Unveiling hidden interactions: Microorganisms, enzymes, and mangroves at different stages of succession in the Shankou Mangrove Nature Reserve, China.

Understanding the interactions between microorganisms, soil extracellular enzymes, and mangroves is crucial for conserving and restoring mangrove ecosystems. However, the unique environments associated with mangroves have resulted in a lack of pertinent data regarding the interactions between these components. Root, stem, leaf, and soil samples were collected at three distinct stages of mangrove succession. Stoichiometry was employed to analyze the carbon, nitrogen, and phosphorus contents of these samples and to quantify extracellular enzyme activities, microbial biomass, and various physicochemical factors in the soil. The results showed that the trends of C, N, and P in the mangrove plants were consistent. Microbial biomass carbon (MBC), microbial biomass nitrogen (MBN), and microbial biomass phosphorus (MBP) were the highest in the Kandelia obovate community. Catalase (CAT) and ß-D-G showed the highest content in K. obovate and Bruguiera gymnorrhiza, whereas cellulase showed the opposite trend. Urease was least abundant in the K. obovate community, whereas neutral protease (NPR) and acid phosphatase (ACP) were most abundant. The overall soil environment in mangroves exhibited a state of N limitation, with varying degrees of limitation observed across different succession stages. The demand for P became more intense in the later stages of succession, particularly in the K. obovate and B. gymnorrhiza communities. In conjunction with correlation analysis, it indicated that the input of mangrove plant litter had a significant regulatory influence on the C, N, and P contents in the soil. There was a significant positive correlation between MBC, MBN, and MBP, indicating synergistic effects of C, N, and P on soil microorganisms. Therefore, evaluating the nutrient ratios and sufficiency of mangroves allowed us to comprehensively understand the present environmental conditions. This study aims to develop sustainable management strategies for the conservation and restoration of mangroves.

Cross-Linkable Fullerene Enables Elastic and Conductive Grain Boundaries for Efficient and Wearable Tin-Based Perovskite Solar Cells.

Tin-based perovskite solar cells (TPSCs) have received increasing attention due to their low toxicity, high theoretical efficiency, and potential applications as wearable devices. However, the inherent fast and uncontrollable crystallization process of tin-based perovskites results in high defect density in the film. Meanwhile, when fabricated into flexible devices, the prepared perovskite film exhibits inevitable brittleness and high Young's modulus, seriously weakening the mechanical stability. In this work, we design and synthesize a cross-linkable fullerene, thioctic acid functionalized C60 fulleropyrrolidinium iodide (FTAI), which has multiple interactions with perovskite components and can finely regulate the crystallization quality of perovskite film. The obtained perovskite film shows an increased grain size and a more matched energy level with the electron transport material, effectively improving the carrier extraction efficiency. The FTAI-based rigid device achieves a champion efficiency of 14.91 % with enhanced stability. More importantly, the FTAI located at the perovskite grain boundaries could spontaneously cross-link during the perovskite annealing process, which effectively improves the conductivity and elasticity of grain boundaries, thereby giving the film excellent bending resistance. Finally, the FTAI-based wearable device yields a record efficiency of 12.35 % and displays robust bending durability, retaining about 90 % of the initial efficiency after 10,000 bending times.

Suppressing Halide Segregation via Pyridine-Derivative Isomers Enables Efficient 1.68 eV Bandgap Perovskite Solar Cells.

Light-induced phase segregation is one of the main issues restricting the efficiency and stability of wide-bandgap perovskite solar cells (WBG PSCs). Small organic molecules with abundant functional groups can passivate various defects, and therefore suppress the ionic migration channels for phase segregation. Herein, a series of pyridine-derivative isomers containing amino and carboxyl are applied to modify the perovskite surface. The amino, carboxyl, and N-terminal of pyridine in all of these molecules can interact with undercoordinated Pb2+ through coordination bonds and suppress halide ions migration via hydrogen bonding. Among them, the 5-amino-3-pyridine carboxyl acid (APA-3) treated devices win the champion performance, enabling an efficiency of 22.35% (certified 22.17%) using the 1.68 eV perovskite, which represents one of the highest values for WBG-PSCs. This is believed to be due to the more symmetric spatial distribution of the three functional groups of APA-3, which provides a better passivation effect independent of the molecular arrangement orientation. Therefore, the APA-3 passivated perovskite shows the slightest halide segregation, the lowest defect density, and the least nonradiative recombination. Moreover, the APA-3 passivated device retains 90% of the initial efficiency after 985 h of operation at the maximum power point, representing the robust durability of WBG-PSCs under working conditions.

