MICROCHEMICAL JOURNAL
·
2025
·
IF 5.1
Jiaying Wang,Yu Tian,Kai Zhang,Jiantong Jiao,Yi Zhao
NF-κB p50 is a critical transcription factor that plays an essential role in regulating immune responses, inflammatory pathways, and tumor progression. Its aberrant expression is closely linked to various pathological conditions, making it a valuable biomarker for early disease diagnosis and therapeutic monitoring. In this work, we developed a highly sensitive and reusable electrochemical biosensor capable of detecting NF-κB p50 at ultralow concentrations. The biosensor integrates a pH-responsive regeneration mechanism and a multi-stage signal amplification cascade involving Exonuclease III (Exo III)-assisted recycling, CRISPR/Cas12a-mediated trans -cleavage, and DNA tetrahedron nanostructure-functionalized electrodes. This synergistic design significantly enhances detection sensitivity and stability. The platform offers a broad dynamic detection range from 5 aM to 100 fM with a remarkably low detection limit of 2.38 aM. More importantly, the biosensor demonstrates excellent reusability through efficient regeneration under alkaline conditions (pH 10.0), with minimal loss in signal output. Validation in tenfold-diluted human serum samples yielded high recovery rates (99.61 %–106.23 %) and low relative standard deviations, confirming its practical applicability. This study not only presents a robust approach for ultrasensitive protein detection but also introduces a generalizable strategy for the regenerative electrochemical analysis of protein-based biological macromolecules in clinical diagnostics.
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JOURNAL OF ETHNOPHARMACOLOGY
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2025
·
IF 5.4
Meng Kong,Zixuan Xu,Haifei Lu,Yumeng Chen,Yini Zhang,Xia Jiang,Ping Wang
Ethnopharmacological relevance ShengHui decoction (SHD), a traditional Chinese herbal formula, has long been used clinically to mitigate Alzheimer’s disease (AD), demonstrating significant efficacy in alleviating cognitive impairment. However, its molecular mechanisms remain insufficiently understood. Aim of the study To clarify the effects of SHD on oxidative stress–related markers and inflammatory cytokines in an aluminum chloride (AlCl 3 )-induced zebrafish model of AD and as well as uncover its underlying mechanisms in alleviating oxidative stress and neuroinflammation.. Materials and methods Ultra-performance liquid chromatography–tandem mass spectrometry (UPLC-MS/MS) was employed to identify the bioactive constituents of SHD. Behavioral tests and histopathological analyses were then conducted to evaluate the effects of SHD (0.74, 1.48, and 2.96 mg/mL) on apoptosis and amyloid-beta (Aβ) deposition in an AlCl 3 -induced AD zebrafish model. Biochemical assays and enzyme-linked immunosorbent assay were used to quantify superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-1 beta (IL-1β), and IL-18.. Western blot analysis was performed to determine the protein expression of nuclear factor erythroid 2–related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), nuclear factor-kappa B p65 (NF-κB p65), phosphorylated NF-κB p65 (p–NF-κB p65), and NOD-like receptor family pyrin domain containing 3 (NLRP3). Results UPLC–MS/MS profiling identified phenolic acids, saponins, lignans/coumarins, flavonoids, and aliphatic alcohols as the main constituents of SHD. SHD significantly ameliorated cognitive deficits and histopathological abnormalities in AlCl 3 -induced zebrafish. Moreover, SHD attenuated oxidative stress by upregulating Nrf2, HO-1, and NQO1 expression, while downregulating AlCl 3 -induced levels of NF-κB p65, p–NF-κB p65, NLRP3 and pro-inflammatory factors. Conclusions SHD effectively improved cognitive performance and reduced AD-like pathological lesions in AlCl 3 -induced zebrafish. Importantly, SHD exhibits both antioxidant and anti-inflammatory activities by activating the Nrf2/HO-1 axis and inhibiting NF-κB signaling, thereby alleviating oxidative stress and neuroinflammatory responses in AD. These findings provide experimental evidence supporting SHD as a potential therapeutic agent for AD, and substantiate the traditional Chinese medicine principle of tonifying the kidney and replenishing essence in the treatment of AD.
