Electron Manipulation and Surface Reconstruction of Bimetallic Iron-Nickel Phosphide Nanotubes for Enhanced Alkaline Water Electrolysis.

Developing high-efficiency and stable bifunctional electrocatalysts for water splitting remains a great challenge. Herein, NiMoO4 nanowires as sacrificial templates to synthesize Mo-doped NiFe Prussian blue analogs are employed, which can be easily phosphorized to Mo-doped Fe2xNi2(1-x)P nanotubes (Mo-FeNiP NTs). This synthesis method enables the controlled etching of NiMoO4 nanowires that results in a unique hollow nanotube architecture. As a bifunctional catalyst, the Mo-FeNiP NTs present lower overpotential and Tafel slope of 151.3 (232.6) mV at 100 mA cm-2 and 76.2 (64.7) mV dec-1 for HER (OER), respectively. Additionally, it only requires an ultralow cell voltage of 1.47 V to achieve 10 mA cm-2 for overall water splitting and can steadily operate for 200 h at 100 mA cm-2. First-principles calculations demonstrate that Mo doping can effectively adjust the electron redistribution of the Ni hollow sites to optimize the hydrogen adsorption-free energy for HER. Besides, in situ Raman characterization reveals the dissolving of doped Mo can promote a rapid surface reconstruction on Mo-FeNiP NTs to dynamically stable (Fe)Ni-oxyhydroxide layers, serving as the actual active species for OER. The work proposes a rational approach addressed by electron manipulation and surface reconstruction of bimetallic phosphides to regulate both the HER and OER activity.

Rubus chingii Hu relieved the polycystic ovary syndrome with enhanced insulin sensitivity through inhibiting TXNIP/NLRP3 inflammasome signaling.

BACKGROUND: Polycystic ovary syndrome (PCOS) is one of the most prevalent endocrine disorders in gynecology with severe metabolic abnormalities. Therefore, identifying effective treatments and drugs for PCOS is important. We aimed to investigate effect of the traditional Chinese medicine (TCM) Rubus chingii Hu (R. chingii) on ovarian function and insulin resistance (IR) of PCOS rat models, and to explore the underlying mechanisms. METHODS: A PCOS rat model was established by subcutaneous injection of dehydroepiandrosterone (DHEA) solution for 20 days. PCOS rats were randomly divided into a control group (CON), model group (MOD), metformin group (MET), TCM R. chingii group (RCG), and RCG + Ad-TXNIP groups. After 28 days of treatment, the samples were collected for subsequent experiments. RESULTS: R. chingii treatment alleviated hormone imbalance and IR while improving ovarian pathology in the PCOS model. R. chingi inhibited the activation of the thioredoxin-interacting protein (TXNIP)/NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in the ovarian tissue of PCOS rats. Furthermore, TXNIP overexpression hindered the protective effect of R. chingii intervention in PCOS rats, as evidenced by the increase of homeostasis model assessment of insulin resistance (HOMA-IR), luteinizing hormone (LH), testosterone (T), C-reactive protein (CRP) levels, and atretic follicles. CONCLUSION: R. chingii intervention improved ovarian polycystic development by suppressing the TXNIP/NLRP3 inflammasome, which may be an effective treatment for PCOS.

An injectable nanocomposite alginate-Ca2+ hydrogel for melittin-assisted Ca2+-overload and photothermal cancer therapy.

An injectable nanocomposite alginate-Ca2+ hydrogel embedded with melittin and polyaniline nanofibers was fabricated for Ca2+-overload and photothermal combination cancer therapy. Melittin disrupts the cell membranes and enhances Ca2+ influx significantly, improving Ca2+-overload treatment, while the polyaniline nanofibers endow the hydrogel with glutathione (GSH) depletion and photothermal ability.

Dual-Atom Support Boosts Nickel-Catalyzed Urea Electrooxidation.

