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Interference among multiple heavy metal ions (HMIs) is a significant problem that must be solved in electroanalysis, which extremely restricts the practical popularization of electrochemical sensors. However, due to the limited exploration of the intrinsic mechanism, it is still difficult to confirm the influencing factors. In this work, a series of experimental and theoretical electroanalysis models have been established to investigate the electroanalysis results of Cu(II), Cd(II), As(III), and their mixtures, which were based on the simple structure and stable coordination of nickel single-atom catalysts. X-ray absorption spectroscopy and density functional theory calculations were used to reveal the underlying detection mechanism of the 50-fold boosting effect of Cu(II) on As(III) while Cd(II) inhibits As(III). Combining the application of the thermodynamic model and Fourier transform infrared reflection, the specific interaction of the nanomaterials and HMIs on the interface is considered to be the fundamental source of the interference. This work opens up a new way of thinking about utilizing the unique modes of interplay between nanomaterials and HMIs to achieve anti-interference intelligent electrodes in stripping analysis.

Microplastics widely exist in various environmental media and have become a global environmental problem. To investigate the pollution characteristics, deposition patterns, and influencing factors of microplastics in the sediments of bay beach, five typical beaches were selected in Xiamen Bay. According to the tidal variation, 0-10 cm, 10-20 cm, and 20-30 cm sediment column samples were collected in layers at the high tide line, middle tide line, and low tide line at the same time, and the characteristics of the horizontal and vertical distribution of microplastics in the beach sediments were studied. The results showed that the abundance of microplastics in 45 sediment samples in Xiamen Bay beach ranged from 39 to 260 n·kg

Constructing high-effective electrode sensing interfaces has been considered an effective method for electrochemical detection toward heavy metal ions (HMIs). However, most research has been devoted to enhancing the stripping currents of HMIs by simply improving the adsorptive capacity and conductivity of the electrode modified materials, while lacking theoretical guidelines in fabricating catalytic sensing interfaces. Besides, the understanding of detection mechanisms is quite unscientific from the perspective of catalysis. This perspective summarizes five general strategies in designing highly efficient sensing interfaces in the recent five years, including modulating crystal phases, orientations and planes, defect engineering, ionic valence state cycle engineering, adsorption in situ catalysis strategy, and construction of atomic level catalytic active sites. What's more, the catalytic mechanisms for improving the signals of HMIs, such as boosting the electron transfer rates and conversion rates, lowering the energy barriers, etc., are introduced and emphasized. This study has a great significance in directionally controlling functionalized electrochemical sensors to achieve excellent sensitivity and selectivity in detecting environmental pollutants from the view of catalysis, and it also brings enlightenments and guidance to develop new electroanalytical methods.

Rationale: Postoperative ileus (POI) is a frequent complication arising after gastrointestinal surgery but pathogenesis of POI is still not fully understood. While Th1 immune cells are implicated in POI, the involvement of Th2 cells has not yet been clarified. Given the impact of reactive oxygen species (ROS) in the regulation of Th1 and Th2 balance, we hypothesized that not only Th1 but also Th2 immune response can be involved in the development of experimental POI. Methods: The intestinal transit test was performed using carbon gum arabic. Electron microscopy was employed to assess tissue morphology and the presence of immune cells. Cytokines, IgE and ROS were measured. Immune cells from Peyer's patches were analyzed by Flow Cytometry and toluidine blue staining was used for detection of mast cells. Transcriptional factors were analyzed by Western blot. Results: POI is associated with an increase in both Th2 cytokines and Th2 cells. We have further demonstrated that POI induces a Th2-dependent activation of memory and non-memory B cells. This was accompanied by an increase in a number of mast cells in the colon of POI mice as well by an increased IgE and histamine plasma levels. We found that POI-induced accumulation of ROS was associated with an increased expression of the transcriptional factors HMBGI, NF-κB, and p38. This increased expression seemed to be associated with a Th2 response. Conclusion: Th2 immune response can be involved in the activation of mast cells in POI, which was associated with ROS mediated activation of NF-κB and p38 MAPK signaling pathway.

Constructing catalysts with simple structures, uniform effective sites, and excellent performance is crucial for understanding the reaction mechanism of target pollutants. Herein, the single-atom catalyst of Mn-intercalated graphitic carbon nitride (Mn/g-C

Ulcerative colitis (UC) is a complex disease that results from a dysregulated immune response in the gastrointestinal tract. A mouse model orally administered with dextran sodium sulfate (DSS) is the most widely used experimental animal model of UC. However, the ultrastructure of the colon in mouse colitis is poorly understood. In the present study, colonic specimens from DSS-induced UC mice underwent hematoxylin and eosin staining, Masson's trichrome staining and Verhoeff's elastic staining. In addition, the ultrastructure of samples was examined by transmission electron microscopy. UC was successfully induced by 7 consecutive days of DSS oral administration. The goblet cell architecture of the UC tissue was damaged in the mucosa. Additionally, a significant number of inflammatory cells infiltrated into the stroma and the structure of the intestinal gland was destroyed. The tissue in the submucosa showed significant edema. Hyperplasia was also identified in the submucosa, promoting a disorganized microstructure within the colon wall. Numerous collagen fibers in the muscular layer were disrupted, and the fiber bundles were thinner compared with those in the normal control group. Furthermore, in the DSS-induced UC group, the smooth muscle cell showed edema, the cell membrane structure was unclear and the shape of the nucleus was irregular. In conclusion, the present study revealed important histological and ultrastructural changes in the colon of DSS-induced UC mice. These features may contribute to improved understanding of the pathogenesis and mechanism of UC.