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高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2019
·
IF 3.17
Zhiyu Xi,Xibei Hu,Xiao Chen,Yong Yang,Jie Ren,Baofeng Wang,Zhihong Zhong,Yuhao Sun,Guo-Yuan Yang,Qingfang Sun,Liuguan Bian
Protocatechuic acid (PCA) has been well studied for its neuroprotection value in several diseases, but the effect in intracerebral haemorrhage (ICH) has not been reported. Here we verified the protection of PCA in ICH, and investigated the relative mechanisms. ICH model mice were established by injection of collagenase IV. The mice were treated with PCA once per day for 3 days, starting immediately after operation. The modified neurological severity score (mNSS) of mice at 1st, 3rd and 7th day after operation were recorded. And some of mice were euthanized at 3rd day to compare brain water content, pro-inflammatory cytokines expression, and cell apoptosis in perihematomal tissue. Additionally, SH-SY5Y cells were treated hemin to mimic secondary injury of ICH. Cells were incubated with PCA for treatment. The cell viability , ROS , apoptosis rate and protein expression of apoptosis-relative protein and MAPKs and NF-κB were detected and analysed. The results revealed PCA alleviated the cerebral oedema at 3rd post ICH, and significantly improved neurological functions. PCA also attenuated the protein and gene expression of TNF-а, IL-1β and IL-6 vivo. PCA dose-dependently decreased the generation of ROS and apoptosis rate. Furthermore, PCA treatment dose-dependently decreased the expression of bax, cleaved caspase-3, increased bcl-2 expression; PCA downregulated P38/JNK-NF-κB pathway. In conclusion, PCA effectively improves prognosis of ICH mice by inhibiting oxidative stress , inflammation and apoptosis. The mechanism possibly results of downregulating of P38/JNK-NF-κB pathway, and PCA can be a potential therapeutic agent for ICH.
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Virulence
·
2022
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IF 5.428
Qiankun Yang,Jianguo Zhang,Feixue Liu,Huizhen Chen,Wei Zhang,Haitao Yang,Nana He,Jingquan Dong,Panpan Zhao
Aeromonas caviae, an important food-borne pathogen, induces serious invasive infections and inflammation. The pro-inflammatory IL-1β functions against pathogenic infections and is elevated in various Aeromonas infection cases. However, the molecular mechanism of A. caviae-mediated IL-1β secretion remains unknown. In this study, mouse macrophages (PMs) were used to establish A. caviae infection model and multiple strategies were utilized to explore the mechanism of IL-1β secretion. IL-1β was elevated in A. caviae infected murine serum, PMs lysates or supernatants. This process triggered NLRP3 levels upregulation, ASC oligomerization, as well as dot gathering of NLRP3 and speck-like signals of ASC in the cytoplasm. MCC950 blocked A. caviae mediated IL-1β release. Meanwhile, NLRP3 inflammasome mediated the release of IL-1β in dose- and time-dependent manners, and the release of IL-1β was dependent on active caspase-1, as well as NLRP3 inflammasome was activated by potassium efflux and cathepsin B release ways. A. caviae also enhanced TLR2 levels, and deletion of TLR2 obviously decreased IL-1β secretion. What’s more, A. caviae resulted in NF-κB p65 nuclear translocation partly in a TLR2-dependent manner. Blocking NF-κB using BAY 11-7082 almost completely inhibited NLRP3 inflammasome first signal pro-IL-1β expression. Blocking TLR2, NF-κB, NLRP3 inflammasome significantly downregulated IL-1β release and TNF-α and IL-6 levels. These data illustrate that A. caviae caused IL-1β secretion in PMs is controlled by NLRP3 inflammasome, of which is mediated by NF-κB pathway and is partially dependent on TLR2, providing basis for drugs against A. caviae.
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高影响因子
Journal of Essential Oil Bearing Plants
·
2020
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IF 0.824
Yu Chen,Lejing Chi,Xiaoxin Liang,Yaohui Shi,Tongyun Wu,Mao Ye,Ping Han,Li Lin,Lanyue Zhang,Peng Xu,Zhiyun Du
Cedrus deodara is a cedar plant from the Pinaceae family. Because Cedrus is widely used in health care products, cosmetics, medicine, and insecticides, the essential oils of Cedrus deodara (CDEOs) are gaining increasing levels of attention. However, there have only been a few studies on the anti-inflammatory effects of CDEOs. This study aimed to systematically study the composition and biological effects of CDEOs, in line with this, the study assessed the chemical composition of CDEOs and evaluated their anti-inflammatory mechanisms in mice. Gas chromatography-mass spectrometry (GC-MS) was used to determine and analyze a total of 41 compounds from CDEOs. It was found that the major components of CDEOs are thujopsene (28.23%), α-cedrene (17.01%), and cedrol (15.55%); moreover, our results showed that the active ingredients in CDEOs have anti-inflammatory and antioxidant effects and that the active ingredients in CDEOs can be used as an antioxidant, as an important biological resource in functional food, and as ingredients in cosmetics and pharmaceuticals. Taken together, these CDEOs serve as ideal additives for anti-inflammatory drugs.