Nickel-based catalysts have been regarded as one of the most promising electrocatalysts for urea oxidation reaction (UOR), however, their activity is largely limited by the inevitable self-oxidation reaction of Ni species (NSOR) during the UOR. Here, we proposed an interface chemistry modulation strategy to trigger the occurrence of UOR before the NSOR via constructing a 2D/2D heterostructure that consists of ultrathin NiO anchored Ru-Co dual-atom support (Ru-Co DAS/NiO). Operando spectroscopic characterizations confirm this unique triggering mechanism on the surface of Ru-Co DAS/NiO. Consequently, the fabricated catalyst exhibits outstanding UOR activity with a low potential of 1.288 V at 10 mA cm-2 and remarkable long-term durability for more than 330 h operation. DFT calculations and spectroscopic characterizations demonstrate that the favorable electronic structure induced by this unique heterointerface endows the catalyst energetically more favorable for the UOR than the NSOR.

Pyroptosis participates in PM2.5-induced air-blood barrier dysfunction.

Epidemiological studies have shown that particulate matters with diameter less than 2.5 µm (PM2.5) play an important role in inducing and promoting respiratory diseases, but its underlying mechanism remains to be explored. The air-blood barrier, also known as the alveolar-capillary barrier, is the key element of the lung, working as the site of oxygen and carbon dioxide exchange between pulmonary vasculatures. In this study, a mouse PM2.5 exposure model was established, which leads to an induced lung injury and air-blood barrier disruption. Oxidative stress and pyroptosis were observed in this process. After reducing the oxidative stress by N-acetyl-L-cysteine (NAC) treatment, the air-blood barrier function was improved and the effect of PM2.5 was alleviated. The level of pyroptosis and related pathway were also effectively relieved. These results indicate that acute PM2.5 exposure can cause lung injury and the alveolar-capillary barrier disruption by inducing reactive oxygen species (ROS) with the participation of pyroptosis pathway.

PM2.5 induced lung injury through upregulating ROS-dependent NLRP3 Inflammasome-Mediated Pyroptosis.

The main cause of air pollution is PM2.5, which directly causes lung injury through respiration. Oxidative stress and inflammation are considered to be the key mechanism of cell damage. Pyroptosis is a process of the programmed death of inflammatory cells and as a dangerous endogenous signal, it is widely involved in different inflammatory diseases. However, few studies have been conducted on PM2.5 exposure and cell pyroptosis. In this study, we aimed to investigate the effect of PM2.5 on apoptosis, pyroptosis and cell cycle arrest regulated by reactive oxygen species production. Balb/c mice were exposed to PM2.5 dynamically and verified by the RAW264.7 cells in vitro. The results showed the activation of NF-κB and NLRP3 inflammasome and the release of IL-1ß and reactive oxygen species were caused by exposure to PM2.5. The maturation of IL-1ß relied on Caspase-1, and the active Caspase-1 was related to cell pyroptosis. Oxidative stress, inflammation, apoptosis and pyroptosis all affected the cell cycle. This study describes a potentially important mechanism of PM2.5-induced lung damage that PM2.5 promotes lung injury via upregulating ROS-NLRP3-mediated the RAW264.7 cells pyroptosis.

Oxidative stress activates Ryr2-Ca2+ and apoptosis to promote PM2.5-induced heart injury of hyperlipidemia mice.

The increased cases of hyperlipemia in China and the crucial role of PM2.5 in inducing and promoting cardiovascular diseases have attracting more and more researchers' attention. However, the effects and mechanisms of PM2.5 on cardiovascular system of hyperlipidemia people are still unclear. In this study, hyperlipidemia mice model was established by high-fat diet. Then we exposed these mice to PM2.5 or saline to explore the underling mechanism of cardiac injury in hyperlipidemia mice. The hyperlipemia mice are more susceptible to heart damage caused by PM2.5 exposure. The participation of oxidative stress, cell apoptosis and Ca2+ related mechanism could be observed in this model. After NAC (N-acetyl-L-cysteine) treatment, the oxidative stress level induced by PM2.5 exposure significantly decreased in hyperlipemia mice. NAC effectively alleviated cardiac injury, improved the imbalance of calcium and attenuated apoptosis induced by PM2.5 exposure in hyperlipemia mice. The strong oxidative stress in hyperlipemia mice could lead to calcium homeostasis imbalance and activation of apoptosis-related pathways. This mechanism of PM2.5-induced myocardial injury was also verified in vitro. In our present study, we demonstrated the contribution of the PM2.5-ROS-Ryr2-Ca2+ axis in PM2.5-induced heart injury of hyperlipidemia mice, offering a potential therapeutical target for related pathology.