Efficient Tin-Based Perovskite Solar Cells Enabled by Precisely Synthesized Single-Isomer Fullerene Bisadducts with Regulated Molecular Packing.

Designing and synthesizing fullerene bisadducts with a higher-lying conduction band minimum is promising to further improve the device performance of tin-based perovskite solar cells (TPSCs). However, the commonly obtained fullerene bisadduct products are isomeric mixtures and require complicated separation. Moreover, the isomeric mixtures are prone to resulting in energy alignment disorders, interfacial charge loss, and limited device performance improvement. Herein, we synthesized single-isomer C60- and C70-based diethylmalonate functionalized bisadducts (C60BB and C70BB) by utilizing the steric-hindrance-assisted strategy and determined all molecular structures involved by single crystal diffraction. Meanwhile, we found that the different solvents used for processing the fullerene bisadducts can effectively regulate the molecular packing in their films. The dense and amorphous fullerene bisadduct films prepared by using anisole exhibited the highest electron mobility. Finally, C60BB- and C70BB-based TPSCs showed impressive efficiencies up to 14.51 and 14.28%, respectively. These devices also exhibited excellent long-term stability. This work highlights the importance of developing strategies to synthesize single-isomer fullerene bisadducts and regulate their molecular packing to improve TPSCs' performance.

In situ diets of the bloom-forming dinoflagellate Noctiluca scintillans in Daya Bay.

Red Noctiluca scintillans is a common heterotrophic dinoflagellate that forms blooms in temperate, subtropical, and tropical coastal ecosystems. The diet of this species plays an important role in its cell growth, development, and reproduction. Because limited gene diversity data are available regarding prey of this species, its diet in Daya Bay during a boreal winter bloom is reported using an integrated approach involving light microscopy, single cell isolation and plastid 16S rDNA cloning, and 18S rDNA V4 and V9 region amplification using isolated cells and environmental DNA as templates with high-throughput sequencing. While conventional light microscopy reveals the diet of this species to comprise Coscinodiscus sp. and Stephanopyxis turris (diatoms), copepod eggs, and detritus, plastid gene diversity identifies a diet comprising diatoms, cyanobacteria, and bacteria, and 18S rDNA high-throughput sequencing reveals a diet comprising 36 eukaryote families (primarily copepods, as well as diatoms, dinoflagellates, Ochrophyta, Haptophytes, Chordata, Cercozoans, Chlorophyta, Polychaeta, and ciliates). Dietary staples include copepods, diatoms, dinoflagellates, Ochrophyta, and Synechococcus. High copepod abundance in prey may reflect their relatively high abundance in environmental seawater. Thus, N. scintillans is generally omnivorous but prefers dominant phytoplankton taxa, including Rhizosoleniaceae, Leptocylindraceae, and Cymatosiraceae (diatoms), as well as Gonyaulacaceae (dinoflagellates). An integrated multi-disciplinary approach provides a more comprehensive picture of N. scintillans diet in Daya Bay, and an improved understanding of this species' ecological niche and trophic role in marine ecosystems.

Well-Defined Fullerene Bisadducts Enable High-Performance Tin-Based Perovskite Solar Cells.

Tin-based perovskite solar cells (TPSCs) are attracting intense research interest due to their excellent optoelectric properties and eco-friendly features. To further improve the device performance, developing new fullerene derivatives as electron transporter layers (ETLs) is highly demanded. Four well-defined regioisomers (trans-2, trans-3, trans-4, and e) of diethylmalonate-C60 bisadduct (DCBA) are isolated and well characterized. The well-defined molecular structure enables us to investigate the real structure-dependent effects on photovoltaic performance. It is found that the chemical structures of the regioisomers not only affect their energy levels, but also lead to significant differences in their molecular packings and interfacial contacts. As a result, the devices with trans-2, trans-3, trans-4, and e as ETLs yield efficiencies of 11.69%, 14.58%, 12.59%, and 10.55%, respectively, which are higher than that of the as-prepared DCBA-based (10.28%) device. Notably, the trans-3-based device also demonstrates a certified efficiency of 14.30%, representing one of the best-performing TPSCs.

