Bioengineered
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2022
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IF 6.832
Kenan Zheng,Baojiang Lv,Lulu Wu,Chen Wang,Haoyou Xu,Xiaojun Li,Zhibing Wu,Yuanqi Zhao,Zequan Zheng
Experimental autoimmune encephalomyelitis (EAE) is characterized by demyelination of the central nervous system. Emodin is an anthraquinone derivative with comprehensive anti-inflammatory, anti-cancer, and immunomodulatory effects and is widely used in the treatment of inflammatory, tumor, and immune system diseases. However, none of the clinical or experimental studies have explored the therapeutic efficacy of emodin in EAE/multiple sclerosis (MS). Thus, we evaluated the protective effect of emodin on EAE mediated via inhibition of microglia activation and inflammation. Wild-type mice were randomly divided into the normal control, EAE, low-dose emodin, and high-dose emodin groups. Clinical scores and pathological changes were assessed 21 days after immunization. The network pharmacology approach was used to elucidate the underlying mechanisms by using an online database. Molecular docking, polymerase-chain reaction tests, western blotting, and immunofluorescence were performed to verify the network pharmacology results. An in vivo experiment showed that high-dose emodin ameliorated clinical symptoms, inflammatory cell infiltration, and myelination. Pharmacological network analysis showed AKT1 was the main target and that emodin played a key role in MS treatment mainly via the PI3K–Akt pathway. Molecular docking showed that emodin bound well with PI3K, AKT1, and NFKB1. Emodin decreased the expression of phosphorylated(p)-PI3K, p-Akt, NF-κB, and myeloid differentiation factor 88 and the levels of markers (CD86 and CD206) in M1- and M2-phenotype microglia in EAE. Thus, the emodin inhibited microglial activation and exhibited anti-inflammatory and neuroprotective effects against EAE via the Myd88/PI3K/Akt/NF-κB signalling pathway. In conclusion, emodin has a promising role in EAE/MS treatment, warranting further detailed studies.
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高影响因子
EXPERIMENTAL CELL RESEARCH
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2023
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IF 3.7
Lirong Zou,Xinling Wang,Xiao Han
The retina may undergo structural and functional damage as a result of hypoxia, which could lead to permanent blindness. As competing endogenous RNAs (ceRNAs), lncRNAs are essential in eye disorders. The biological function of lncRNA MALAT 1 and its potential mechanisms in hypoxic-ischemic retinal diseases are still unknown. MALAT 1 and miR-625–3p expression alterations in hypoxia-treated RPE cells were examined using qRT-PCR. The target binding relationships between MALAT 1 and miR-625–3p, as well as between miR-625–3p and HIF-1α, were identified utilizing bioinformatics analysis and dual luciferase reporter assay. We observed that si-MALAT 1 and miR-625–3p mimic both reduced apoptosis and epithelial-mesenchymal transition (EMT) in hypoxic RPE cells, whereas si-MALAT 1 was reversed by miR-625–3p inhibitor. Further, we carried out a mechanistic investigation, and rescue assays demonstrated that MALAT 1 sponging miR-625–3p influenced HIF-1α expression and consequently took part in the NF-κB/Snail signaling pathway , which regulated apoptosis and EMT. In conclusion, our research had shown that the MALAT 1/miR-625–3p/HIF-1α axis drove the progression of hypoxic-ischemic retinal disorders and may serve as a promising predictive biomarker for their therapeutic and diagnostic targets.