Background Chinese medicine decoction Da-Cheng-Qi-Tang (DCQT) is effective for treating gastrointestinal (GI) disorders, including postoperative ileus (POI); however, the mechanism by which DCQT improves intestinal motility of POI remains unknown. Purpose The aim of this study is to explore the therapeutic effect and mechanism of the decoction with the traditional formula DCQT (T-DCQT) and a modified DCQT (M-DCQT) in an experimental POI mouse model. Methods Mice were divided into 5 experimental groups with 16 mice per group as follows: (1) control group; (2) sham group; (3) POI group; (4) T-DCQT group and (5) M-DCQT group. Each group was subdivided into 2 groups in which the therapeutic effect was examined at 24h and 48h after operation. POI was induced by classic intestinal manipulation operation and the gastrointestinal(GI) motility was measured with a charcoal marking mixture gavage. The intestinal tissues were collected for evaluation of the histopathological alteration, and analysis of the expression of inflammatory signal pathways, as NF-κB, p38 MAPK, and TLR4 by qPCR, immunohistochemical staining and western-blotting, respectively. Plasma inflammatory cytokines were determined using a high-throughput liquid chip. All analyses were performed with samples collected 24 and/or 48h after operation. Results GI transit was significantly reduced in mice with POI and this dysfunction was alleviated after administration of either T-DCQT or M-DCQT enema. When compared to controls, the pathological changes in the ileum mucosal of POI mice were significantly improved, and the increased expression of NF-κB, p38 MAPK, and TLR4 in the intestinal tissues were reversed, following T- DCQT or M-DCQT treatment. Plasma inflammatory cytokines, such as IL-1α, IL-6, MCP-1, MIP-1β and IL-17 levels were significantly highly expressed in POI group, and most of them, as IL-1α, IL-6, MIP-1β and IL-17 were significantly reduced after T-DCQT or M-DCQT treatment. Conclusion The current study indicated that administration of T-DCQT or M-DCOT could ameliorate the POI-associated inflammatory response and improve GI motility, by controlling inflammatory cytokines release and modulating the expression of some inflammatory signal pathways in the POI mouse model.

The electrochemical method for highly sensitive determination of arsenic(III) in real water samples with noble-metal-free nanomaterials is still a difficult but significant task. Here, an electrochemical sensor driven by noble-metal-free layered porous Fe3O4/Co3S4 nanosheets was successfully employed for As(III) analysis, which was prepared via a facile two-step method involves a hydrothermal treatment and a subsequent sulfurization process. As expected, the electrochemical detection of As(III) in 0.1 M HAc-NaAc (pH 6.0) by square wave anodic stripping voltammetry (SWASV) with a considerable sensitivity of 4.359 μA/μg·L−1 was obtained, which is better than the commonly used noble metals modified electrodes. Experimental and characterization results elucidate the enhancement of As(III) electrochemical performance could be attributed to its nano-porous structure, the presence of oxygen vacancies and strong synergetic coupling effects between Fe3O4 and Co3S4 species. Besides, the Fe3O4/Co3S4 modified screen printed carbon electrode (Fe3O4/Co3S4-SPCE) shows remarkable stability and repeatability, valuable anti-interference ability and could be used for detection in real water samples. Consequently, the results confirm that as-prepared porous Fe3O4/Co3S4 nanosheets is identified as a promising modifier to detect As(III) in real sample analysis.

Activated pancreatic stellate cells (PSCs) play a crucial role in the progression of pancreatic fibrosis. Transforming growth factor-β (TGF-β) is one of the strongest stimulator inducing fibrosis. The mitogen-activated protein kinase (MAPK) proteins (including ERK, JNK and p38 MAPK) are known to contribute to PSC activation and pancreatic fibrosis. Previous studies have identified PSC activation induced by TGF-β1 is related to MAPK pathway, but the respective role of MAPK family members in PSC activation still unclear, and which family member may be the key mediator in mice PSC activation still controversial. In this study, we investigated the influence of different MAPK family member (JNK, ERK, and p38 MAPK) on mice PSC activation using an in vivo and in vitro model. The results showed p-JNK, p-ERK and p-p38 MAPK were all over-expressed in CP group, and p-JNK, p-ERK, and p-p38 MAPK were co-expressed with activated PSC. In vitro, TGF-β1 induced JNK and ERK over-expression in PSCs. In contrast, p38 MAPK expression in PSC showed only a very weak increase. JNK- and ERK-specific inhibitors inhibited FN and α-SMA mRNA expression in PSCs, and a p38 MAPK inhibitor had no effect on PSC activation. These findings indicate that JNK and ERK were directly involved in the PSCs activation induced by TGF-β1 and the development of pancreatic fibrosis. p38 MAPK participate in the progression of CP, but it does not respond to TGF-β1 directly and may not be regarded as the target of TGF-β1 induced PSC activation.

Cu2Se nanobelts have been developed via a facile cation-exchange approach at room temperature, employing ZnSe·0.5N2H4 hybrid nanobelts as the templated precursors. Detailed characterizations demonstrate that the morphologies of the templated precursors are well-preserved in the cation-exchange reaction, because of the spatial confinement effect from the coated layer of poly(vinylpyrrolidone) (PVP) surfactant. Simultaneously, Cu2+ cations diffusing through the coated layer of PVP are in situ reduced to be Cu+ cations by the ligands of N2H4, thereby forming Cu2Se nanobelts with the complete replacement of Zn2+ cations in the templated precursors. After thermal oxidation in air, the obtained Cu2Se nanobelts are further converted into porous CuO nanobelts. Considering that this special morphology processes a large active surface area and is favorable for gas diffusion, gas-sensing properties of porous CuO nanobelts have been explored. The results indicate that porous CuO nanobelts exhibit highly selective sen...

The aim of the current study was to investigate the effects of early-stage dextran sodium sulfate (DSS)-induced mouse colitis on the biomechanical properties and microstructure of colon walls. In the present study, colitis was induced in 8-week-old mice by the oral administration of DSS, and then 10 control and 10 experimental colitis samples were harvested. Uniaxial tensile tests were performed to measure the ultimate tensile strength and ultimate stretches of colon tissues. In addition, histological investigations were performed to characterize changes in the microstructure of the colon wall following treatment. The results revealed that the ultimate tensile stresses were 232±33 and 183±25 kPa for the control and DSS groups, respectively (P=0.001). Ultimate stretches at rupture for the control and DSS groups were 1.43±0.04 and 1.51±0.06, respectively (P=0.006). However, there was no statistically significant difference in tissue stiffness between the two groups. Histological analysis demonstrated high numbers of inflammatory cells infiltrated into the stroma in the DSS group, leading to significant submucosa edema. Hyperplasia was also identified in the DSS-treated submucosa, causing a disorganized microstructure within the colon wall. Furthermore, a large number of collagen fibers in the DSS-treated muscular layer were disrupted, and fiber bundles were thinner when compared with the control group. In conclusion, early-stage experimental colitis alters the mechanical properties and microstructural characteristics of the colon walls, further contributing to tissue remodeling in the pathological process.