Annexin A2 degradation contributes to dopaminergic cell apoptosis via regulating p53 in neurodegenerative conditions.

BACKGROUND: P53 overexpression has been shown to involve in mitochondria-mediated dapaminergic neuron cell death in Parkinson's disease. However, the exactly molecular mechanisms responsible for the p53-dependent intrinsic cell death in neurodegenerative conditions remain unclearly. Annexin A2 is a multifunctional protein that negatively regulates p53 expression. The purpose of this study was to explore the mechanism of p53 dependent dopaminergic cell death and implication of Annexin A2 in cellular apoptosis in 1-methyl-4-phenylpyridinium (MPP+)-induced PC12 cells. METHODS: The cell viability of neural PC12 cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltet-razolium bromide assay. Flow cytometry was used to evaluate the apoptosis and mitochondrial transmembrane potential of neural PC12 cells. The expression of p53 and Annexin A2 was analyzed by western blot assay. RESULTS: The present study showed that the exposure of PC12 cells to neurotoxin MPP+ increased the expression levels of p53 and the discharge of mitochondrial transmembrane potential. Notably, Annexin A2 degradation was also observed in this cellular model of Parkinson's disease, in a time and dose-dependent manner. This expressing change of Annexin A2 was in direct proportion to the loss of cell viability of PC12 cells, and this expression pattern was in inverse proportion to p53 levels in this cellular model of Parkinson's disease. CONCLUSION: These results indicated that Annexin A2 degradation plays a crucial role the degeneration of dapaminergic cells of Parkinson's disease, and Annexin A2 downregulation-mediated the cell death is closely associated with mitochondrial dysfunction via p53-dependent pathway; thus provide a novel therapeutic target for Parkinson's disease treatment.

Atomic-Level Modulation of the Interface Chemistry of Platinum-Nickel Oxide toward Enhanced Hydrogen Electrocatalysis Kinetics.

Precise manipulation of the interactions between different components represents the frontier of heterostructured electrocatalysts and is crucial to understanding the structure-function relationship. Current studies, however, are quite limited. Here, we report targeted modulation of the atomic-level interface chemistry of Pt/NiO heterostructure via an annealing treatment, which results in substantially enhanced hydrogen electrocatalysis kinetics in alkaline media. Specifically, the optimized Pt/NiO heterostructure delivers by far the highest specific exchange current density of 8.1 mA cmPt-2 for hydrogen oxidation reaction. X-ray spectroscopy results suggest Pt-Ni interfacial bonds are formed after annealing, inducing more significant electron transfer from NiO to Pt. Also, the regulated interface chemistry, as proven by theoretical calculations, optimizes the binding behaviors of hydrogen and hydroxyl species. These findings emphasize the importance of interface engineering at the atomic level and inspire further explorations of heterostructured electrocatalysts.

LIN28B induces a differentiation program through CDX2 in colon cancer.