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高影响因子
FISH & SHELLFISH IMMUNOLOGY
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2023
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IF 4.7
Hao Cai,Ke Li,Yilin Yin,Xiaotong Ni,Shiwen Xu
Bis(2-ethylhexyl) phthalate (DEHP) is not only a widely used plasticizer but also a common endocrine disruptor that frequently lingers in water, posing a threat to the health of aquatic organisms . Quercetin (Que) is a common flavonol found in the plant kingdom known for its antioxidant, anti-inflammatory, and immunomodulatory effects. However, it is still unclear whether DEHP can cause pyroptosis and affect the expression of cytokines of grass carp L8824 cells and whether Que has antagonistic effect in this process. In our study, grass carp L8824 cells were treated into four groups after 24 h, namely NC group, DEHP group (1000 μM DEHP), Que group (5 μM Que), and DEHP + Que group (1000 μM DEHP + 5 μM Que). Our results indicate a significant increase in the level of ROS in L8824 cells after exposure to DEHP. DEHP upregulated oxidative stress markers (H 2 O 2 and MDA) and downregulated antioxidant markers (CAT, GSH, SOD , and T-AOC). DEHP also upregulated MAPK and NF-κB signal pathway-related proteins and mRNA expressions (p-p38, p-JNK, p-EPK, and p65). As for cell pyroptosis and its related pathways, DEHP upregulated pyroptosis-related protein and mRNA expressions (GSDMD, IL-1β, NLRP3, Caspase-1, LDH , pro-IL-18, IL-18, and ASC). Finally, DEHP can up-regulated cytokines (IL-6 and TNF-α) expression, down-regulated cytokines (IL-2 and IFN-γ) expression, and antimicrobial peptides (β-defensin, LEAP2, and HEPC). The co-treatment of L8824 cells with DEHP and Que inhibited the activation of the ROS/MAPK/NF-κB axis, alleviated pyroptosis, and restored expression of immune-related indicators. Finally, NAC was applied to reverse intervention of oxidative stress. In summary, Que inhibited DEHP-induced pyroptosis and the influence on cytokine and antimicrobial peptide expression in L8824 cells by regulating the ROS/MAPK/NF-κB pathway. Our results demonstrate the threat to fish health from DEHP exposure and confirmed the harm of DEHP to the aquatic ecological environment and the detoxification effect of Que to DEHP, which provides a theoretical basis for environmental toxicology.
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高影响因子
CELL STRESS & CHAPERONES
·
2023
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IF 3.8
He Xin,Wang Juan,Sun Lei,Ma Wenqi,Li Miao,Yu Shanshan,Zhou Qi,Jiang Jue
Mastitis is a disease involved in inflammation of breast which affects human and animals. Wogonin is one bioactive compound from many Chinese herbal medicines, which have multiple properties, including anti-inflammatory activity. However, the roles of wogonin in mastitis progression are largely undefined. Mastitis models were established using LPS-treated mice and mammary epithelial cells (MECs). Infiltration of inflammatory cells was analyzed by hematoxylin-eosin staining and myeloperoxidase (MPO) activity. Inflammatory cytokine (TNF-α and IL-1β) levels were detected via ELISA. The phosphorylation and total of Akt and NF-κB levels and content of Nrf2 and HO-1 were measured via western blot. Cell viability was examined by CCK-8 assay. Oxidative stress was assessed by ROS generation and levels of MDA, GSH, and SOD. Wogonin attenuated LPS-induced infiltration of inflammatory cells, increase of MPO activity and levels of TNF-α and IL-1β, and activation of the Akt/NF-κB pathway in murine mammary gland tissues, and promoted activation of Nrf2/HO-1 signaling. Wogonin did not affect MEC viability, but mitigated LPS-induced inflammation in MECs by reducing TNF-α and IL-1β levels. Wogonin relieved LPS-induced oxidative stress in MECs through decreasing ROS generation and MDA level and increasing GSH and SOD levels. Wogonin repressed LPS-induced activation of the Akt/NF-κB pathway in MECs and increased Nrf2/HO-1 signaling activation. Activated Akt/NF-κB signaling or Nrf2/HO-1 signaling inactivation reversed the suppressive effects of wogonin on LPS-induced inflammation and oxidative stress in MECs. Wogonin mitigates LPS-induced inflammation and oxidative stress of MECs via suppressing activation of the Akt/NF-κB signaling and activating Nrf2/HO-1 pathway, indicating the therapeutic potential of wogonin in mastitis.