Ulcerative colitis (UC) is strongly associated with inflammation and intestinal barrier disorder. The nonselective cannabinoid receptor agonist HU210 has been shown to ameliorate inflamed colon in colitis, but its effects on intestinal barrier function and extraintestinal inflammation are unclear. To investigate the effects and the underlying mechanism of HU210 action on the UC in relation to a role of TLR4 and MAP kinase signaling. Wild-type (WT) and TLR4 knockout (Tlr4 −/−) mice were exposed to 4% dextran sulfate sodium (DSS) for 7 days. The effects of HU210 on inflammation and intestinal barrier were explored. Upon DSS challenge, mice suffered from bloody stool, colon shortening, intestinal mucosa edema, pro-inflammatory cytokine increase and intestinal barrier destruction with goblet cell depletion, increased intestinal microflora accompanied with elevated plasma lipopolysaccharide, reduced mRNA expression of the intestinal tight junction proteins, and abnormal ratio of CD4+/CD8+ T cells in the intestinal Peyer’s patches. Pro-inflammatory cytokines in the plasma and the lung, as well as pulmonary myeloperoxidase activity, indicators of extraintestinal inflammation were increased. Protein expression of p38α and pp38 was up-regulated in the colon of WT mice. Tlr4 −/− mice showed milder colitis. HU210 reversed the intestinal barrier changes in both strains of mice, but alleviated inflammation only in WT mice. Our study indicates that in experimental colitis, HU210 displays a protective effect on the intestinal barrier function independently of the TLR4 signaling pathway; however, in the extraintestinal tissues, the anti-inflammatory action seems through affecting TLR4-mediated p38 mitogen-activated protein kinase pathway.

Inhibition of the protein C system (PCS) might be one of the mechanisms of ulcerative colitis (UC).The aim of the study was to explore the role of IgG plasma cells in changes in the PCS in UC.Dextran sulfate sodium (DSS) was chosen to induce mouse UC. Inflammation was assessed using hematoxylineosin (HE) staining and immunofluorescence. The profiling of colonic plasma cells and macrophages from colitis mice was analyzed with flow cytometry. After stimulation of macrophages with IgG type immune complex (IgG-IC), western blot was used to determine tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) protein levels. After co-incubation of colonic mucosa microvascular endothelial cells (MVECs) with TNF-α or IL-6, mitogen-activated protein kinase (MAPK) expression was detected.The DSS-colitis mice showed higher inflammatory indexes (p0.05 or p0.01), accompanied by greater infiltration of CD38+IgG+ plasma cells (p0.01), CD14+CD64+ macrophages (p0.01) and IgG-IC than healthy mice. Enhancement of TNF-α and IL-6 protein expression was demonstrated in this subset of macrophages when stimulated by IgG-IC (p0.01). After MVECs were incubated with TNF-α or IL-6, the expression of β-arrestin1, pP38 MAPK and pJNK MAPK exhibited an increase (p0.05 or p0.01), but downregulation of endothelial protein C receptor (EPCR) expression was observed (p0.05 or p0.01); this inhibition of EPCR expression was reversed by SB203580, SP600125 or U0126 (p0.05 or p0.01). In addition, changes in activated protein C (APC) presented results similar to those for EPCR expression (p0.05 or p0.01).These results reveal that the PCS is inhibited during UC processing. There is a possibility that the interaction between IgG plasma cells and CD14+CD64+ macrophages, as well as further secretion of cytokines from CD14+CD64+ macrophages by the formation and stimulation of IgG-IC, subsequently influence MVECs through the β-arrestin-MAPK pathway. Enhancement of PCS activity may represent a novel approach for treating UC.

Background This study attempted to provide the effects and mechanisms of two cannabinoids, O-1602 and cannabidiol (CBD), on colonic motility of 2,4,6-trinitro-benzene sulfonic acid (TNBS) colitis. Methods TNBS was used to induce the model of motility disorder. G protein-coupled receptor 55 (GPR55) expression was detected using real-time PCR and immunohistochemistry in colon. Pro-inflammatory cytokines and myeloperoxidase were also measured. The colonic motility was measured by upper GI transit in vivo and recorded using electrical stimulation organ bath technique in vitro. Freshly isolated smooth muscle from the rat colon were applied to determine the membrane potential and Ca2+ -ATPase activity, respectively. Key results CBD or O-1602 separately improved inflammatory conditions significantly in TNBS-induced colitis rats. However, sole CBD pretreatment reduced GPR55 expression, which was up-regulated in TNBS colitis. O-1602 and CBD each lowered MPO and IL-6 levels remarkably in TNBS colitis, while TNF-α levels experienced no change. CBD rescued the downward colonic motility in TNBS colitis in vivo; however, it decreased the upward contraction of the smooth muscle strip under electrical stimulation in vitro. Pretreatment with CBD prevented against TNBS-induced changes of Ca2+ -ATPase activity of smooth muscle cells. However, membrane potential of the smooth muscle cells decreased by TNBS experienced no change after O-1602 or CBD import. Conclusions & inferences The present study suggested that CBD participated in the regulation of colonic motility in rats, and the mechanisms may be involved in the regulation of inlammatory factors and Ca2+ -ATPase activity through GPR55.

The potential capability to rapid, highly sensitive, and selective diagnose neurotransmitters in human serum environment is extremely crucial for clinical biology. Herein an electrochemical sensor based on Ag nanoparticles anchored onto CuO porous nanobelts (Ag/CuO PNBs) was constructed for the ultrasensitive determination of dopamine (DA), which was prepared via a facile two-step cation-exchange reaction followed by in-situ thermal conversion. The Ag/CuO PNBs exhibited an excellent electrochemical sensing performance to DA. The linear range for the detection of DA was ranged from 0.04 to 10 μM with an outstanding detection limit of 7.0 nM. Cyclic voltammograms (CVs) were employed to investigate kinetic information of multiphase electron transfer reactions, revealing that Ag nanoparticles significantly enhanced electrocatalytic activity toward DA owing to the participation of Ag(0)/Ag(I) cycle. Meanwhile, the Ag/CuO PNBs showed the significant selectivity, remarkable stability and repeatability, as well as attractive reproducibility (RSD ≤ 3.7 %). Furthermore, the practicality of the developed sensor has been evaluated by analyzing DA in serum-containing electrolyte, and the recovery in the range of 95.7∼111.1 % was obtained. The results confirmed that the as-prepared sensor presented a significant promise for the detection of DA in real sample analysis.