Fullerene Derivative with Flexible Alkyl Chain for Efficient Tin-Based Perovskite Solar Cells.

Fullerene derivatives are considered excellent materials for the extraction and transportation of electrons in the production of efficient tin-based perovskite solar cells (TPSCs). However, it is not clear how the molecular structure of fullerene derivatives affects the efficiency and stability of TPSCs. In this study, the effects of fullerene derivatives, (6,6)-phenyl-C61-butyric acid hexyl ester (PCBH) and (6,6)-phenyl-C61-butyric acid methyl ester (PCBM), with different functional groups, on photovoltaic performance were investigated. The flexible alkyl chain of PCBH effectively improved the film morphology and stability, the electron extraction and transport capabilities, and the interface contact of fullerene and perovskite. As a result, the PCBH-based TPSC yielded a higher efficiency, of 9.21%, than the PCBM-based devices (7.54%). More importantly, the PCBH-based films exhibited higher stability and effectively suppressed the oxidation of Sn2+ by inhibiting oxygen permeation. Therefore, the PCBH-based devices exhibited significantly enhanced stability. This result indicates that optimizing the functional group of fullerene derivatives is crucial for improving the efficiency and stability of TPSCs.

Angiotensin-(1-7) ameliorates high glucose-induced vascular endothelial injury through suppressing chloride channel 3.

Diabetes Mellitus (DM) is a significant risk factor for cardiovascular disease (CVD), which is leading cause of deaths in DM patients. However, there are limited effective medical therapies for diabetic CVD. Vascular endothelial injury caused by DM is a critical risk factor for diabetic CVD. Previous study has indicated that Angiotensin-(1-7) (Ang-(1-7)) may prevent diabetic CVD, whereas it is not clear that Ang-(1-7) whether attenuates diabetic CVD through suppressing vascular endothelial injury. In this study, we found that Ang-(1-7) alleviated high glucose (HG)-induced endothelial injury in bEnd3 cells. Moreover, Ang-(1-7) ameliorated HG-induced endothelial injury through downregulating chloride channel 3 (CIC-3) via Mas receptor. Furthermore, HG-induced CIC-3 enhanced reactive oxygen species (ROS) and cytokine production and reduced the level of nitric oxide (NO), while Ang-(1-7) preserved the impact of HG-induced CIC-3 on productions of ROS, cytokine and NO through inhibiting CIC-3 via Mas receptor. Summarily, the present study revealed that Ang-(1-7) alleviated HG-induced vascular endothelial injury through the inhibition of CIC-3, suggested that Ang-(1-7) may preserve diabetic CVD through suppressing HG-induced vascular endothelial injury.

Naringin attenuates high glucose-induced injuries and inflammation by modulating the leptin-JAK2/STAT3 pathway in H9c2 cardiac cells.

INTRODUCTION: Our previous study showed that naringin (NRG) protects cardiomyocytes against high glucose (HG)-induced injuries by inhibiting p38 mitogen-activated protein kinase (MAPK). Leptin induces hypertrophy in rat cardiomyocytes via p38/MAPK activation. The present study aimed to test the hypothesis that leptin-Janus kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT3), which are responsible for leptin's functions, are involved in HG-induced injuries and cardioprotective effects of NRG in cardiomyocytes. MATERIAL AND METHODS: H9c2 cells were exposed to HG for 24 h to establish a cardiomyocyte injury model. Cells were pretreated with NRG and other drugs before exposure to HG. Protein expression was measured by western blot analysis. Cell viability was detected by Cell Counting Kit-8 assay. Apoptotic cells were assessed by Hoechst 33258 staining assay. Intracellular reactive oxygen species levels were determined by dichlorofluorescein diacetate staining. Mitochondrial membrane potential was evaluated using JC-1. An enzyme-linked immunosorbent assay was performed to determine the inflammatory cytokines. RESULTS: NRG significantly attenuated HG-induced increases in leptin and Ob-R expression. Pretreatment with either a leptin antagonist (LA) or NRG markedly ameliorated HG-induced elevation of phosphorylated (p)-JAK2 and p-STAT3, respectively. Pretreatment with NRG, LA, Ob-R antagonist, or AG490 clearly alleviated HG-induced injuries and inflammation. CONCLUSIONS: This study provides new evidence of the NRG protective effects of H9c2 cells against HG-induced injuries possibly via modulation of the leptin-JAK2/STAT3 pathway.