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高影响因子
Materials Today Bio
·
2024
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IF 8.7
Xiang Han,Feiyang Wang,Yuzhuo Ma,Xuerong Lv,Kewei Zhang,Yue Wang,Ke Yan,Youmin Mei,Xiaoqian Wang
Traditional fibrous membranes employed in guided tissue regeneration (GTR) in the treatment of periodontitis have limitations of bioactive and immunomodulatory properties. We fabricated a novel nTPG/PLGA/PCL fibrous membrane by electrospinning which exhibit excellent hydrophilicity, mechanical properties and biocompatibility. In addition, we investigated its regulatory effect on polarization of macrophages and facilitating the regeneration of periodontal tissue both in vivo and in vitro. These findings showed the 0.5%TPG/PLGA/PCL may inhibit the polarization of RAW 264.7 into M1 phenotype by suppressing the PI3K/AKT and NF-κB signaling pathways. Furthermore, it directly up-regulated the expression of cementoblastic differentiation markers (CEMP-1 and CAP) in periodontal ligament stem cells (hPDLSCs), and indirectly up-regulated the expression of cementoblastic (CEMP-1 and CAP) and osteoblastic (ALP, RUNX2, COL-1, and OCN) differentiation markers by inhibiting the polarization of M1 macrophage. Upon implantation into a periodontal bone defect rats model, histological assessment revealed that the 0.5%TPG/PLGA/PCL membrane could regenerate oriented collagen fibers and structurally intact epithelium. Micro-CT (BV/TV) and the expression of immunohistochemical markers (OCN, RUNX-2, COL-1, and BMP-2) ultimately exhibited satisfactory regeneration of alveolar bone, periodontal ligament. Overall, 0.5%TPG/PLGA/PCL did not only directly promote osteogenic effects on hPDLSCs, but also indirectly facilitated cementoblastic and osteogenic differentiation through its immunomodulatory effects on macrophages. These findings provide a novel perspective for the development of materials for periodontal tissue regeneration.
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高影响因子
Communications Biology
·
2024
·Vol. 7
·期 1
·1-11
·
IF 5.2
Qin Danhui,Song Hui,Wang Caiwei,Ma Xiaojie,Fu Yu,Zhao Chunyuan,Zhao Wei,Zhang Lei,Zhang Weifang
Stimulator of interferon genes (STING) is vital in the cytosolic DNA-sensing process and critical for initiating the innate immune response, which has important functions in host defense and contributes to the pathogenesis of inflammatory diseases. Zinc finger CCCH-type antiviral protein 1 (ZC3HAV1) specifically binds the CpG dinucleotides in the viral RNAs of multiple viruses and promotes their degradation. ZAPS (ZC3HAV1 short isoform) is a potent stimulator of retinoid acid-inducible gene I (RIG-I) signaling during the antiviral response. However, how ZC3HAV1 controls STING signaling is unclear. Here, we show that ZC3HAV1 specifically potentiates STING activation by associating with STING to promote its oligomerization and translocation from the endoplasmic reticulum (ER) to the Golgi, which facilitates activation of IRF3 and NF-κB pathway. Accordingly, Zc3hav1 deficiency protects mice against herpes simplex virus-1 (HSV-1) infection- or 5,6-dimethylxanthenone-4-acetic acid (DMXAA)-induced inflammation in a STING-dependent manner. These results indicate that ZC3HAV1 is a key regulator of STING signaling, which suggests its possible use as a therapeutic target for STING-dependent inflammation.