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高影响因子
FUEL
·
2023
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IF 7.4
Weiwen Wang,Mengqi Xiang,Yaqian Fu,Wenze Wang,Jihai Duan
The sluggish energy of photocatalytic CO 2 reduction and the low methanol yields got are straightforwardly connected with the applied photocatalyst and reactor design, restricting the broad utilization of this technology. In light of this, the aim of this work is to innovate a new application of this Cu-Zn/Ni foam (Cu-Zn/NF) with a rod-like structure, which combines a intact foam-based photocatalyst with a microfluidic flow channel. This design ensures a larger specific surface area, besides a uniform phase distribution and efficient CO 2 reduction. A novel foam-based monolithic photomicroreactor was evaluated by measuring methanol concentration and yield. Under the conditions of 25 mL·min −1 , 0.5 M NaOH, 5 mm thickness of Ni foam, and 350 W xenon lamp irradiation conditions were applied, the methanol yield could reach 15.88 μmol·g −1 ·h −1 . This outcome is superior to the announced values in most CO 2 photoreactors. This work guides the optimization of photomicroreactors, besides provides new ideas for the use of monolithic microreactors for CO 2 reduction.
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高影响因子
INTERNATIONAL JOURNAL OF HYDROGEN ENERGY
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2021
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IF 5.816
Qi Zhang,Shihui Jiao,Boran Wang,Zisheng Wang,Xinyan Lv,Wenwen Wang,Yumei Tan,Canyu Cui,Yan Chen
Electrocatalytic water splitting for hydrogen production plays a vital role in the development of new energy field, but there is still a lack of low-content precious metal or cost-effective non-noble metal catalysts for the hydrogen evolution reaction (HER). Therefore, how to develop the catalysts with a smaller amount of precious metal to achieve higher performance is still a major challenge. Herein, we have fabricated Ru–Ni 2 P@Ni(OH) 2 /NF-2 heterostructure by phosphating Ni(OH) 2 /NF and then anchoring Ru on the surface through wet chemical strategy. Benefiting from its optimal Δ G H∗ and synergistic effect , this Ru–Ni 2 P@Ni(OH) 2 /NF-2 catalyst shows superior electrocatalytic HER kinetics in alkaline electrolyte . A small overpotential of 31 mV is needed for this electrocatalyst to obtain the current densities of 10 mA cm −2 with remarkable durability over 24 h. This work provides a new strategy for the preparation of effective HER electrocatalyst with a low precious metal content.
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高影响因子
Food Science and Human Wellness
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2020
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IF 2.455
Ruichang Gao,Wanghui Shu,Yang Shen,Quancai Sun,Wengang Jin,Dajing Li,Ying Li,Li Yuan
Previous studies have suggested that polypeptides extracted from milk, soybean, fish, eggs, and meat possess potential anti-inflammatory effects. To date, few studies have reported the anti-inflammatory function of sturgeon peptides and their underlying mechanisms are unknown. The current study was therefore to determine the anti-inflammatory potential of sturgeon peptides with lipopolysaccharide (LPS)-induced RAW264.7 inflammatory model. Pepsin hydrolysate (PeH) was purified by ultrafiltration and Sephadex G-15 gel filtration chromatography. PeH significantly reduced the inflammatory mediator (NO) and inflammatory cytokines (IL-6、TNF-α and IL-1β) expression in a dose-dependent manner. Moreover, the purified sturgeon peptide (F2) possessed strong antioxidant potential and effectively inhibited DPPH and ABTS free radicals. F2 significantly suppressed the expression of MAPKs, IκBα, and NF-κB p65, indicating that F2 exerted anti-inflammatory influence by the inhibition of MAPK and NF-κB pathways.