[Corrigendum] Exogenous hydrogen sulfide exerts proliferation, anti-apoptosis, migration effects and accelerates cell cycle progression in multiple myeloma cells via activating the Akt pathway.

Following the publication of this article, an interested reader drew to the authors' attention that, in Fig. 4 on p. 1913, the t-Akt panel in Fig. 4A looked unexpectedly similar to the ß-actin panel in Fig. 4C. The authors were able to refer back to their original data, and realized that the Figure had been compiled incorrectly; essentially, the data for the t-Akt panel had been duplicated, and the data for the ß-actin panel in Fig. 4C had not been included in the Figure as intended. The revised version of Fig. 4, showing the correct data for the ß-actin panel in Fig. 4C, is shown opposite. This error did not have a significant impact on the results or the conclusions reported in this study. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and all of the authors agree to the publication of this Corrigendum. The authors sincerely apologize for this mistake, and regret any inconvenience this mistake has caused. [the original article was published in Oncology Reports 36: 1909-1916, 2016; DOI: 10.3892/or.2016.5014].

MiR-203-3p inhibits the oxidative stress, inflammatory responses and apoptosis of mice podocytes induced by high glucose through regulating Sema3A expression.

Diabetic nephropathy (DN) is the most serious long-term microvascular complication of diabetes, which mainly causes podocyte injury. Many studies have shown that microRNAs play a vital role in the development of DN. Studies have shown that miR-203-3p is involved in mesangial cell proliferation and apoptosis of DN mice. Therefore, we speculated that miR-203-3p might be related to the development of DN, but our study does not provide any evidence. In animal experiments, diabetic mice (db/db) were transfected with iR-203-3p overexpression lentiviral vectors (LV-miR-203-3p) and their control (LV-miR-con), with normal mice (db/m) being used as the control. High glucose (HG)-induced podocytes were used to construct a DN cell model in vitro. The expression levels of miR-203-3p, Semaphorin 3A (Sema3A) and inflammatory cytokines were detected by quantitative real-time polymerase chain reaction. Also, serum creatinine and blood urea nitrogen levels were used to evaluate the degree of renal injury in DN mice. Sema3A and apoptosis-related protein levels were assessed by the western blot analysis. Enzyme-linked immunosorbent assay was used to determine the different oxidative stress-related indicators and inflammatory cytokines. Flow cytometry and caspase-3 activity detection were used to analyze the degree of podocyte apoptosis. Our results suggested that the expression of miR-203-3p was lower in DN mice and in HG-induced podocytes. Overexpression of miR-203-3p reduced the body weight, blood glucose and renal injury of DN mice in vivo, as well as relieve the oxidative stress, inflammatory response and apoptosis of HG-induced podocytes in vitro. Functionally, Sema3A was a target of miR-203-3p, and Sema3A overexpression reversed the inhibitory effect of miR-203-3p on HG-induced podocyte injury. Our findings revealed that miR-203-3p alleviated the podocyte injury induced by HG via regulating Sema3A expression, suggesting that miR-203-3p might be a new therapeutic target to improve the progression of DN.

Exogenous hydrogen sulfide promotes hepatocellular carcinoma cell growth by activating the STAT3-COX-2 signaling pathway.