Most colorectal cancers (CRCs) are moderately differentiated or well differentiated, a status that is preserved even in metastatic tumors. However, the molecular mechanisms underlying CRC differentiation remain to be elucidated. Herein, we unravel a potentially novel posttranscriptional regulatory mechanism via a LIN28B/CDX2 signaling axis that plays a critical role in mediating CRC differentiation. Owing to a large number of mRNA targets, the mRNA-binding protein LIN28B has diverse functions in development, metabolism, tissue regeneration, and tumorigenesis. Our RNA-binding protein IP (RIP) assay revealed that LIN28B directly binds CDX2 mRNA, which is a pivotal homeobox transcription factor in normal intestinal epithelial cell identity and differentiation. Furthermore, LIN28B overexpression resulted in enhanced CDX2 expression to promote differentiation in subcutaneous xenograft tumors generated from CRC cells and metastatic tumor colonization through mesenchymal-epithelial transition in CRC liver metastasis mouse models. A ChIP sequence for CDX2 identified α-methylacyl-CoA racemase (AMACR) as a potentially novel transcriptional target of CDX2 in the context of LIN28B overexpression. We also found that AMACR enhanced intestinal alkaline phosphatase activity, which is known as a key component of intestinal differentiation, through the upregulation of butyric acid. Overall, we demonstrated that LIN28B promotes CRC differentiation through the CDX2/AMACR axis.

Oxidative stress activates the TRPM2-Ca2+-NLRP3 axis to promote PM2.5-induced lung injury of mice.

PM2.5, a main particulate air pollutant, poses a serious hazard to human health. The exposure to PM2.5 increases mortality and morbidity of many respiratory diseases such as asthma, chronic obstructive pulmonary diseases and even lung cancer. The contribution of reactive oxygen species (ROS) in the PM2.5-induced acute lung injury process was confirmed in our previous research, but the molecular mechanism based for it remains unclarified. In this research, ROS-induced lung injury after exposure to PM2.5 was explored in vivo and in vitro. The in vivo study indicated that N-acetyl-L-cysteine (NAC) could attenuate the accumulation of inflammatory cells, the thickening of alveolar wall and the degree of lung injury. Furthermore, we found ROS could regulate the intracellular Ca2+ level, expression of the Transient Receptor Potential Melastatin 2 (TRPM2), NLRP3 and its downstream inflammatory factors in vivo. In vitro experiments with A549 cells and primary type II alveolar epithelium cells (SD cells) showed that ROS induced by PM2.5 exposure could mediate intracellular Ca2+ mobilization via TRPM2, with a subsequent activation of NLRP3. In our present study, we demonstrated the contribution of the ROS-TRPM2-Ca2+-NLRP3 pathway in PM2.5-induced acute lung injury and offered a potential therapeutical target valid for related pathology.

Diagnostic Value of Whole-Body DWI With Background Body Suppression Plus Calculation of Apparent Diffusion Coefficient at 3 T Versus 18F-FDG PET/CT for Detection of Bone Metastases.

OBJECTIVE. The purpose of this study is to evaluate the diagnostic performance of whole-body (WB) DWI with background body suppression (DWIBS) combined with calculation of the apparent diffusion coefficient (ADC) value at 3 T compared with the diagnostic performance of 18F-FDG PET/CT for detecting bone metastases in patients with malignant tumors. SUBJECTS AND METHODS. Thirty-nine consecutive patients with suspected bone metastases underwent both WB DWIBS and FDG PET/CT. Imaging findings were independently interpreted using qualitative and quantitative analyses. Pathologic findings or clinical or radiologic follow-up data were used as the diagnostic reference standard. The sensitivity, specificity, overall accuracy, positive predictive value, and negative predictive value of both modalities were calculated. The ADCs of benign lesions and metastases were compared. RESULTS. A total of 213 metastatic bone segments were confirmed among 39 patients. The sensitivity, specificity, overall accuracy, positive predictive value, and negative predictive value were 93.0%, 87.8%, 89.6%, 79.8%, and 96.0%, respectively, for WB DWIBS and 92.5%, 92.0%, 92.1%, 85.7% and 95.9%, respectively, for FDG PET/CT. The specificity of WB DWIBS in detecting bone metastases was significantly lower than that of FDG PET/CT (p < 0.05), whereas the sensitivity, overall accuracy, positive predictive value, and negative predictive value in detecting bone metastases were not significantly different between WB DWIBS and FDG PET/CT (p > 0.05). The ADCs for benign lesions were significantly higher than those for metastases (p < 0.001). In ROC curve analysis, the AUC value was 0.901. A cutoff ADC value of 920.5 × 10-6 mm2s-1 distinguished benign lesions from bone metastases with a sensitivity of 92.9% and a specificity of 73.4%. CONCLUSION. WB DWIBS coupled with ADC analysis at 3 T is effective for detecting bone metastases.