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高影响因子
Biomed Research International
·
2019
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IF 2.197
Hao Lu,Hui Yao,Rong Zou,Xiwen Chen,Hanlin Xu
Renal inflammation can result in renal injury. Uric acid (UA) is the final product of purine metabolism in humans and because of the lack of urate oxidase, UA may accumulate in tissues, including kidney, causing inflammation. Galangin was isolated from a traditional Chinese medicine plant and possesses several beneficial effects, working as an anti-oxidant, anti-mutagenic, anti-tumor, anti-inflammatory, anti-microbial, and anti-viral agent. Therefore, this study aimed at investigating the molecular mechanism of galangin in the attenuation of UA induced renal inflammation in normal rat kidney epithelial cells NRK-52E. Our findings suggested that galangin treatment efficiently protected NRK-52E cells against UA induced renal inflammation by decreasing tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-18, prostaglandin E2 (PGE2), and nitric oxide (NO) release, and it inhibited nitric oxide synthase (iNOS), prostaglandin endoperoxide synthase 2 (PTGS2), TNF-α, IL-1β, and IL-18 mRNA expression. In addition, galangin was not exerting any cytotoxicity at the concentrations that were effective against inflammation as assessed by CCK8 assay. Moreover, western blotting showed that galangin treatment effectively inhibited nuclear factor-kappa B (NF-κB), phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) and nucleotide-binding domain- (NOD-) like receptor protein 3 (NLRP3) signaling pathway activation. Taken together, these findings suggested that galangin plays a pivotal role in renal inflammation by suppressing inflammatory responses, which might be closely associated with the inhibition of NLRP3 inflammasome, NF-κB and PI3K/AKT signaling pathway activation.
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高影响因子
FREE RADICAL BIOLOGY AND MEDICINE
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2014
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IF 5.71
Simin Yan,Xu Zhang,Haili Zheng,Danhong Hu,Yongtian Zhang,Qinghua Guan,Lifang Liu,Qilong Ding,Yunman Li
Proinflammatory cytokine TNF-α-induced adhesion of leukocytes to endothelial cells plays a critical role in the early stage of atherosclerosis . Oxidative stress and redox-sensitive transcription factors are implicated in the process. Thus, compounds that mediate intracellular redox status and regulate transcription factors are of great therapeutic interest. Clematichinenoside (AR), a triterpene saponin isolated from the root of Clematis chinensis Osbeck , was previously demonstrated to have anti-inflammatory and antioxidative properties. However, little is known about the exact mechanism underlying these actions. Thus we performed a detailed study on its effect on leukocytes–endothelial cells adhesion with TNF-α-stimulated human umbilical vein endothelial cells (HUVECs) and cell-free systems. First, we found that AR reduced TNF-α-induced VCAM-1 and ICAM-1 expression and their promoter activity, inhibited translocation of p65 and phosphorylation of IκBα , suppressed IκB kinase-β (IKK-β) activity, lowered O 2 ∙− and H 2 O 2 levels, tackled p47 phox translocation, and decreased NOX4 NADPH oxidase expression. Second, we showed that AR exhibited no direct free radical scavenging ability in cell-free systems at concentrations that were used in intact cells. Besides, AR had no direct effect on the activity of IKK-β that was extracted from TNF-α-stimulated HUVECs. We also found that p47 translocation, NOX4 expression, and reactive oxygen species (ROS) levels were up-regulated before IκB phosphorylation in TNF-α-induced HUVECs. Moreover, TNF-α-enhanced IKK-β activity was also inhibited by (polyethylene glycol) PEG–catalase, N -acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-κB pathways in TNF-α-induced HUVECs, which finally suppress monocyte–HUVECs adhesion. This compound is potentially beneficial for early-stage atherosclerosis.
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
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IF 4.8
Shuyan Liu,Shunqing Zhou,Bo Wang,Zanhui Jia
Curcumin (CUR) exhibits potential inhibitory effects on tumor growth; however, its hydrophobicity and instability limit its clinical applications. In the present study, we developed CUR nanoparticles (CUR-NPs) and evaluated their biochemical characteristics. Cell uptake and proliferation were assessed using scratch and Transwell assays, respectively. Western blotting was performed to investigate the expression levels of proteins related to the NF-κB/PRL-3 signaling pathway, inflammatory response, cell proliferation, and cell migration in SKOV3 cells. Our findings showed that the blank vector was not cytotoxic to cells, allowing us to disregard any effects caused by the vector itself. CUR-NPs exhibited concentration- and time-dependent inhibitory effects on cell proliferation, surpassing those of CUR alone. Increasing the concentration of CUR-NPs resulted in a reduced cell scratch-healing ability and lower chamber migration capacity. Compared to the control group, expression levels of proteins associated with NF-κB/PRL-3 signaling pathway, inflammatory response (TNF-α and IL-6), cell proliferation (cyclin E1 and cyclin A1), as well as cell migration (N-cadherin and vimentin) were significantly elevated in the lipopolysaccharide (LPS) stimulation and NF-κB p65 overexpression groups. Conversely, E-cadherin expression was significantly decreased under these conditions. However, treatment with high concentrations of CUR-NPs effectively reversed these changes. These results highlight the significant ability of CUR-NPs to inhibit human ovarian cancer cell proliferation and migration, while suppressing inflammatory responses through the regulation of the NF-κB/PRL-3 signaling pathway.