The effects of hydrogen sulfide (H2S) on cancer are controversial. Our group previously demonstrated that exogenous H2S promotes the development of cancer via amplifying the activation of the nuclear factor-κB signaling pathway in hepatocellular carcinoma (HCC) cells (PLC/PRF/5). The present study aimed to further investigate the hypothesis that exogenous H2S promotes PLC/PRF/5 cell proliferation and migration, and inhibits apoptosis by activating the signal transducer and activator of transcription 3 (STAT3)-cyclooxygenase-2 (COX-2) signaling pathway. PLC/PRF/5 cells were treated with 500 µmol/l NaHS (a donor of H2S) for 24 h. The expression levels of phosphorylated (p)-STAT3, STAT3, cleaved caspase-3 and COX-2 were measured by western blot assay. Cell viability was detected by Cell Counting kit-8 assay. Apoptotic cells were observed by Hoechst 33258 staining. The expression of STAT3 and COX-2 messenger RNA (mRNA) was detected by semiquantitative reverse transcription-polymerase chain reaction. The production of vascular endothelial growth factor (VEGF) was evaluated by ELISA. The results indicated that treatment of PLC/PRF/5 cells with 500 µmol/l NaHS for 24 h markedly increased the expression levels of p-STAT3 and STAT3 mRNA, leading to COX-2 and COX-2 mRNA overexpression, VEGF induction, decreased cleaved caspase-3 production, increased cell viability and migration, and decreased number of apoptotic cells. However, co-treatment of PLC/PRF/5 cells with 500 µmol/l NaHS and 30 µmol/l AG490 (an inhibitor of STAT3) or 20 µmol/l NS-398 (an inhibitor of COX-2) for 24 h significantly reverted the effects induced by NaHS. Furthermore, co-treatment of PLC/PRF/5 cells with 500 µmol/l NaHS and 30 µmol/l AG490 markedly decreased the NaHS-induced increase in the expression level of COX-2. By contrast, co-treatment of PLC/PRF/5 cells with 500 µmol/l NaHS and 20 µmol/l NS-398 inhibited the NaHS-induced increase in the expression level of p-STAT3. In conclusion, the findings of the present study provide evidence that the STAT3-COX-2 signaling pathway is involved in NaHS-induced cell proliferation, migration, angiogenesis and anti-apoptosis in PLC/PRF/5 cells, and suggest that the positive feedback between STAT3 and COX-2 may serve a crucial role in hepatocellular carcinoma carcinogenesis.

[Corrigendum] Heat shock protein 90/Akt pathway participates in the cardioprotective effect of exogenous hydrogen sulfide against high glucose­induced injury to H9c2 cells.

Subsequently to the publication of this article, the authors have realized that the address affiliation for the corresponding author, Chengheng Hu, and the authors Longyun Peng and Xinxue Liao appeared incorrectly. These authors' affiliation information should have appeared as follows (the corrected address affiliation is featured in bold): XIAO KE1,2*, JINGFU CHEN3*, LONGYUN PENG4, WEI ZHANG5, YIYING YANG5, XINXUE LIAO4, LIQIU MO6, RUIXIAN GUO7, JIANQIANG FENG6, CHENGHENG HU4 and RUQIONG NIE2 1Department of Cardiology, Shenzhen Sun Yat­sen Cardiovascular Hospital, Shenzhen; 2Department of Cardiology, Sun Yat­sen Memorial Hospital, Sun Yat­sen University, Guangzhou, Guangdong; 3Department of Cardiovascular Medicine and Dongguan Cardiovascular Institute, The Third People's Hospital of Dongguan City, Dongguan; 4Department of Cardiology and Key Laboratory on Assisted Circulation, Ministry of Health, The First Affiliated Hospital, Sun Yat­sen University; 5Department of Cardiovasology and Cardiac Care Unit (CCU), Huangpu Division of The First Affiliated Hospital, Sun Yat­sen University; 6Department of Anesthesiology, Huangpu Division of The First Affiliated Hospital, Sun Yat­sen University; 7Department of Physiology, Zhongshan School of Medicine, Sun Yat­sen University, Guangzhou, Guangdong, P.R. China *Contributed equally In addition, the address for correspondence in the correspondence box should have appeared as follows: Correspondence to: Professor Chengheng Hu, Department of Cardiology and Key Laboratory on Assisted Circulation, Ministry of Health, The First Affiliated Hospital, Sun Yat­sen University, Guangdong, 58 Zhongshan 2rd Road, Guangzhou 510080, P.R. China E­mail: huchengheng138@163.com The authors regret this error in the affiliations, and apologize for any inconvenience caused. [the original article was published in the International Journal of Molecular Medicine 39: 1001­1010, 2017; DOI: 10.3892/ijmm.2017.2891].

Ang-(1-7) protects HUVECs from high glucose-induced injury and inflammation via inhibition of the JAK2/STAT3 pathway.