LncRNA H19/microRNA-675/PPARα axis regulates liver cell injury and energy metabolism remodelling induced by hepatitis B X protein via Akt/mTOR signalling.

Emerging evidence indicates that the lncRNAs/microRNA/mRNA axis plays important roles in a variety of diseases. This study was aimed to investigate the potential roles and underlying molecular mechanisms of lncRNA H19 and H19-derived miR-675 in regulating hepatitis B virus (HBV)-associated liver injury. mRNA and miR-675 levels were determined by quantitative real-time PCR (qRT-PCR), protein levels were determined by western blot, cell viability was measured by the MTT assay, cell apoptosis was measured by flow cytometry, inflammatory cytokine production was determined by ELISA, oxidative stress and energy metabolism were assessed by commercial kits, and the target relationship between PPARα and miR-675 was confirmed by the dual-luciferase reporter assay. The results showed that the expression of lncRNA H19 and miR-675 was up-regulated in patients with chronic hepatitis B (n = 20). Inhibition of lncRNA H19 or miR-675 in L02 cells increased cell viability, suppressed hepatitis B X protein (HBx)-induced cell apoptosis, inflammatory cytokine production, and oxidative stress, and remodelled energy metabolism. Furthermore, PPARα was found to be a target gene of miR-675. The expression of PPARα was down-regulated in patients with chronic hepatitis B, and there was a negative correlation between the expression of lncRNA H19 and PPARα, or between miR-675 and PPARα. Moreover, by knocking down the expression of PPARα, the actions (apoptosis, inflammatory factors, oxidative stress, and energy metabolism) of lncRNA H19 or miR-675 inhibition in HBx-induced L02 cells were at least partially reversed. In addition, HBx-induced elevated levels of p-AktSer473, p-AktThr308 and p-mTORSer2448 were down-regulated by lncRNA H19 or miR-675 inhibition. Furthermore, PPARα knockdown partly reversed the down-regulated effects of H19 or miR-675 inhibition. Taken together, these data indicate that the lncRNA H19/miR-675/PPARα axis regulates liver cell injury and energy metabolism remodelling induced by HBx, which may be related to the modulation of Akt/mTOR signalling.

The harmful effects of acute PM2.5 exposure to the heart and a novel preventive and therapeutic function of CEOs.

Epidemiological researches have demonstrated the relationship between PM2.5 exposure and increased morbidity and mortality of cardiovascular injury. However, no effective therapeutic method was established. The purpose of this study is to investigate the effect of acute PM2.5 exposure on the mice heart tissue and explore the therapeutic effects of compound essential oils (CEOs) in this model. In this study, after mice were exposed to PM2.5 intratracheally, some obvious histopathological changes as well as some great alterations of proinflammatory cytokines were observed in the heart tissue. The imbalance of oxidative stress, the altered Ca2+ channel related proteins and the increased intracellular free Ca2+ were all involved in the heart impairment and would also be investigated in this model. The CEOs alleviated the heart impairment via its antioxidant effect rather than its anti-inflammatory function because our results revealed that oxidative stress related indicators were restored after CEOs administration. At the same time, increased concentration of intracellular free Ca2+ and ROS induced by PM2.5 were reduced after NAC (N-Acetyl-L-cysteine) administration. These data suggested that the acute PM2.5 exposure would damage heart tissue by inducing the inflammatory response, oxidative stress and intracellular free Ca2+ overload. PM2.5-induced oxidative stress probably increase intracellular free Ca2+ via RYR2 and SERCA2a. CEOs have the potential to be a novel effective and convenient therapeutic method to prevent and treat the acute heart impairment induced by PM2.5 via its antioxidant function.

Platinum/Nickel Bicarbonate Heterostructures towards Accelerated Hydrogen Evolution under Alkaline Conditions.