AIM To investigate the anti-inflammatory effect and the possible mechanisms of an agonist of cannabinoid (CB) receptors, WIN55-212-2 (WIN55), in mice with experimental colitis, so as to supply experimental evidence for its clinical use in future. METHODS We established the colitis model in C57BL/6 mice by replacing the animals’ water supply with 4% dextran sulfate sodium (DSS) for 7 consecutive days. A colitis scoring system was used to evaluate the severity of colon local lesion. The plasma levels of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), and the myeloperoxidase (MPO) activity in colon tissue were measured. The expressions of cannabinoid receptors, claudin-1 protein, p38 mitogen-activated protein kinase (p38MAPK) and its phosphorylated form (p-p38) in colon tissue were determined by immunohistochemistry and Western blot. In addition, the effect of SB203580 (SB), an inhibitor of p38, was investigated in parallel experiments, and the data were compared with those from intervention groups of WIN55 and SB alone or used together. RESULTS The results demonstrated that WIN55 or SB treatment alone or together improved the pathological changes in mice with DSS colitis, decreased the plasma levels of TNF-α, and IL-6, and MPO activity in colon. The enhanced expression of claudin-1 and the inhibited expression of p-p38 in colon tissues were found in the WIN55-treated group. Besides, the expression of CB1 and CB2 receptors was enhanced in the colon after the induction of DSS colitis, but reduced when p38MAPK was inhibited. CONCLUSION These results confirmed the anti-inflammatory effect and protective role of WIN55 on the mice with experimental colitis, and revealed that this agent exercises its action at least partially by inhibiting p38MAPK. Furthermore, the results showed that SB203580, affected the expression of CB1 and CB2 receptors in the mouse colon, suggesting a close linkage and cross-talk between the p38MAPK signaling pathway and the endogenous CB system.

In order to meet the demands for rapid and safe nondestructive testing of fruit and vegetable quality，tomato detection system with a special circular light source was built based on the visible / near infrared diffuse transmission principle. Taking soluble solids content (SSC) and total sugar (TS) as the internal quality index, the prediction of 58 tomato samples was carried out by using this system. First, we collected the spectral data of four points for each tomato. Second, Savitzky-Golay smooth(SG-Smooth), standard normal variable transformation(SNV), multiplication scattering correction(MSC), first derivative (FD) and other methods were used to process the original spectral curve before the partial least squares regression(PLSR) model was established. Finally, we validated the established model. The results show that the correlation coefficient (r) of calibration and prediction of the SSC prediction model -are 0.995 6 and 0.976 0 when using 10 point SG-smooth, and the root mean square error of calibration and prediction are 0.052 4% and 0.082 3%. The partial least square regression (PLSR)model, with respect to the first derivative (FD) spectra, provides better prediction performance for total sugar of tomato, with correlation coefficient (r) of calibration of 0.969 1 and 0.972 9, and prediction, root mean standard error of 0.423 8% and 0.454 9%. In the experimental verification of the prediction model, the relationship of SSC between predicted and true value is 0.985 5, root mean square error is 0.066 3°Brix, the relationship of TS between predicted and true value is 0.944 9 while root mean square error is 0.571 5%. The results show that the content of soluble solids and total sugar in tomato can be realized by using visible / near infrared diffuse reflectance spectroscopy. It provides a real-time, nondestructive and rapid detection method for the evaluation of the internal quality of tomato, and provides a theoretical basis for its online grading.

Porous ZnO nanobelts sensitized with Ag nanoparticles have been prepared via a partial cation-exchange reaction assisted by a thermal oxidation treatment, employing ZnSe·0.5N2H4 nanobelts as precursors. After partially exchanged with Ag+ cations, the belt-like morphology of the precursors is still preserved. Continuously calcined in air, they are in situ transformed into Ag nanoparticles sensitized porous ZnO nanobelts. The size of the Ag nanoparticles can be tuned through manipulating the amount of exchanging Ag+ cations. Considering the porous and belt-like nanostructure, sensing characteristics of ZnO and the catalytic activity of Ag nanoparticles, the gas sensing performances of the as-prepared Ag nanoparticles sensitized porous ZnO nanobelts have been carefully investigated. The results indicate that Ag nanoparticles significantly enhance the sensing performances of porous ZnO nanobelts toward typical volatile organic compounds. Especially, a good selectivity has been demonstrated toward acetic acid gas with a low detection limit less than 1 ppm. Furthermore, they also display a good reproducibility with a short response/recovery time due to the thin, uniform and porous sensing film, which is fabricated with the assembled technique and in situ calcined approach. Finally, their sensing mechanism has been further discussed.

In this research, the surface enhanced Raman spectroscopy (SERS) technique is used to develop a nondestructive and fast detecting method for the detection of residual chlorpyrifos on spinach. Silver colloids used for SERS spectroscopy is prepared by the reduction of silver nitrate with hydroxylamine hydrochloride at alkaline pH. The prepared silver colloids are dropped onto spinach samples, then the SERS spectra are collected non-destructively with a self-developed Raman system. This method can be made without physical contact to samples, and rapidly completed without time-consuming sample pre-treatments, and suited to the development of real-time on-line detection methods for trace pesticide residues. SERS signals are collected from 20 points on each spinach sample with 450 mW laser power and 2.5 s exposure time. Chlorpyrifos concentrations in 24 samples are determined with gas chromatography after SERS spectra taken. Savitzky-Golay (SG) smoothing filter and effective peak linear fitting method are used to remove the random noise and the fluorescence background for improving the accuracy of SERS results. The SERS signals are collected from different parts of 50 spinach samples with the same concentration of chlorpyrifos but at different fresh degrees. The relative standard deviation (RSD) of chlorpyrifos’ characteristic peak intensities is 13.4%. Although the differences of samples lead to differences in the curves of Raman spectrum, they have little influence on the characteristic peak intensities, which indicates the stability of the proposed detecting method. After the fluorescent background removed, the 20 curves of each sample are averaged. Correlation analysis is done between chlorpyrifos concentration and signal intensity at every Raman shift. Results show that correlation coefficients are higher than 0.85 in the range of 615.5~626.4 cm-1. Signals in this range are used to establish multiple linear regression (MLR) model for the prediction of residual chlorpyrifos. MLR model was developed for chlorpyrifos concentration versus Raman signal intensity at 615.5~626.4 cm-1 for predicting residual chlorpyrifos content in samples, the correlation coefficients of calibration (RC) and validation (RP) are 0.961 and 0.954, which indicate a good linear relationships between them. The minimum detectable threshold for this method is 0.05 mg·kg-1 which is close to the value limited by the national standard of China (0.1 mg·kg-1 for chlorpyrifos in spinach). The proposed practical method is sample, fast, without sample preparation, thus it shows great potential in safety detection of fruits and vegetables.