Angiotensin (Ang)­1­7, which is catalyzed by angiotensin­converting enzyme 2 (ACE2) from angiotensin­II (Ang­II), exerts multiple biological and pharmacological effects, including cardioprotective effects and endothelial protection. The Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway has been demonstrated to be involved in diabetes­associated cardiovascular complications. The present study hypothesized that Ang­(1­7) protects against high glucose (HG)­induced endothelial cell injury and inflammation by inhibiting the JAK2/STAT3 pathway in human umbilical vein endothelial cells (HUVECs). HUVECs were treated with 40 mmol/l glucose (HG) for 24 h to establish a model of HG­induced endothelial cell injury and inflammation. Protein expression levels of p­JAK2, t­JAK2, p­STAT3, t­STAT3, NOX­4, eNOS and cleaved caspase­3 were tested by western blotting. CCK­8 assay was performed to assess cell viability of HUVECs. Apoptotic cell death was analyzed by Hoechst 33258 staining. Mitochondrial membrane potential (MMP) was obtained using JC­1. Superoxide dismutase (SOD) activity was tested by SOD assay kit. Interleukin (IL)­1ß, IL­10, IL­12 and TNF­α levels in culture media were tested by ELISA. The findings demonstrated that exposure of HUVECs to HG for 24 h induced injury and inflammation. This injury and inflammation were significantly ameliorated by pre­treatment of cells with either Ang­(1­7) or AG490, an inhibitor of the JAK2/STAT3 pathway, prior to exposure of the cells to HG. Exposure of the cells to HG also increased the phosphorylation of JAK2/STAT3 (p­JAK2 and p­STAT3). Increased activation of the JAK2/STAT3 pathway was attenuated by pre­treatment with Ang­(1­7). To the best of our knowledge, the findings from the present study provided the first evidence that Ang­(1­7) protects against HG­induced injury and inflammation by inhibiting activation of the JAK2/STAT3 pathway in HUVECs.

Exogenous H2S promotes cancer progression by activating JAK2/STAT3 signaling pathway in esophageal EC109 cells.

Hydrogen sulfide (H2S) plays an important role in diverse physiological and pathophysiological processes in cancer cells both in vitro and in vivo. We have previously shown that exogenous H2S exerts its biological effects on hepatoma, glioma, and esophageal cancer cells through the activation of NF-κB, p38-MAPK/ERK1/2-COX-2, and HSP90 pathways. However, the role of H2S and the underlying mechanism in esophageal squamous cell carcinoma remain unclear. Here we investigated whether exogenous H2S contributes to the biological behavior of esophageal squamous cancer cell line EC109, through the activation of JAK2/STAT3 signaling pathway. EC109 cells were treated with NaHS (a donor of H2S) and AG490 (a specific inhibitor of JAK2/STAT3 signaling pathway). The expression levels of p-JAK2, p-STAT3, caspase-3/9/12, Bax, Bcl-2, MMP-2/9, and VEGFR were measured by western blot analysis. Cell viability was detected by CCK-8 and quantified by direct counting of cells under a microscope. Cell migration was analyzed by the scratch-wound assay, while the level of VEGF was measured by ELISA. Cells treated with NaHS for 24 h showed significant upregulation of p-JAK2, and p-STAT3 expression, as well as increased cell viability when compared to the control cells. The expression levels of caspase-3/9/12 and Bax decreased, while those of Bcl-2, MMP-2/9, VEGFR, and VEGF increased. NaHS induced the migration of EC109 cells. However, co-treatment with NaHS and AG490 significantly inhibited these effects. Thus, JAK2/STAT3 signaling pathway may contribute to H2S-induced cell proliferation, anti-apoptosis, migration, and angiogenesis in EC109 cells.

Effect of Prophylactic Thoracic Duct Ligation in Reducing the Incidence of Postoperative Chylothorax during Esophagectomy: A Systematic Review and Meta-analysis.

OBJECTIVES: There is no consensus on the effectiveness of prophylactic thoracic duct ligation (PLG) in esophagectomy for reducing the incidence of postoperative chylothorax. We performed a systemic review and meta-analysis to study its efficacy. METHODS: A systemic review of the publications was performed on three databases to identify all the relevant literature on comparative outcomes of PLG and nonprophylactic thoracic duct ligation (NPLG). The primary end point was the incidence of postoperative chylothorax. RESULTS: Seven studies with comparative data on PLG (n = 2,178) versus NPLG (n = 3,048) were identify from the current publications. Comparison showed no significant difference between PLG and NPLG on the incidence of postoperative chylothorax (relative risk = 0.431; 95% confidence interval, 0.186 to 1.002; p = 0.050). CONCLUSIONS: Although some studies showed that PLG during the esophagectomy was effective to lower the incidence of postoperative chylothorax, no evidence was observed in the present meta-analysis. Further research is warranted to validate the findings.

