CHEMICAL ENGINEERING JOURNAL
·
2022
·
IF 16.744
Ling Li,Longcheng Zhang,Lichen Gou,Siqi Wei,Xiandeng Hou,Li Wu
Electrocatalytic methanol oxidation reaction (MOR) is a promising alternative approach to oxygen evolution reaction for efficient hydrogen production. However, developing highly efficient and cost-effective MOR catalysts, coupled with the cathodic hydrogen evolution reaction, is still a challenge. Herein, we used a Ni 2 P nanosheet array with Cu 2 O-Cu dendrites on nickel foam (Cu 2 O-Cu@Ni 2 P/NF) as an efficient and stable electrocatalyst for MOR, which attained a low potential of 1.41 V at 100 mA cm −2 and a small Tafel slope of 44.99 mV dec –1 with excellent stability for at least 24 h in 1.0 M KOH solution with 1.0 M methanol. In situ Raman spectroscopy reveals that Cu 2 O-Cu promotes the generation of the β-NiOOH active phase, and converts to Cu(II)O under the electrolysis conditions. Furthermore, the methanol electrolysis cell utilizing Cu 2 O-Cu@Ni 2 P/NF as both the cathode and anode delivered a current density of 10 mA cm −2 at a low cell voltage of 1.40 V, and the cell voltage decreased by 210 mV at a current density of 100 mA cm −2 compared to water electrolysis. This work provides a new strategy to design the promising Ni-based phosphide as a bifunctional electrocatalyst in methanol electrolysis, enabling energy-saving H 2 production.
研究领域:
材料科学
·
电化学
·
能源工程
✓ 已验证
DOI
高影响因子
FASEB JOURNAL
·
2025
·Vol. 39
·期 7
·e70539
·
IF 4.2
Yingjie Shen,Yitong Zhou,Kuziwakwashe Alice Chiwa,Junxin Wang,Shihong Ren,Mingxuan Wang,Hongru Ren,Yeyi Zheng,Ying Yu,Lutao Jiang,Jingmou Yu,Yuchun Qiao,Litai Jin,Jianlin Lou,Xiangkuo Zheng
Psoriasis is an immune-mediated inflammatory dermatological disorder characterized by the interaction between immune cells and keratinocytes, which perpetuates cutaneous inflammation and cellular hyperproliferation. In this study, we identified a strong δ-catenin signature in psoriatic skin; however, the precise role of δ-catenin remains to be elucidated. Additionally, we observed that Interleukin (IL)-17A, a pivotal cytokine involved in the development of psoriatic lesions, induces δ-catenin expression in HEKn and HACAT cells. From a mechanistic perspective, δ-catenin initiated NF-κB signaling, subsequently leading to the activation of IL-6 and IL-8 production. Furthermore, silencing δ-catenin expression mitigated IL-17A-induced hyperproliferation of keratinocytes through the NF-κB pathway. Our study further identified miR-101 and miR-122 as upstream regulators of δ-catenin, exerting their effects by downregulating δ-catenin protein levels. We demonstrated that miR-101 and miR-122 can inhibit the hyperproliferation of keratinocytes induced by δ-catenin. These findings validate the role of δ-catenin in the pathogenesis of psoriasis, particularly in keratinocyte-mediated inflammatory responses and cellular hyperproliferation. Consequently, miR-101 and miR-122 hold potential as therapeutic agents in the treatment of psoriasis. Graphical The schematic diagram delineates the signaling pathway associated with IL-17A-induced psoriasis, highlighting the upregulation of delta-catenin, which initiates NF-κB signaling. This activation subsequently leads to the production of IL-6 and IL-8, as well as the hyperproliferation of keratinocytes. Furthermore, miR-101 and miR-122 function as inhibitors of delta-catenin, effectively obstructing this signaling cascade.
