Pharmaceutics
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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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METABOLIC BRAIN DISEASE
·
2026
·Vol. 41
·期 1
·104
·
IF 3.8
Zhong Guangcheng,Shi Jiahui,Jiang Yue,Li Shiyin,Wang Xuejing,Zhang Ting,Chen Zhuo,Wang Qi,Liu Shan
Alzheimer’s disease (AD) is a prevalent neurodegenerative condition distinguished by intricate pathological mechanisms. Cinnamaldehyde, a natural active chemical sourced from the bark of Cinnamomum species, exhibits remarkable neuroprotective properties that have been validated in various neurological disorders. In this study, network pharmacology alongside zebrafish experiments was employed to investigate the molecular mechanisms and signaling pathways through which cinnamaldehyde ameliorates AD. Potential targets of cinnamaldehyde were found using the SuperPred, TargetNet, SwissTargetPrediction, and SEA databases, whilst AD-related targets were obtained from TTD, OMIM, GeneCards, and DrugBank databases. Subsequently, protein-protein interaction analysis was performed using the STRING database, followed by GO and KEGG enrichment studies via the DAVID platform. Finally, molecular docking validation was conducted using CB-Dock2. The network pharmacology results indicated that cinnamaldehyde might impact its beneficial effects on AD via regulating the toll-like receptor 4 (TLR4)/Nuclear factor kappa B (NF-κB) signaling pathway. To further validate this mechanism, an AD model was established in zebrafish induced by aluminum chloride (AlCl₃). Behavioral assays demonstrated that cinnamaldehyde significantly improved AlCl₃-induced cognitive impairment. Hematoxylin-eosin and Nissl staining revealed that cinnamaldehyde attenuated neuropathological damage. Biochemical analyses indicated that cinnamaldehyde alleviated oxidative stress and restored cholinergic dysfunction. Furthermore, RT-qPCR findings indicated that cinnamaldehyde reduced inflammatory mediator expression and diminished TLR4 and NF-κB p65 mRNA levels, while western blotting confirmed reduced TLR4 and phosphorylated NF-κB p65 protein expression. In summary, cinnamaldehyde may mitigate neuroinflammation through suppressing the TLR4/NF-κB signaling pathway, thereby ameliorating AlCl₃-induced cognitive impairment, neuropathological injury, oxidative stress imbalance, and cholinergic system dysfunction in zebrafish. Graphical The alternative text for this image may have been generated using AI.
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FITOTERAPIA
·
2026
·
IF 2.9
Qian Sun,Shi-Liu Xu,Shuang-Ning Liu,De-Jian Chen,Zheng-Jun Li,Xiao-Jun Qiu,Xia Yang,Feng-Xiang Zhang,Jian-Xin Chen
SWLDH was firstly confirmed to treat bacterial infection-induced ALI. • PI3K-AKT/NF- κ B and MAPK signaling pathways were confirmed as the core mechanism for SWLDH to treat ALI. • Five potential anti-ALI compounds in SWLDH were identified. Shi-Wei-Long-Dan-Hua capsule (SWLDH) is clinically used to alleviate bacterial or viral infection induced bronchitis. Recent studies have reported its effects on viral infection induced acute lung injury, broadening our understanding of its clinical applications. However, its effects against bacterial infection-induced ALI were still unclear, along with not fully elucidated chemical profile, significantly limiting its clinical application and product improvement. In this work, we aimed to systematically characterize the chemical components in SWLDH and explore its effects and mechanisms against bacterial infection-induced ALI. Results showed that SWLDH (2 g/kg/day) significantly reduced lung index, alleviated pathological injury and depressed cytokine expression in LPS-challenged mice. SWLDH also inhibited LPS-induced over-expression of iNOS and pro-inflammatory cytokines (TNF- α , IL-1 β , IL-6) in RAW264.7 cells. Moreover, 128 chemical components in SWLDH and its 32 prototypes in rats were identified by using UPLC-Q/TOF MS. Network pharmacology and Western blot were used to confirm that SWLDH can alleviate LPS- induced ALI by suppressing pulmonary inflammation and the PI3K-Akt-NF- κ B/MAPK axis. Further, five potential anti-ALI substances in SWLDH were found. This is the first time to comprehensively profile the chemical components in SWLDH and reveal its effects and mechanisms against bacterial infection-induced ALI, providing the potential substances and pharmacological data for further quality improvement and product development. Download: Download high-res image (166KB) Download: Download full-size image
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APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY
·
2026
·
IF 3.5
Li Tong,Li Ning,Li Yi,Liu Jinwen,Hao Dajie
