitor, reveals better anticancer effect in acute leukemia, but it remains unknown about the precise mechanism of Chidamide-induced acute leukemia cell apoptosis due to the lack of in situ molecular changes information. Based on Raman spectral analysis, we find that the action of Chidamide on Jurkat cell will lead to an addition of an acetyl group to a specific lysine residue at the end of histone amino acid, and greatly enhance the acetylation of histones H1, H2A, H2B, H3, and H4, and then destroy the electrostatic force between the alkaline terminal of the positive charged arginine side chain and the negative charged DNA of phosphate group, finally cause the depolymerization of DNA and histone octamer in chromatin nucleosome depolymerization and the relaxation of chromatin. Accordingly, the accumulation of reactive oxygen species (ROS) and the decreasing of mitochondrial membrane potential (MMP) are observed. For comparison, we also present the corresponding results of suberoylanilide hydroxamic acid (SAHA) and MS-275 inhibitors. The achieved results show that proliferation of Chidamide-treated Jurkat cells is low relative to MS-275 or SAHA, and the action of Chidamide or MS-275 on Jurkat cells lead to obvious increasing in histones H1, H2A, H2B, H3, and H4, whereas the action effect of SAHA is mainly observed in histones H1, H2A, H2B, H3 but weak in histone H4. Moreover, it is found that Chidamide-induced histone H3 acetylation in Jurkat cells is stronger than MS-275 and SAHA. Collectively, by Raman spectral analysis, we achieve the dynamic behavior of biochemical components, molecular conformation and morphological changes of HDAC inhibitors-treated Jurkat cells. Importantly, our research is the first to demonstrate that the action site of HDAC inhibitors on Jurkat cell is located in the DNA minor groove. Most importantly, the application of Raman spectrum in exploring in-situ molecular changes information, histone acetylation modification in epigenetics, drug action sites and cell cycle affected by HDAC inhibitors will supply new idea and reference for the design and modification of HDAC inhibitors.

Dynamic monitoring and quantitative characterization of intracellular H2O2 content by using SERS based boric acid nanoprobe.

Quantitative characterization of intracellular H2O2 content, which is still difficult by the conventional biochemical methods due to the lack of real-time and non-invasive technique of single cell measurement, is a useful solution for cell state assessment. Based on the surface enhanced Raman scattering (SERS), we construct a novel boric acid (BA) nanoprobe to perform quantitative characterization of H2O2 content, in which the p-thiol benzene boric acid (4-MPBA) reporter molecule modified with gold nanorods (AuNRs) is employed for Raman signal enhancement. The achieved result demonstrates obvious advantages of the synthesized AuNRs/4-MPBA/BA nanoprobe in measurement sensitivity of H2O2 content. Importantly, this AuNRs/4-MPBA/BA nanoprobe will provide a powerful tool for dynamic monitoring and quantitative characterization of intracellular H2O2 content during cell apoptosis or other cell growth processes, and then achieve important reference data for studying the corresponding molecular mechanism.