研究领域:
皮肤病学
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分子生物学
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免疫学
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产品关联
DOI
PubMed
高影响因子
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
·
2025
·Vol. 93
·期 5
·e70084
·
IF 2.4
Heng Wang,Zhaofei Liu,Xiangjun Xu,Haitao Zhang,Lei He,Ming Li
Background Chronic prostatitis (CP), a frequent male urological disease, is featured with chronic pelvic pain and various discomfort. Calycosin has anti-inflammatory effect and its exact mechanism in CP remains unknown. Objective Our research was designed to explain the underlying mechanism of calycosin in CP and illustrate our findings in the rats and LPS-ATP-induced RWPE-1 cells. Methods The pathology of prostate tissues was analyzed by HE staining and histological inflammation score. The concentration of inflammatory factors were detected via ELISA assay. Besides, the representative biomarkers of oxidative stress were measured through detection kits. The ROS production, NLRP3 and GSDMD expression were evaluated by immunofluorescence or immumohistochemical staining. Furthermore, the expression of NF-kBp65 pathway-associated proteins and pyroptosis-associated proteins were detected by western blotting. RWPE-1 cells growth and pyroptosis were assessed by CCK-8 and flow cytometry, respectively. mRNA levels of pyroptosis markers were detected by qRT-PCR analysis. Results The CP model in vivo and in vitro was successfully established by carrageenan and LPS-ATP, respectively. Calycosin substantially ameliorated the pathological damage of prostate tissue. Moreover, calycosin treatment promoted RWPE-1 cells viability and reduced pyroptosis. Calycosin remarkably reduced the inflammatory factors secretion and oxidative stress markers. Calycosin stimulation effectively suppressed the pyroptosis, which was linked with inactivation of the NF-kBp65 signaling pathway. These beneficial effects of calycosin were similar to the NLRP3 inhibitor (MCC950). Conclusion To sum up, our observations indicated that calycosin protects against CP via suppressing inflammation, oxidative stress, and pyroptosis through NF-kBp65 pathway, thereby serving as a promising therapy for CP treatment.
研究领域:
医学
·
药理学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CARBOHYDRATE POLYMERS
·
2015
·
IF 4.074
Wuxia Zhang,Feifei Sun,Hong Niu,Qingjie Wang,Jinyou Duan
As a major component in extracellular matrix of the tissue, chondroitin sulfate A (CS-A) has been shown to exhibit either pro- or anti-inflammatory immune response which was largely dependent on its molecular size and cell types. In this study, we determined the signaling pathway involved in immune response of CS and its N -deacetylated derivative (dCS). Our data indicated that both CS and dCS could activate the NF-κB transcription factor in antigen presenting cells and induce TNF-α production through the TLR/MyD88 pathway. Further studies demonstrated that both CS and dCS had a potential in promoting the proliferation of spleen lymphocytes, and promoting the cytokines secretion by OVA-sensitized splenocytes. Thus, our finding provided a mechanistic insight into the understanding of cellular immunity of CS and dCS, which might be helpful to develop CS-based immune modulators against chronic inflammatory conditions, autoimmunity, infectious diseases, allergies and asthmatic conditions.
研究领域:
免疫学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Nano Energy
·
2024
·
IF 16.8
Jie Liu,Yunmei Du,Xiaoli Sun,Shuangshuang Li,Yanru Liu,Lei Wang
Developing a simple and effective strategy to optimize the structure of phosphide to stimulate its industrial-scale current density for water decomposition is a great challenge. In this work, the ‘phosphorization-quenching ammonia treatment’ strategy was innovatively proposed to prompt N-doping and the phase transition of phosphide, thereby constructing the unique N-FeNiP/NF-T electrode. As anticipated, the well-designed N-FeNiP/NF-T obtained an industrial current density of 1 A cm −2 at only 282 mV for HER and 307 mV for OER, which is 0.90-fold of Pt/C and 0.52-fold of RuO 2 , respectively. Notably, the density functional theory calculation revealed that the N dopants further optimized the reaction kinetics of the N-Ni 2 P/NiP 2 heterostructure with high OER activity and the N-NiP 2 phase with high HER activity, leading to the maximization of the synergistic effect. Overall, this work provides a novel strategy to induce phase transition to construct efficient heterostructure electrodes with optimal reaction kinetics.
研究领域:
材料科学
·
电化学
·
催化
✓ 已验证
DOI
高影响因子
LIFE SCIENCES
·
2021
·
IF 5.037
Zhenjie Sun,Qian Chai,Ziying Zhang,Dexue Lu,Ziang Meng,Weihua Wu
Aims Glycemic variability has been shown to be more harmful in the development of diabetic complication than sustained chronic hyperglycemia. In this present study, we tried to reveal the effects of glycemic variability on cardiac damage in diabetic mice and investigate whether sodium-glucose cotransporter 1 (SGLT1), an important cardiac glucose transporter, functions as an important mediator in the process. Materials and methods Type 2 diabetes mellitus (DM) mice were induced by a high-fat diet and intraperitoneal injection of streptozotocin (STZ), and then glycemic variability in type 2 diabetes mellitus (GVDM) was induced by alternately injecting insulin and glucose to DM mice. In order to determine the roles of SGLT1 in GVDM mice, SGLT1 inhibition was performed using shRNA against SGLT1. The blood glucose level, the cardiac function and myocardial injury were assessed. And the expressions of SGLT1 and the activations of NLRP3/caspase-1 pathway and NF-κB in left ventricular tissues were measured. Key findings The results showed that SGLT1 was highly expressed in heart of GVDM mice compared to control and DM groups, and knockdown of SGLT1 reduced glycemic variability in GVDM mice. Moreover, glycemic variability impaired cardiac function, aggravated cardiac injury and induced NLRP3/caspase-1-mediated inflammatory response and pyroptosis. And knockdown of SGLT1 significantly attenuated the cardiac damages that induced by glycemic variability. Significance The results indicated that glycemic variability could cause cardiac damage and induce inflammatory response and pyroptosis of cardiomyocytes in diabetic mice, which could be partially blocked by SGLT1 silence.