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Colorectal cancer (CRC) has become the fourth leading cause of cancer-related death in the worldwide. It is urgent to find more effective therapeutic strategies for it. Reactive oxygen species (ROS) play multiple roles in normal cellular physiology processes. Thus, a certain level of ROS is essential to keep normal cellular function. However, the accumulation of ROS shows dual roles for cells, which is mainly dependent on the concentration of ROS, the origin of the cancer cell and the activated signaling pathways during tumor progression. In general, moderate level of ROS leads to cell damage, DNA mutation and inflammation, which promotes the initiation and development of cancer. Excessive high level of ROS induces cancer cell death, showing an anti-cancer role. ROS are commonly higher in CRC cells than their normal counterpart cells. Therefore, it is possible that ROS induce cell death in cancer cells while not affecting the normal cells, demonstrating lower side effects. Besides, ROS also play a role in tumor microenvironment and drug resistance. These multiple roles of ROS make them a promising therapeutic target for cancer. To explore potential ROS-target therapies against CRC, it is worth to comprehensively understanding the role of ROS in CRC and therapy. In this review, we mainly discuss the strategies of ROS in CRC therapy, including direct CRC cell target and indirect tumor environment target. In addition, the influences of ROS in drug resistance will also been discussed.

Background The changes in the gut barrier (GB) and associated mechanisms in postoperative ileus (POI) are still unclear. Toll-like receptor 4 (TLR4) is involved in inflammation, which may cause GB dysfunction and POI. Here, the roles of the GB in POI in relation to TLR4-dependent signaling pathways were explored. Methods POI was induced by small bowel manipulation in wild-type (WT) and TLR4-knockout (TLR4-/-) mice. Twenty-four hours after manipulation, indices of gastrointestinal (GI) transit, GB structure and function, inflammation, and related signaling pathways were analyzed. Key results Normal GI motility and GB function were not affected by TLR4 knockout. Compared with WT POI mice, TLR4-/-POI mice showed milder GI transit retardation, GB dysfunction, and inflammatory responses. In WT mice, GB disorder was characterized by colonic goblet cells depletion, increased gut claudin-2 expression, and decreased CD4+/CD8+ ratios in intestinal Peyer's patches. Green fluorescent protein-tagged Escherichia coli in the gut was detected in plasma and extraintestinal organs, followed with increased plasma lipopolysaccharide. These changes displayed in WT POI mice were less severe in TLR4-/-POI mice. Furthermore, the mRNA and protein expression of interleukin-6, monocyte chemotactic protein-1, pp38 and pJNK in the intestine, and TNF-α level in plasma were significantly increased in WT, but not TLR4-/-POI mice. Conclusions & inferences These results indicate that GB is impaired in the experimental POI, with inflammation being involved in this pathological process. TLR4 deficiency alleviated GB dysfunction and suppressed inflammation by disrupting the activation of mitogen-activated protein kinase signaling pathways, thereby ameliorating POI.

Berberine is an isoquinoline alkaloid present in several plant species, including Coptis sp. and Berberis sp. In traditional medicine, extracts of berberine are used in the treatment of diarrhea of different origins. Recent studies have shown that berberine and its derivatives have significant biological effects on gastrointestinal (GI) and other functions and may become therapeutics for the treatment of diarrhea, gastroenteritis, diabetes, hyperlipidemia, cardiovascular diseases and inflammatory conditions. This paper summarizes the current knowledge on the actions of berberine in the GI tract. Binding and target sites, activated intracellular pathways, as well as the absorption and metabolism of berberine are discussed. Effects that may be useful in future clinical treatment, like antidiarrheal, anti-inflammatory and antitumor effects are critically reviewed and potential clinical applications are presented in detail.

The measurement of ultralow concentrations of heavy metal ions (HMIs) in blood is challenging. A new strategy for the determination of mercury ions (Hg2+ ) based on an oriented ZnO nanobelt (ZnO-NB) film solution-gated field-effect transistor (FET) chip is adopted. The FET chips are fabricated with ZnO-NB film channels with different orientations utilizing the Langmuir-Blodgett (L-B) assembly technique. The combined simulation and I-V behavior results show that the nanodevice with ZnO-NBs parallel to the channel has exceptional performance. The sensing capability of the oriented ZnO-NB film FET chips corresponds to an ultralow minimum detectable level (MDL) of 100 × 10-12 m in deionized water due to the change in the electrical double layer (EDL) arising from the synergism of the field-induced effect and the specific binding of Hg2+ to the thiol groups (-SH) on the film surface. Moreover, the prepared FET chips present excellent selectivity toward Hg2+ , excellent repeatability, and a rapid response time (less than 1 s) for various Hg2+ concentrations. The sensing performance corresponds to a low MDL of 10 × 10-9 m in real samples of a drop of blood.

The role of metabolic acidosis in the progression of chronic kidney disease (CKD) remains unclear. The aim of the present study was to investigate the direct effects of acid loading on the proliferation of rat glomerular mesangial cells (GMCs) in vitro and the possible role of sodium-hydrogen ion exchanger isoform 1 (NHE1). Rat GMCs were treated with acidic medium as acid loading. Growth and proliferation of GMCs was studied by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay, thymidine ((3)H-TdR) incorporation, and flow cytometry. NHE1 protein expression and activity were quantified by Western blot and dual wavelength epifluorescent illumination with 2',7'-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein, respectively. 5-(N,N-dimethyl) amiloride hydrochloride (DMA), a specific inhibitor of NHE1, was used to investigate the possible involvement of NHE1 in the proliferation of GMCs. The MTT assay, (3)H-TdR incorporation, and cell cycle distribution analysis indicated that acid loading stimulated the proliferation of GMCs. Acid loading increased NHE1 activity, but had no effects on NHE1 expression at the protein level. The effects of acid loading on the proliferation of GMCs were inhibited by DMA. Acid loading induced GMC proliferation through NHE1-dependent pathways. Our findings may contribute to the understanding of metabolic acidosis in the progression of CKD.