Heterostructured nanomaterials, generally have physicochemical properties that differ from those of the individual components, and thus have potential in a wide range of applications. New platinum (Pt)/nickel bicarbonate (Ni(HCO3 )2 ) heterostructures are designed for an efficient alkaline hydrogen evolution reaction (HER). Notably, the specific and mass activity of Pt in Pt/Ni(HCO3 )2 are substantially improved compared to the bare Pt nanoparticles (NPs). The Ni(HCO3 )2 provides abundant water adsorption/dissociation sites and modulate the electronic structure of Pt, which determine the elementary reaction kinetics of alkaline HER. The Ni(HCO3 )2 nanoplates offer a platform for the uniform dispersion of Pt NPs, ensuring the maximum exposure of active sites. The results demonstrate that, Ni(HCO3 )2 is an effective catalyst promoter for alkaline HER.

Recent Progress on Nickel-Based Oxide/(Oxy)Hydroxide Electrocatalysts for the Oxygen Evolution Reaction.

Developing clean and sustainable energies as alternatives to fossil fuels is in strong demand within modern society. The oxygen evolution reaction (OER) is the efficiency-limiting process in plenty of key renewable energy systems, such as electrochemical water splitting and rechargeable metal-air batteries. In this regard, ongoing efforts have been devoted to seeking high-performance electrocatalysts for enhanced energy conversion efficiency. Apart from traditional precious-metal-based catalysts, nickel-based compounds are the most promising earth-abundant OER catalysts, attracting ever-increasing interest due to high activity and stability. In this review, the recent progress on nickel-based oxide and (oxy)hydroxide composites for water oxidation catalysis in terms of materials design/synthesis and electrochemical performance is summarized. Some underlying mechanisms to profoundly understand the catalytic active sites are also highlighted. In addition, the future research trends and perspectives on the development of Ni-based OER electrocatalysts are discussed.

Iron-Doped Nickel Molybdate with Enhanced Oxygen Evolution Kinetics.

Electrochemical water splitting is one of the potential approaches for making renewable energy production and storage viable. The oxygen evolution reaction (OER), as a sluggish four-electron electrochemical reaction, has to overcome high overpotential to accomplish overall water splitting. Therefore, developing low-cost and highly active OER catalysts is the key for achieving efficient and economical water electrolysis. In this work, Fe-doped NiMoO4 was synthesized and evaluated as the OER catalyst in alkaline medium. Fe3+ doping helps to regulate the electronic structure of Ni centers in NiMoO4 , which consequently promotes the catalytic activity of NiMoO4 . The overpotential to reach a current density of 10 mA cm-2 is 299 mV in 1 m KOH for the optimal Ni0.9 Fe0.1 MoO4 , which is 65 mV lower than that for NiMoO4 . Further, the catalyst also shows exceptional performance stability during a 2 h chronopotentiometry testing. Moreover, the real catalytically active center of Ni0.9 Fe0.1 MoO4 is also unraveled based on the ex situ characterizations. These results provide new alternatives for precious-metal-free catalysts for alkaline OER and also expand the Fe-doping-induced synergistic effect towards performance enhancement to new catalyst systems.

miR-101-3p sensitizes hepatocellular carcinoma cells to oxaliplatin by inhibiting Beclin-1-mediated autophagy.