[Angiotensin-(1-7) protects cardiac myocytes against high glucose-induced injury by inhibiting ClC-3 chloride channels].

OBJECTIVE: To explore whether angiotensin-(1-7) [Ang-(1-7)] protects cardiac myocytes against high glucose (HG)-induced injury by inhibiting ClC-3 chloride channels. METHOD: H9c2 cardiac cells were exposed to 35 mmol/L glucose for 24 h to establish a cell injury model. The cells were treated with Ang-(1-7) or the inhibitor of chloride channel (NPPB) in the presence of HG for 24 h to observe the changes in HG-induced cell injury. Cell counter kit 8 (CCK-8) assay was used to test the cell viability, and the morphological changes of the apoptotic cells were detected using Hoechst 33258 staining and fluorescent microscopy. The intracellular level of reactive oxygen species (ROS) was examined by DCFH-DA staining, SOD activity in the culture medium was measured using commercial kits, and the mitochondrial membrane potential (MMP) of the cells was tested with rodamine 123 staining. The expression level of cardiac ClC-3 chloride channels was detected with Western blotting. RESULTS: Exposure of H9c2 cardiac cells to 35 mmol/L glucose for 24 h markedly enhanced the expressions of cardiac ClC-3 channel protein (P<0.01). Co-treatment of the cells with 1 µmol/L Ang-(1-7) and HG for 24 h significantly attenuated HG- induced upregulation of ClC-3 channel protein expression (P<0.01). Co-treatment of the cells exposed to HG with 1 µmol/L Ang-(1-7) or 100 µmol/L NPPB for 24 h obviously ameliorated HG-induced injuries as shown by increased cell viability, enhanced SOD activity, decreased number of apoptotic cells, and reduced intracellular ROS generation and loss of MMP (P<0.01). CONCLUSION: ClC-3 channels are involved in HG-induced injury in cardiac cells. Ang-(1-7) protects cardiac cells against HG-induced injury by inhibiting ClC-3 channels.

Heat shock protein 90/Akt pathway participates in the cardioprotective effect of exogenous hydrogen sulfide against high glucose-induced injury to H9c2 cells.

It has been reported that exogenous hydrogen sulfide (H2S) protects against high glucose (HG)-induced cardiac injury and has a modulatory effect on heat shock protein (HSP) and Akt, which play a cardioprotective role. In this study, we examined whether the HSP90/Akt pathway contributes to the protective effects of exogenous H2S against HG-induced injury to H9c2 cardiac cells. Our results revealed that the exposure of H9c2 cardiac cells to 35 mM glucose (HG) for 1 to 24 h decreased the expression of HSP90 and markedly reduced the expression level of phosphorylated (p)-Akt in a time-dependent manner. Co-exposure of the cells to HG and geldanamycin (GA; an inhibitor of HSP90) aggravated the inhibition of the p-Akt expression level by HG. Of note, treatment of the cells with 400 µM NaHS (a donor of H2S) for 30 min prior to exposure to HG significantly attenuated the HG-induced decrease in the expression levels of both HSP90 and p-Akt, along with inhibition of HG-induced cell injury, as indicated by the increase in cell viability and superoxide dismutase (SOD) activity, and by a decrease in the number of apoptotic cells, reactive oxygen species (ROS) generation, as well as by the decreased dissipation of mitochondrial membrance potential (MMP). Importantly, treatment of the cells with GA or LY294002 (an inhibitor of Akt) prior to exposure to NaHS and HG considerably blocked the cardioprotective effects of NaHS against the HG-induced injury mentioned above. On the whole, the findings of this study demonstrate that the inhibition of the HSP90/Akt pathway may be an important mechanism responsible for HG-induced cardiomyocyte injury. We also provide novel evidence that exogenous H2S protects H9c2 cells against HG-induced injury by activating the HSP90/Akt pathway.