Although Berberine (BER) is popular in treating gastrointestinal (GI) disorders, its mechanisms are not clear yet. In order to investigate the effects and possible mechanism of BER on GI motility in rodents, we first explored GI motility by recording the myoelectrical activity of jejunum and colon in rats, and upper GI transit with a charcoal marker in mice. Then, the plasma levels of gastrin, motilin, somatostatin and glucagon-like-peptide-1 (Glp-1) were measured by ELISA or radioimmunoassay (RIA). Furthermore, endogenous opioid-peptides (β-endorphin, dynorphin-A, met-enkephalin) were detected by RIA after treatment with BER. Our results showed that BER concentration-dependently inhibited myoelectrical activity and GI transit, which can be antagonized by opioid-receptor antagonists to different extents. The elevated somatostatin and Glp-1, and decreased gastrin and motilin in plasma, which were caused by BER application, also could be antagonized by the opioid-receptor antagonists. Additionally, plasma level of β-endorphin, but not dynorphin-A and met-enkephalin, was increased by applying BER. Taken together, these studies show that BER plays inhibiting roles on GI motility and up-regulating roles on somatostatin, Glp-1 and down-regulating roles on gastrin, motilin. The pharmacological mechanisms of BER on GI motility and plasma levels of GI hormones were discovered to be closely related to endogenous opioid system.

Raman spectroscopy combined with chemometric methods has been thought to an efficient method for identification and determination of pesticide residues in fruits and vegetables. In the present research, a rapid and nondestructive method was proposed and testified based on self-developed Raman system for the identification and determination of deltamethrin and acetamiprid remaining in apple. The peaks of Raman spectra at 574 and 843 cm(-1) can be used to identify deltamethrin and acetamiprid, respectively, the characteristic peaks of deltamethrin and acetamiprid were still visible when the concentrations of the two pesticides were 0.78 and 0.15 mg · kg(-1) in apples samples, respectively. Calibration models of pesticide content were developed by partial least square (PLS) algorithm with different spectra pretreatment methods (Savitzky-Golay smoothing, first derivative transformation, second derivative transformation, baseline calibration, standard normal variable transformation). The baseline calibration methods by 8th order polynomial fitting gave the best results. For deltamethrin, the obtained prediction coefficient (Rp) value from PLS model for the results of prediction and gas chromatography measurement was 0.94; and the root mean square error of prediction (RMSEP) was 0.55 mg · kg(-1). The values of Rp and RMSEP were respective 0.85 and 0.12 mg · kg(-1) for acetamiprid. According to the detect performance, applying Raman technology in the nondestructive determination of pesticide residuals in apples is feasible. In consideration of that it needs no pretreatment before spectra collection and causes no damage to sample, this technology can be used in detection department, fruit and vegetable processing enterprises, supermarket, and vegetable market. The result of this research is promising for development of industrially feasible technology for rapid, nondestructive and real time detection of different types of pesticide with its concentration in apples. This supplies a rapid nondestructive and environmentally friendly way for the determination of fruit and vegetable quality and safety.

Inflammatory bowel disease (IBD) includes ulcerative colitis and Crohn's disease which is characterized by the recurrent intestinal inflammation and overactive immune responses. The signaling pathways of p38 mitogen-activated protein kinase (MAPK) play an important role in bowel inflammation. The inhibition of p38 MAPK can effectively suppress the expression of inflammatory mediators. However, due to the obvious preclinical and clinical side effects, p38 inhibitors are unacceptable in safety profiles and cannot be applied in the treatment of IBD. MAPK-activated protein kinase 2 (MK2), as the direct substrate of p38α and p38β, is a multifunctional signaling protein in the progression of inflammation and several lines of evidence demonstrate that the inhibition of MK2 may produce the same beneficial effect as the inhibition of p38 MAPK. Hence, MK2 is likely to be a potential drug target for the treatment of IBD.

A unique subset of B cells expressing interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) plays an essential role in preventing inflammation and autoimmunity. We investigated the presence of this cell subset in intestines and its role in the pathogenesis of ileitis using SAMP1/Yit and age-matched control AKR/J mice. Mononuclear cells were isolated from mesenteric lymph nodes (MLNs) and the expressions of B220, CD1d, CD5, Toll-like receptor 4 (TLR4) and TLR9 in isolated cells were analysed. Purified B cells were stimulated with lipopolysaccharide (LPS) or CpG-DNA, then IL-10 and TGF-β(1) expressions were examined by enzyme immunoassay and flow cytometry. Production of IL-1β by TLR-mediated macrophages co-cultured with or without purified MLN B cells from SAMP1/Yit and AKR/J mice was evaluated. In addition, interferon-γ (IFN-γ) production in intestinal T cells co-cultured with MLN B cells were also assessed in SAMP1/Yit and AKR/J strains. The production levels of IL-10 and TGF-β(1) stimulated by LPS and CpG-DNA were significantly lower in B cells separated from MLNs from the SAMP1/Yit strain. B cells expressing IL-10 and TGF-β(1) were mainly located in a population characterized by the cell surface marker CD1d(+) . Interleukin-1β production by TLR-activated macrophages co-cultured with MLN B cells from SAMP1/Yit mice was significantly higher than that of those from AKR/J mice. Interestingly, IFN-γ production by T cells was noted only when they were co-cultured with SAMP1/Yit but not the AKR/J B cells. These results are the first to show that disorders of regulatory B-cell function under innate immune activation may cause disease pathogenesis in a murine model of Crohn's disease.

Many etiological factors are involved in the pathogenesis of acute pancreatitis. The pathogenesis of acute pancreatitis has been attributed to such causes as trypsin autodigestion, pancreatic microcirculation malfunction, the calcium overload in pancreatic acinar cells, oxygen free radical injury, cytokine injury, and has been treated in detail in numerous reviews. More recently, heat shock proteins (HSP), particularly heat shock protein 60 (HSP60), have receive increasing attention as another possible factor in the pathogenesis and development of acute pancreatitis. This brief review aims to: (i) outline our current understanding of HSP and their role in pancreatitis; (ii) discuss the available evidences that suggest HSP's interplay between pancreas tissues and etiological agents; (iii) delineate the functional mechanisms of HSP proposed by different research groups, and offer new thinking in preventing and treating acute pancreatitis in general.