研究领域:
内分泌学
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心脏病学
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糖尿病
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
·
2024
·
IF 6
Zhiran Ju,Junde Xu,Keshuang Tang,Fener Chen
COX-2/NLPR3-targeted therapy might be beneficial for the inflammation diseases. To discover novel anti-inflammatory compounds with favorable safety profiles, three new series of non-carboxylic diclofenac analogues bearing various ring systems, such as oxadiazoles 4a - 4w , triazoles 6a - 6m , and cyclic imides 7a and 7b , were synthesized. The synthesized analogues were evaluated for their inhibitory activity against COX-2 enzyme. Among them, compound 6k exhibited potent selective COX-2 inhibition (IC 50 = 1.53 μM; selectivity ((IC 50 (COX-1)/IC 50 (COX-2) = 17.19). Treatment with compound 6k effectively suppressed the NF-κB/NLRP3 signaling pathway, resulting in reduced expression of pro-inflammatory factors. The in vivo ulcerative colitis assay demonstrated that compound 6k significantly ameliorated histological damages and showed strong protection against DSS-induced acute colitis. The collected results indicated that compound 6k displays anti-inflammatory activity through COX-2/NLRP3 inhibition. Therefore, compound 6k represents a promising candidate for further development as a new lead compound with reduced colitis side effects.
研究领域:
药理学
·
药物化学
·
炎症研究
✓ 已验证
DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF HISTOCHEMISTRY
·
2023
·
IF 2
Qian Hu,Ran Tao,Xiaoyun Hu,Haibo Wu,Jianjun Xu
Acute pancreatitis is an inflammatory response in the pancreas, involving activation of pancreatic enzymes. Severe acute pancreatitis (SAP) often causes systemic complications that affect distant organs, including the lungs. The aim of this study was to explore the therapeutic potential of piperlonguminine on SAP-induced lung injury in rat models. Acute pancreatitis was induced in rats by repetitive injections with 4% sodium taurocholate. Histological examination and biochemical assays were used to assess the severity of lung injury, including tissue damage, and levels of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4), reactive oxygen species (ROS), and inflammatory cytokines. We found that piperlonguminine significantly ameliorated pulmonary architectural distortion, hemorrhage, interstitial edema, and alveolar thickening in rats with SAP. In addition, NOX2, NOX4, ROS, and inflammatory cytokine levels in pulmonary tissues were notably decreased in piperlonguminine- treated rats. Piperlonguminine also attenuated the expression levels of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB). Together, our findings demonstrate for the first time that piperlonguminine can ameliorate acute pancreatitis-induced lung injury via inhibitory modulation of inflammatory responses by suppression of the TLR4/NF-κB signaling pathway.
研究领域:
药理学
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炎症
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肺医学
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胃肠病学
✓ 已验证
DOI
PubMed
高影响因子
Antioxidants
·
2021
·Vol. 11
·期 1
·65
·
IF 6.313
Zhi-Yuan Chen,Hui-Wen Xiao,Jia-Li Dong,Yuan Li,Bin Wang,Sai-Jun Fan,Ming Cui
Radiation pneumonia is a common and intractable side effect associated with radiotherapy for chest cancer and involves oxidative stress damage and inflammation, prematurely halting the remedy and reducing the life quality of patients. However, the therapeutic options for the complication have yielded disappointing results in clinical application. Here, we report an effective avenue for fighting against radiation pneumonia. Faecal microbiota transplantation (FMT) reduced radiation pneumonia, scavenged oxidative stress and improved lung function in mouse models. Local chest irradiation shifted the gut bacterial taxonomic proportions, which were preserved by FMT. The level of gut microbiota-derived PGF2α decreased following irradiation but increased after FMT. Experimental mice with PGF2α replenishment, via an oral route, exhibited accumulated PGF2α in faecal pellets, peripheral blood and lung tissues, resulting in the attenuation of inflammatory status of the lung and amelioration of lung respiratory function following local chest irradiation. PGF2α activated the FP/MAPK/NF-κB axis to promote cell proliferation and inhibit apoptosis with radiation challenge; silencing MAPK attenuated the protective effect of PGF2α on radiation-challenged lung cells. Together, our findings pave the way for the clinical treatment of radiotherapy-associated complications and underpin PGF2α as a gut microbiota-produced metabolite.Keywords:radiation pneumonia;gut microbiota;gut-lung axis;gut microbiota metabolites;PGF2α