研究领域:
免疫学
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病毒学
·
炎症性疾病
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Pharmaceutics
·
2026
·Vol. 18
·期 3
·323
·
IF 6.9
Xiao Yang,Hui Wang,Wenjuan Zhang,Peng Gao,Xudong Yu,Weijia Qing,Ping Deng,Jingdian Li,Yan Luo,Li Tian,Jia Xie,Mengyan Chen,Zhengping Yu,Huifeng Pi,Ting Liu,Shenglin Luo
Background/Objectives: High-voltage, low-current electric shocks inflict superficial second-degree burns on the skin, accompanied by a vicious cycle of excessive oxidative stress and inflammation. As efficient treatment of such electrical burns remains a clinical challenge, we explored the efficacy of an injectable thermosensitive chitosan hydrogel engineered with an antioxidant agent (astaxanthin) and an anti-inflammatory agent (ibuprofen) for the treatment of high-voltage, low-current electrical burn injuries.Methods: The proposed CS/AST/IBU hydrogel was prepared and its thermosensitivity was characterized. Subsequently, the hydrogel was injected into the wounds of male Sprague–Dawley (SD) rats subjected to electrical burn injury (20 kV, 3 mA). Finally, a series of experiments were performed to elucidate the dynamics of wound healing and the mechanisms by which the hydrogel promotes wound repair.Results: The injectable hydrogel, through its thermally responsive gelation effect at 37 °C, adapts to the complex irregularities of the wound surface. This facilitates the release of astaxanthin and ibuprofen throughout the wound, which collectively diminish the formation of reactive oxygen species and MDA. Furthermore, it enhances the synthesis of endogenous antioxidants such as SOD, CAT, and GSH; encourages collagen deposition; stimulates the development of dermal appendages; and fosters neovascularization. It interrupts the deleterious cycle of oxidative stress and inflammation mediated by the NF-κB signaling pathway, thereby suppressing the expression of pro-inflammatory markers such as TNF-α, CD11b, and IL-1β while upregulating CD163, an anti-inflammatory receptor.Conclusions: The use of this multipronged, contour-adaptive hydrogel represents an effective strategy for complex wound management and demonstrates broad therapeutic potential for superficial second-degree electrical burns caused by high-voltage, low-current discharge.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2026
·
IF 8.5
Yu Cheng,Yao Wen,Zhaohan Wang,Lizhen Yang,Junming Liao,Jieyu Xing,Zheng Liu,Xiaoyan Sheng,Lingli Zhou,Sigui Zhou,Jian Zou,Haiyun Chen
Our previous investigations have revealed that Perilla frutescens -derived polysaccharide PFP50-1 exhibited significant neuroprotective activity by attenuating lipopolysaccharide (LPS)-induced neuroinflammatory responses in microglia. Nonetheless, the protection and mechanisms of its anti-neuroinflammatory activities are still poorly understood. The neuroprotection effects of PFP50-1's underlying mechanisms were evaluated in MPTP-stimulated Parkinson's disease (PD) mice and LPS-induced microglia, respectively. In vitro , PFP50-1 effectively suppressed the excessive release of pro-inflammatory cytokines. Meanwhile, PFP50-1 significantly downregulated the levels of Toll-like receptor 4 (TLR4), myeloid differentiation primary response protein gene 88 (MyD88), nuclear factor kappa-B (NF-κB), p-PI3K (phosphorylated phosphatidylinositol 3-Kinase), and p-Akt (phosphorylated Protein Kinase B). Subsequently, investigations revealed that TLR4 inhibitor (TAK242) and PI3K inhibitor (LY294002) significantly potentiated PFP50-1's inhibitory effects on LPS-induced pro-inflammatory mediators. Moreover, the excessive releases of Caspase-1, IL-18, and IL-1β were reversed by suppressing NLRP3 inflammasome activation. In conditioned medium-stimulated N2a cells, PFP50-1 exhibited a strong neuroprotective effect against neuroinflammation-mediated neurotoxicity by preventing MMP depolarization and ROS production. Notably, PFP50-1 effectively ameliorated MPTP-induced dopaminergic (DA) neuronal degeneration in vivo , which was associated with the downregulation of the TLR4-mediated and PI3K-mediated signaling pathways, as well as the NLRP3 inflammasome. Collectively, our data indicated that PFP50-1's anti-neuroinflammation effect is related to downregulating the TLR4/NF-κB and PI3K/Akt signaling pathways and suppressing NLRP3 inflammasome activation, making it a promising candidate for PD.