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2025
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IF 4.7
Zhifeng Geng,Guoyi Deng,Ziyu Wang,Xin Xu,Xiaojiao Yin,Sen Zhang,Jiale Shao,Jiyue Wen
Astrocytes may fail to perform their neuroprotective roles against cerebral ischemia/reperfusion (I/R) injury due to phenotypic transformation. We aimed to demonstrate the distinct roles of A1 astrocytes and A2 astrocytes on the blood-brain barrier (BBB) injury following cerebral I/R, and explore whether H 2 S-mediated A2 astrocytes polarization protects against BBB injury via inhibiting ROCK/NF-κB pathway. The mice cerebral I/R model and the oxygen-glucose deprivation/re‑oxygenation (OGD/R) model of astrocytes were used in present study. Cerebral I/R-induced BBB injury is evidenced by increased EB dye leakage and reduced expressions of ZO-1 and occludin in mice hippocampal tissues. We found that H 2 S-mediated A2 polarization and lipopolysaccharide (LPS)-induced polarization of A1 astrocytes respectively display beneficial and harmful role in BBB injury. Besides, harmful roles of A1 astrocytes in BBB injury can be reduced by H 2 S. Additionally, A1 astrocytes exhibit excessive activation of NF-κB and enhanced expressions of MMP9 and AQP4, which can be inhibited by H 2 S. Moreover, H 2 S-mediated polarization of A2 astrocyte displays enhanced phosphorylation and nuclear translocation of STAT3 and reduced expressions of MMP9 and AQP4. Importantly, ROCK inhibitor Fasudil likewise inhibits the activation of NF-κB and promotes STAT3 activation in OGD/R astrocytes, and NF-κB inhibitor BAY11–7082 reduces the expressions of MMP9 and AQP4 in OGD/R astrocytes. In conclusion, H 2 S-mediated polarization of A2 astrocyte protects against BBB injury following cerebral I/R, the mechanisms may be related to inhibition of ROCK/NF-κB pathway, and activation of STAT3.
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高影响因子
MICROBIOLOGICAL RESEARCH
·
2024
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IF 6.1
Ting Fang,Juan Xiong,Xin Huang,Xinyu Fang,Xuqing Shen,Yuanying Jiang,Hui Lu
Strategies aimed at targeting fungal extracellular heat shock protein 90 (eHsp90) using vaccines and antibodies have demonstrated encouraging potential in the prevention and management of invasive fungal diseases (IFDs). However, the precise underlying mechanism by which eHsp90 contributes to the heightened virulence of Candida albicans ( C. albicans ) remains an enigma, awaiting further elucidation. In our current research, we have found that the 47-kDa fragment of C. albicans Hsp90 (CaHsp90), which serves as the primary antigenic determinant, is not degraded within C. albicans cells. Moreover, we have discovered that extracellular CaHsp90 (eCaHsp90) is derived from the components of lysed C. albicans cells. We also generated recombinant CaHsp90 in Escherichia coli , and found that eCaHsp90 spreads beyond the initial C. albicans colonization site, thereby enhancing the overall virulence of the organism. Our results further clarify that eCaHsp90 activates the nuclear factor kappa-B (NF-κB) signaling pathway and upregulates the expression of NACHT, LRR, and PYD domains-containing protein 3 (NLRP3). This upregulation results in the activation of Gasdermin D (GSDMD) and subsequent macrophage pyroptosis, ultimately increasing the virulence of C. albicans . This study provides valuable insights into the mechanism by which eCaHsp90 contributes to the virulence of C. albicans , offering a pharmacological basis for antifungal strategies targeting fungal eHsp90.
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