Angiotensin-(1-7) protects cardiomyocytes against high glucose-induced injuries through inhibiting reactive oxygen species-activated leptin-p38 mitogen-activated protein kinase/extracellular signal-regulated protein kinase 1/2 pathways, but not the leptin-c-Jun N-terminal kinase pathway in vitro.

AIMS/INTRODUCTION: Angiotensin-(1-7) (Ang-[1-7]), recognized as a new bioactive peptide in the renin-angiotensin system, shows biological and pharmacological properties in diabetic cardiovascular diseases. The leptin-induced p38 mitogen-activated protein kinase (MAPK) pathway has been reported to contribute to high glucose (HG)-induced injury. In the present study, we showed the mechanism of how Ang-(1-7) can protect against HG-stimulated injuries in H9c2 cells. MATERIALS AND METHODS: H9c2 cells were treated with 35 mmol/L glucose (HG) for 24 h to establish a model of HG-induced damage. Apoptotic cells were observed by Hoechst 33258 staining. Cell viability was analyzed by cell counter kit-8. The expression of protein was detected by western blot. Reactive oxygen species was tested by 2',7'-dichlorodihydrofluorescein diacetate staining. Mitochondrial membrane potential was measured by 5,5',6,6'-Tetrachloro-1,1',3,3'-tetraethyl-imidacarbocyanine iodide staining. RESULTS: The present results showed that treating H9c2 cells with HG obviously enhanced the expressions of both the leptin and phosphorylated (p)-MAPK pathway. However, the overexpression levels of leptin and p-p38 MAPK/p-extracellular signal-regulated protein kinase 1/2 (ERK1/2), but not p-c-Jun N-terminal kinase, were significantly suppressed by treatment of the cells with Ang-(1-7). Additionally, leptin antagonist also markedly suppressed the overexpressions of p38 and ERK1/2 induced by HG, whereas leptin antagonist had no influence on the overexpression of c-Jun N-terminal kinase. More remarkable, Ang-(1-7), leptin antagonist, SB203580 or SP600125, respectively, significantly inhibited the injuries induced by HG, such as the increased cell viability, decreased apoptotic rate, reduction of ROS production and increased mitochondrial membrane potential. Furthermore, the overexpressions of p38 MAPK, ERK1/2 and leptin were suppressed by N-actyl-L-cystine. CONCLUSIONS: The present findings show that Ang-(1-7) protects from HG-stimulated damage as an inhibitor of the reactive oxygen species-leptin-p38 MAPK/ERK1/2 pathways, but not the leptin-c-Jun N-terminal kinase pathway in vitro.

[Exogenous hydrogen sulfide inhibits high-glucose-induced injuries via regulating leptin/leptin receptor signaling pathway in human umbilical vein endothelial cells].

OBJECTIVE: To investigate whether exogenous hydrogen sulfide (H2S) inhibits the high-glucose (HG)-induced injury by modulating leptin/leptin receptor (LEPR) signal pathway in human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were treated with 40 mmol/L glucose for 3-24 h, and the cell viability was examined by CCK-8 assay. The changes of cell morphology and the number of apoptotic cells were assessed by Hoechst 33258 nuclear staining followed by photofluorography. The intracellular levels of reactive oxygen species (ROS) was detected by DCFH-DA staining followed by photofluorography. Mitochondrial membrane potential (MMP) was determined by Rhodamine 123 (Rh123) staining and photofluorography. The expression levels of leptin and LEPR protein were measured by Western blotting. RESULTS: s The expression of leptin and LERP in HUVECs began to significantly increase at 3 h after HG exposure and reached the peak levels at 9 h (P<0.01). Pretreatment of HUVECs with 400 µmol/L sodium hydrosulfide (H2S donor) for 30 min inhibited HG-induced increase in leptin and leptin receptor expressions in HUVECs (P<0.01). Pretreatment of HUVECs with 400 µmol/L NaHS for 30 min or 50 ng/mL leptin antagonists (LA) for 1 h obviously alleviated HG-induced injury by increasing cell viability, decreasing cell apoptosis and lowering accumulation of intracellular ROS and MMP loss (P<0.01). CONCLUSION: Exogenous H2S protects against HG-induced injury by inhibiting leptin/LEPR pathway in HUVECs.