研究领域:
肿瘤学
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微生物学
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免疫学
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药理学
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE
·
2018
·Vol. 99
·期 5
·2329-2339
·
IF 2.379
Jing Ye,Changqing Ye,Yayan Huang,Na Zhang,Xueqin Zhang,Meitian Xiao
BACKGROUND Polysaccharides, common components of natural products extensively studied as dietary supplements and functional foods, have been found to have various activities. In the present study, a water-soluble polysaccharide, namely GBSP3a, was isolated and purified from G. biloba sarcotesta. The anti-inflammatory activity of GBSP3a in lipopolysaccharide (LPS)-induced RAW264.7 macrophages and the potential underlying molecular mechanisms were then assessed. RESULTS GBSP3a exerted its anti-inflammatory effect by remarkably inhibiting the secretion of pro-inflammatory mediators and cytokines, including nitric oxide (NO), prostaglandin E 2 (PGE 2 ), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in LPS-stimulated RAW264.7 macrophages. Excessive mRNA and protein expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were dose-dependently inhibited by GBSP3a in LPS-stimulated RAW264.7 cells. Further research suggested that the anti-inflammatory effect of GBSP3a can be attributed to the modulation of the NF-κB and MAPK signaling pathways. CONCLUSION GBSP3a exhibits anti-inflammatory activity and exerts its anti-inflammatory effect probably through suppressing both NF-κB and MAPK signaling pathway, indicating that GBSP3a could be used for the development of anti-inflammatory agent or nutraceuticals. © 2018 Society of Chemical Industry
研究领域:
药理学
·
免疫学
·
分子生物学
✓ 已验证
DOI
PubMed
高影响因子
Aging-US
·
2019
·
IF 5.515
Tingting Xu,Xiangting Ge,Chun Lu,Wei Dai,Hongjin Chen,Zhongxiang Xiao,Liqin Wu,Guang Liang,Songmin Ying,Yali Zhang,Yuanrong Dai
Asthma is a type of chronic lung inflammation with restrictions in effective therapy. NF-κB pathway activation has been suggested to play an important role in the pathogenesis of asthma. Baicalein, one of the major active flavonoids found in Scutellaria baicalensis , exhibits potent anti-inflammatory properties by inhibiting NF-κB activity. Herein, we report that Baicalein significantly reduces OVA-induced airway hyperresponsiveness (AHR), airway inflammation, serum IgE levels, mucus production, and collagen deposition around the airway. Additionally, western blot analysis and immunofluorescence assay showed that Baicalein attenuates the activation of NF-κB, which was mainly reflected by IκBα phosphorylation and degradation, p65 nuclear translocation and downstream iNOS expression. Furthermore, in human epithelial cells, Baicalein blocked TNF-α-induced NF-κB activation. Our study provides evidence that Baicalein administration alleviates the pathological changes in asthma through inactivating the NF-κB/iNOS pathway. Baicalein might be a promising potential therapy agent for patients with allergic asthma in the future.
研究领域:
免疫学
·
药理学
·
呼吸医学
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF INVESTIGATIVE DERMATOLOGY
·
2021
·
IF 8.551
Yingjie Shen,Zhongxin Zhu,Weitao Cong,Mengying Jiang,Jianan Wang,Xixi Chen,Nan Wang,Ying Yu,Yetong Dong,Zhili Liu,Jia Sun,Wenjie Gong,Siyi Zhang,Kwonseop Kim,Litai Jin
Skin wound healing is a complex process involving intricate molecular mechanisms that remain unknown. Restoration of homeostasis after wounding requires the remodeling function of fibroblasts. In this study, we show that phosphorylation of α-catenin S641 was upregulated in fibroblasts during wounding, which accelerated their proliferation and migration to restore the skin barrier. At the wound edge, phosphorylated α-catenin S641 stabilized IκBα and thereby impaired the expression of NF-κB target genes to promote proliferation and migration of fibroblasts. Mechanically, phosphorylated α-catenin S641 blocked K48-linked polyubiquitination and proteasomal degradation of IκBα. Moreover, we also showed that EGF/EGFR/CK2α functioned as key upstream signaling of α-catenin by phosphorylating α-catenin at S641. Wound repair was significantly disrupted in the skin of mice in which α-catenin phosphorylation and CK2α kinase activity were perturbed in fibroblasts. These findings provide insights into the molecular control of fibroblast proliferation and migration in response to wounding and identify potential targets for the treatment of defective wound repair.
研究领域:
细胞生物学
·
分子生物学
·
伤口愈合
·
皮肤生理学
✓ 已验证
DOI
PubMed
高影响因子
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