BACKGROUND: Increasing evidence has shown that autophagy can contribute to drug resistance. Whether microRNA-101-3p (miR-101-3p) participates in oxaliplatin (OXA) resistance via modulating Beclin-1-mediated autophagy in hepatocellular carcinoma (HCC) has not been reported. METHODS: OXA-resistant Huh7 cells (Huh7/OXA) or HepG2 cells (HepG2/OXA) and OXA-sensitive Huh7 or HepG2 cells were treated with OXA in various concentrations. The expressions of miR-101-3p and Beclin-1 were monitored using qRT-PCR. Western blot was used to evaluate cell autophagy. Cell viability and the IC50 of OXA were determined using an MTT assay. Cell apoptosis was evaluated by flow cytometry. A luciferase reporter assay was introduced to confirm the relationship between miR-101-3p and Beclin-1. RESULTS: miR-101-3p was decreased in HCC resistant tissues and cells. Moreover, an increased expression of miR-101-3p reduced cell viability and the IC50 of OXA, and it promoted cell apoptosis in Huh7/OXA and HepG2/OXA cells. miR-101-3p negatively modulated the expression of Beclin-1. Interestingly, the overexpression of Beclin-1 receded the effect of the ectopic expression of miR-101-3p in OXA-resistant HCC cells. In OXA-sensitive Huh7 and HepG2 cells, OXA significantly increased the expressions of LC3 and Beclin-1, and it decreased the abundance of p62. Furthermore, OXA markedly blocked cell viability, which was exacerbated by the introduction of the autophagy inhibitor CQ. Additionally, the elevated expression of miR-101-3p suppressed cell autophagy by inhibiting the expression of LC3 and Beclin-1 and facilitating the expression of p62. CONCLUSION: miR-101-3p is responsible for the sensitivity of HCC cells to OXA by inhibiting Beclin-1-mediated autophagy.

Curcumin Protects an SH-SY5Y Cell Model of Parkinson's Disease Against Toxic Injury by Regulating HSP90.

BACKGROUND/AIMS: We aimed to explore the protective role of curcumin (Cur) in a cell model of Parkinson's disease (PD) and its underlying mechanism. METHODS: In this study, genes concerned with PD-related keywords were screened within DiGSeE database. The association network between Cur and selected genes was downloaded from STITCH, with the interactions analyzed by STRING. We built a mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP+)-induced SH-SY5Y cell model of PD. Cell morphology was observed under an electron microscope. MTT assay was applied to detect cell proliferation rate. Western blot assay was conducted to determine the level of apoptotic markers, including cleaved caspase 3, Bcl-2-associated X protein (Bax) and B-cell lymphoma-extra-large (Bcl-xl). Tyrosine hydroxylase (TH), dopamine transporter (DAT) protein levels and dopamine (DA) concentration were identified as dopaminergic neuron markers and measured by western blotting or Enzyme-linked immunosorbent assay (ELISA). RESULTS: Cur rescued the toxicity effects of MPP+ on SH-SY5Y cells, by controlling morphological change, promoting cell proliferation and inhibiting apoptosis. Of all PD-related genes, HSP90 played an important role in Cur-gene network. HSP90 protein level was elevated by MPP+, whereas Cur could reverse this effect. Silencing of HSP90 significantly attenuated the curative effect introduced by Cur, while HSP90 overexpression enhanced the impact of Cur on PD. CONCLUSION: Cur can effectively inhibit the toxic effect of MPP+ on SH-SY5Y cells and significantly reduce the adverse effects of MPP+ on dopaminergic neurons via up-regulation of HSP90.

Nickel-Based Bicarbonates as Bifunctional Catalysts for Oxygen Evolution and Reduction Reaction in Alkaline Media.

Oxygen electrocatalysis, including the oxygen evolution reaction (OER) and oxygen reduction reaction (ORR), is one of the most important electrochemical processes for sustainable energy conversion and storage technologies. Herein, nickel-based bicarbonates are, for the first time, developed as catalysts for oxygen electrocatalysis, and demonstrate superior electrocatalytic performance in alkaline media. Iron doping can significantly tune the real valence of nickel ions, and consequently tailor the electrocatalytic ability of bicarbonates. Among the nickel-based bicarbonates, Ni0.9 Fe0.1 (HCO3 )2 exhibits the highest bifunctional catalytic activity, with a potential difference of 0.86 V between the OER potential at a current density of 10 mA cm-2 and the ORR potential at a current density of -1 mA cm-2 , which outperforms most of the reported precious-metal-free catalysts. The present work provides new insights into exploring efficient catalysts for oxygen electrocatalysis, and it suggests that, in addition to the extensively studied transition metal hydroxides and oxides, bicarbonates and carbonates also show great potential as precious metal-free catalysts.