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Environment & Health
·
2026
·
IF 6.3
Shiyin Zhong,Qiongli Zhou,Jirui Yang,Zhimin Zhang,Xueting Chai,Jinghao Luo,Xin Zhang,Jingjing Liu,Yangzong Yixi,Lei Shi,Xuhong Chang,Hui Wang
Manganese (Mn) is an essential trace element, but increasing industrial and agricultural use has led to elevated levels of environmental Mn levels. Chronic overexposure to Mn can cause a Parkinson’s-like neurodegenerative disorder; however, the underlying mechanisms remain incompletely understood. This study combined in vitro and in vivo models to investigate the role of the cGAS–STING/NLRP3 axis in regulating the p38 MAPK/NF–κB pathway in the process of Mn-induced Tau aggregation leading to neurotoxicity. Our results demonstrated that MnCl2 exposure significantly activated both the cGAS–STING/NLRP3 signaling axis and the p38 MAPK/NF–κB pathway, accompanied by increased Tau expression. Genetic ablation of cGAS, STING, or NLRP3 attenuated Mn-induced Tau upregulation, indicating that the cGAS–STING/NLRP3 signaling axis mediates Tau expression. RNA-seq analysis further revealed that the decreased Tau expression in knockout cells is associated with the MAPK/NF–κB signaling pathway. Pharmacological inhibition of p38 MAPK or NF–κB markedly downregulated cGAS–STING signaling, inflammatory cytokine release, and phosphorylated Tau (p-Tau) levels. Moreover, we observed colocalization and interaction among p-p38, p-p65, and p-Tau. Overall, these findings reveal that Mn activates the cGAS–STING/NLRP3 signaling axis regulated by the p38 MAPK/NF–κB pathway, driving pathological Tau aggregation.
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MOLECULES
·
2026
·Vol. 31
·期 12
·1990
·
IF 5.1
Jinghan Zhang,Yue Sun,Jinhao Zheng,Can Yang,Mingshuo Yang,Liming Pan
Dendrobium officinalehas attracted increasing attention as a functional food because of its diverse biological activities; however, the photoprotective potential of its protein-derived peptides remains poorly understood. In this study,D. officinaleprotein hydrolysates were fractionated by ultrafiltration according to molecular weight, and their protective effects against ultraviolet B (UVB)-induced photoaging were systematically evaluated in HaCaT keratinocytes. Among the tested fractions, low-molecular-weight peptide fractions exhibited relatively stronger antioxidant activity and effectively reduced intracellular reactive oxygen species (ROS) accumulation in UVB-irradiated cells. In addition, the peptide fractions alleviated UVB-induced inflammatory responses and decreased matrix metalloproteinase (MMP) expression, which was associated with modulation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling pathways. Higher-molecular-weight fractions showed relatively stronger effects on maintaining skin barrier-related functions and were associated with regulation of transforming growth factor-β/Smad (TGF-β/Smad) signaling and collagen-related protein expression. Overall, these findings demonstrate functional differences amongDendrobium officinalepeptide fractions and suggest their potential application as natural photoprotective ingredients in functional foods and cosmeceutical products.
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高影响因子
Nutrients
·
2026
·Vol. 18
·期 14
·2360
·
IF 5.8
Xiaoxi Zhang,Gaoyang Fu,Xinyu Zhao,Yan Huang,Fenfen Li,Daozong Xia
Background/Objectives:Gouty arthritis (GA) is an inflammatory disease caused by increased purine metabolism. The limitations of current anti-GA therapies remain a major challenge. Astilbin, the main flavonoid in Smilax glabra Roxb., was found to exert potential anti-GA effects in our previous study.Methods:In this study, a mouse model of monosodium urate (MSU)-induced arthritis and an inflammatory model using mouse bone marrow-derived macrophages (BMDMs) were established.Results:Our data showed that astilbin reduced MSU-induced joint swelling and inflammatory infiltration in mice, restored lipopolysaccharide (LPS)/MSU-induced reductions in cell viability, and inhibited the expression levels of inflammatory factors IL-1β, IL-6 and TNF-α. Further studies showed that astilbin significantly reduced MSU-induced increases in NLRP3 and P-p65 protein levels, as well as the expression of ASC, P-IKKα, P-IκBα, and cleaved-caspase-1.Conclusions:This study suggests that astilbin may be a promising natural product for the treatment of GA by inhibiting the activation of the NLRP3 inflammasome and NF-κB signaling pathway.
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