Objective. Heparin-binding epidermal growth factor-like growth factor (HB-EGF) has been shown to stimulate the growth and migration of human keratinocytes in an autocrine or paracrine manner. Bearing in mind the preceding narratives, present study was designed to explore the role of HB-EGF on esophageal epithelial cell growth, migration and anti-apoptosis. Material and methods. HET-1A and TTn cells were treated with recombinant HB-EGF, and cell proliferation and migration were assessed by MTT and Boyden chamber assays, respectively. Anti-apoptotic effects of HB-EGF was studied by Bcl-2/Bcl-xL gene expression and utilizing a TNF-related death apoptosis inducing ligand (TRAIL). Results. Recombinant HB-EGF promotes human esophageal epithelial cell proliferation in a dose dependent manner, where 1 and 10 ng/ml doses were found to be most effective. HB-EGF induced cell migration was noted in TTn, but not in HET-1A cells. Recombinant HB-EGF induced the Bcl-2, Bcl-xL mRNA/protein expression in HET-1A and TTn cells. TRAIL induced the apoptosis in TTn, whereas it was significantly inhibited in HB-EGF treated conditions. Finally, we also revealed HB-EGF induced phosphorylation of EGFR and p38 MAPK in those cell lines, while all cellular functions were repressed by EGFR inhibitor AG1478. Conclusion. HB-EGF promotes esophageal epithelial cell proliferation, migration and induces anti-apoptotic gene expression via EGFR/p38 MAPK phosphorylation.

The objective of this study was to investigate the function of heat shock protein 60 (HSP60) on pancreatic tissues by applying HSP60 small interfering RNA (siRNA) to reduce HSP60 expression. Rat pancreas was isolated and pancreatic tissue snips were prepared, cultured, and stimulated with low and high concentrations of cerulein (10−11 and 10−5 mol/L) or lipopolysaccharide (LPS, 10 and 20 μg/mL). Before the stimulation and 1 and 4 h after the stimulation, the viability and the level of trypsinogen activation peptide (TAP) in the tissue fragments were determined and the levels of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) in the culture supernatants were measured. Real-time PCR and Western blotting were used to evaluate the HSP60 mRNA and protein expression. After the administration of siRNA to inhibit HSP60 expression in the isolated tissues, these injury parameters were measured and compared. The pancreatic tissues in the control (mock-interfering) group showed a decreased viability to varying degrees after being stimulated with cerulein or LPS, and the levels of TAP, TNF-α, and IL-6 increased significantly (p

A unique subset of B cells expressing interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) plays an essential role in preventing inflammation and autoimmunity. We investigated the presence of this cell subset in intestines and its role in the pathogenesis of ileitis using SAMP1/Yit and age-matched control AKR/J mice. Mononuclear cells were isolated from mesenteric lymph nodes (MLNs) and the expressions of B220, CD1d, CD5, Toll-like receptor 4 (TLR4) and TLR9 in isolated cells were analysed. Purified B cells were stimulated with lipopolysaccharide (LPS) or CpG-DNA, then IL-10 and TGF-β(1) expressions were examined by enzyme immunoassay and flow cytometry. Production of IL-1β by TLR-mediated macrophages co-cultured with or without purified MLN B cells from SAMP1/Yit and AKR/J mice was evaluated. In addition, interferon-γ (IFN-γ) production in intestinal T cells co-cultured with MLN B cells were also assessed in SAMP1/Yit and AKR/J strains. The production levels of IL-10 and TGF-β(1) stimulated by LPS and CpG-DNA were significantly lower in B cells separated from MLNs from the SAMP1/Yit strain. B cells expressing IL-10 and TGF-β(1) were mainly located in a population characterized by the cell surface marker CD1d(+) . Interleukin-1β production by TLR-activated macrophages co-cultured with MLN B cells from SAMP1/Yit mice was significantly higher than that of those from AKR/J mice. Interestingly, IFN-γ production by T cells was noted only when they were co-cultured with SAMP1/Yit but not the AKR/J B cells. These results are the first to show that disorders of regulatory B-cell function under innate immune activation may cause disease pathogenesis in a murine model of Crohn's disease.

Postoperative ileus involves reflex inhibition of intestinal motility within hours after surgery and a subsequent intestinal inflammatory response that is characterized by efferent vagal modulation via acetylcholine receptors on intestinal macrophages. We aimed to characterize the role of vagal modulation of intestinal motility during the early hours after surgery.C57BL6 mice underwent laparotomy and standardized small bowel manipulation to induce postoperative ileus. Subgroups were vagotomized 3-4 days prior to experiments or received pharmacological inhibition of the acetylcholine alpha7 subunit with the inhibitor alpha-bungarotoxin, while control animals were sham operated and remained otherwise untreated. Three hours later, a 2-cm jejunal segment was harvested with the mesentery attached. Mesenteric afferent nerve recordings were established in an organ bath generating a multiunit signal with subsequent computerized analysis. Intraluminal pressure was continuously recorded to assess intestinal motility. Afferent nerve responses were quantified at baseline and to chemical stimulation with bradykinin (0.5 microM) or serotonin (5-HT; 500 microM) and following mechanical stimulation by continuous ramp distension to 60 mmHg.Peak amplitudes of intestinal motility and afferent nerve discharge at baseline were not different following chronic vagotomy, alpha-bungarotoxin or sham operation. Maximum afferent discharge to 5-HT following alpha-bungarotoxin was comparable to sham controls, while the response was reduced in chronically vagotomized animals (p0.05). Maximum afferent nerve discharge to bradykinin and peak firing during maximum distension at 60 mmHg was similar in the different subgroups. At luminal distension from 10 to 30 mmHg, afferent discharge was lower in vagotomized animals compared to sham controls (p0.05) but unchanged after alpha-bungarotoxin.Sensitivity to low-threshold distension and 5-HT is mediated via vagal afferents during postoperative ileus, while sensitivity to high-threshold distension and bradykinin is independent of vagal afferent innervation. Early inhibition of intestinal motility at 3 h after onset of postoperative ileus does not appear to depend on vagal innervation.

The objective of this study was to investigate the role of MAPKAP kinase 2 (MK2) and heat shock protein (HSP) HSP60 in the pathogenesis of a new model of severe acute pancreatitis (AP). MK2 plays a significant role in the regulation of cytokines. It has been shown that induction and expression of several HSPs can protect against experimental pancreatitis. Interplay between both systems seems of high interest. Mice with a homozygous deletion of the MK2 gene were used. Severe AP was induced by combined intraperitoneal injections of cerulein with lipopolysaccharide (LPS). Severity of AP was assessed by biochemical markers and histology. The serum IL-6 and lung myeloperoxidase (MPO) levels were determined for assessing the extent of systemic inflammatory response. Expression of HSP25, HSP60, HSP70, and HSP90 was analyzed by Western blotting. Repeated injections of cerulein alone or cerulein plus LPS (Cer+LPS) resulted in local inflammatory responses in the pancreas and corresponding systemic inflammatory changes with pronounced severity in the Cer+LPS group. Compared with the C57Bl wild-type mice, the MK2−/− mice presented with significant milder pancreatitis and attenuated responses of serum amylase and trypsinogen activity. Furthermore, serum IL-6 was decreased as well as lung MPO activity. Injection of LPS alone displayed neither pancreatic inflammatory responses nor alterations of pancreatic enzyme activities but evidently elevated serum IL-6 levels and increased lung MPO activity. In contrast hereto, in the MK2−/− mice, these changes were much milder. Increased expression of HSP25 and HSP60 occurred after induction of AP. Especially, HSP60 was robustly elevated after Cer+LPS treatment, in both MK2−/− and wild-type mice. Thus the homozygous deletion of the MK2 gene ameliorates the severity of acute pancreatitis and accompanying systemic inflammatory reactions in a new model of severe acute pancreatitis. Our data support the hypothesis that MK2 participates in the multifactorial regulation of early inflammatory responses in AP, independently of the regulation of stress proteins like HSP25 and HSP60 and most likely due to its effect on cytokine regulation.

CD5(+) B cells comprise a unique subset of B cells that modulates innate as well as autoimmune systems. The aim of this study was to investigate alterations of the circulating CD5(+) B-cell subset in patients with inflammatory bowel disease (IBD) by evaluating various clinical parameters, including therapeutic regimens.Thirty-four patients with ulcerative colitis (UC), 19 patients with Crohn's disease (CD), and 46 healthy control subjects were enrolled in this study. CD5(+) B cells in peripheral blood collected from each subject were analyzed by flow cytometry. Multiple regression analysis was carried out to evaluate the factors related to the circulating CD5(+) B-cell subset in the IBD patients. In an in vitro examination, dexamethasone-induced apoptosis in peripheral blood B cells was examined by detecting cell surface binding of the annexin-V antibody.Age and gender in the control subjects did not influence the circulating CD5(+) B-cell subset. Multiple regression analysis showed that the presence of UC, corticosteroid therapy, and number of white blood cells in peripheral blood each had a significant influence in decreasing the number of circulating CD5(+) B cells in the IBD patients. Furthermore, in vitro results showed that dexamethasone treatment significantly induced apoptosis in CD5(+) B cells, though apoptosis was similarly observed in CD5(-) B cells.CD5(+) B cells may be involved in the pathogenesis of UC, and modulation of this subset by corticosteroid therapy may play a role in the treatment of IBD patients.

The expression of heat-shock protein 60 (also known as chaperonin 60, Cpn60) in experimental acute pancreatitis (AP) is considered to play an active role in the prevention of abnormal enzyme accumulation and activation in pancreatic acinar cells. However, there are controversial results in the literature regarding the relationship between the abnormality of Cpn60 expression and AP onset and development. The purpose of this study was to investigate the alternations of Cpn60 expression and the relationship between the abnormal expression of Cpn60 and AP progression in rat severe acute pancreatitis (SAP) models. In this report, we induced SAP in Sprague–Dawley (SD) rats by reverse injection of sodium deoxycholate into the pancreatic duct, and examined the dynamic changes of Cpn60 expression in pancreatic tissues from different time points and at different levels with techniques of real-time PCR, western blotting, and immunohistochemistry. At 1 h after SAP induction, the expression of Cpn60 mRNA in the AP pancreatic tissues was higher than those in the sham-operation group and normal control group, but decreased sharply as the time period was extended, and there was a significant difference between 1 h and 10 h after SAP induction (p

Cks1 is a member of the cyclin-dependent kinase subunit family. These proteins are essential components of cyclin/cyclin-dependent kinase (cdk) complexes contributing to cell cycle control in all eukaryotes. Cks1 protein is found overexpressed in a number of tumors. Expression of Cks1 mRNA starts in late G1 reaching a peak in S/G2-phases of the cell cycle. We find that this expression pattern depends on transcriptional regulation and is controlled by a combination of a cell cycle-dependent element (CDE) together with a cell cycle genes homology region (CHR) in the Cks1 promoter. Furthermore, we observe Cks1 mRNA and protein to be downregulated after induced expression of the tumor suppressor p53. This repression is due to p53 downregulating transcription from the Cks1 promoter. p53-dependent repression is seen in a dose-dependent manner and in several cell types of different origin. In contrast to p53, its homologues p63 and p73 do not significantly repress transcription from the Cks1 promoter. The Cks1 promoter does not contain a p53 binding site. For some promoters the CCAAT box-binding transcription factor NF-Y had been implicated in p53-dependent repression. NF-Y is the main activator for Cks1 transcription but does not influence p53-dependent repression from the Cks1 promoter. Generally, the observation that the potential oncogene Cks1 is downregulated by the tumor suppressor p53 corresponds well with the idea that p53 employs multiple ways in order to halt the cell cycle.

Hematite-cuprous oxide (α-Fe2O3/Cu2O) nanocomposites are synthesized based on the design of Z-scheme photocatalyst for CO2 reduction. The band structure for the typical Fe2O3/Cu2O (with 1:1 mole ratio) is characterized by UV-vis reflectance spectroscopy and X-ray/ultraviolet photoelectron spectroscopy, and its heterojunction is determined to be Type II band alignment. The photoreduction CO2 activities of the heterostructures are investigated in the presence of water vapor. The CO yields are changed with Fe/Cu mole ratio, and the maximal CO yield attains 5.0 μmol·g cat(-1) after 3 h of visible-light irradiation. Besides the effect of light wavelength, H2O/CO2 molar ratio and temperature on the products is studied. The selectivity of the prepared catalysts is tunable by modulating the light wavelength. The reaction mechanism is proposed and further confirmed experimentally. The results gained herein may provide some insights into the design of Z-scheme photocatalysts for CO2 reduction.