Oxidative stress and inflammasome-driven inflammation are key contributors to atherosclerotic disease progression. Here, we report a ROS-responsive hyaluronic acid-PEGDA hydrogel designed for the sustained delivery of palmitoleic acid. In the study, catechol-functionalized hyaluronic acid was cross-linked with polyethylene glycol diacrylate to create an extracellular matrix mimic that possessed tunable mechanical strength and redox-sensitive degradability. It showed controlled release of palmitoleic acid under normal physiological conditions and a faster rate of release under oxidative conditions. In vitro studies using vascular endothelial cells and macrophages demonstrated good cytocompatibility and a marked reduction in intracellular reactive oxygen species, lipid peroxidation, and pro-inflammatory cytokine secretion. At the molecular level, treatment with the palmitoleic acid-loaded hydrogel resulted in activation of AMP-activated protein kinase, inhibition of NF-κB nuclear translocation, and suppression of NLRP3 inflammasome activation, as evidenced by decreased caspase-1 cleavage and IL-1β maturation. These findings indicate that ROS-responsive hydrogel-mediated delivery of palmitoleic acid effectively modulates oxidative and inflammatory signalling pathways relevant to atherosclerosis. Graphical
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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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BIOGERONTOLOGY
·
2026
·Vol. 27
·期 2
·72
·
IF 5.3
Zhang Xiaoli,Wang Chengniu,Chen Weiguan
Aging is a major risk factor for the onset and progression of many neurodegenerative diseases. Inflammation is the body’s natural defense mechanism against harmful stimuli . A growing body of research has highlighted the intricate relationship between aging and inflammation, with chronic low - grade inflammation, often referred to as “inflammaging,” being a hallmark of the aging process. Cycloneolitsol (CL) is a C-32 cycloartane-type triterpene from Taxodium ascendens which has been reported to possess the anticancer, neuroprotection and antibacterial activities. Its specific role and the underlying molecular mechanisms in modulating the aging process remain unclear. Our study aimed to explore the possible anti-aging effect and mechanisms of CL. Network pharmacology predicted core targets and several potential pathways, which are associated with the anti-aging effect of CL. RAW264.7 macrophages and Caenorhabditis elegans were selected for evaluating its anti-aging and anti-inflammation activity. The results showed that CL exerted obvious anti-inflammatory effects against LPS-induced M1-type polarization of RAW264.7 cells via NF-κB signaling pathway. In C. elegans , CL improved Biological Characteristics and prolonged the lifespan without reproductive toxicity. Furthermore, experiments on different mutant C. elegans strains and the nuclear translocation of SKN-1 confirmed that CL activates autophagy and enhances the antioxidant stress response ability through the SEK-1/PMK-1/SKN-1 signaling pathway. This study provides novel insights into the biological activities of CL, highlighting its potential as a natural product for treating inflammation-related diseases and delay aging.
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NEUROSCIENCE LETTERS
·
2026
·
IF 2.2
XinQun Xu,QuanLan Wang,Long Wang,WenQiang Cheng,Fei Li,HuanBing Liu,YuangBing Guo
Objective To investigate the regulatory mechanism of IDO1 on brain tissue damage in Alzheimer’s disease (AD) mice. Methods APP/PS1 mice (AD model mice) and C57BL/6J mice were treated with IDO1 inhibitor 1-MT. Behavioral changes were assessed using the open field test, and histopathological changes were analyzed using HE staining, Nissl staining, and transmission electron microscopy. TUNEL staining and immunofluorescence were used to detect cell apoptosis and the expression of IDO1 and GFAP, respectively. Metabolomics was analyzed using liquid chromatography-mass spectrometry. An in vitro AD cell model was established, and inflammatory factor levels were measured using ELISA/qPCR, while NF-κB pathway activation was assessed using WB. Results In vivo experiments showed that compared with the model group mice, 1-MT intervention improved behavioral abnormalities in AD mice, reduced hippocampal tissue damage, decreased neuronal apoptosis, and downregulated the expression of IDO1 and GFAP. In vitro experiments demonstrated that interfering with IDO1 could decrease the levels of IL-1β, TNF-α, and IL-6, reduce GFAP expression, and inhibit p65 phosphorylation. Conclusion Interfering with IDO1 can inhibit the NF-κB pathway, reduce the release of inflammatory factors, and improve brain tissue damage in AD mice.
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MOLECULES
·
2026
·Vol. 31
·期 10
·1560
·
IF 5.1
Sisi Huang,Wei Cai,Yan Wang,Xiaoliang Xing,Zaiqi Zhang
Objective:This study aimed to investigate whether pomolic acid (PA), a predicted bioactive metabolite of the Dong botanical drug Madeng’ai (MDA), suppresses inflammatory cytokine expression by inhibiting nuclear factor-κB (NF-κB) pathway activation in a tumor necrosis factor-α (TNF-α)-induced human rheumatoid arthritis fibroblast-like synoviocyte (RA-HFLS) model.Methods:PA content in MDA from different regions and harvest years was quantified via High-Performance Liquid Chromatography (HPLC). Network analysis was employed as a hypothesis-generating tool to predict potential targets and pathways, followed by molecular docking to validate the binding affinity of PA to core targets of the NF-κB pathway, and ADMET prediction to evaluate its pharmacokinetic properties and safety profile. The RA-HFLS inflammatory model was induced by TNF-α. Cell viability and inflammatory cytokine secretion were assessed using Cell Counting Kit-8 (CCK-8) and enzyme-linked immunosorbent assay (ELISA). NF-κB signaling pathway activation and downstream gene expression were examined by Western blot and reverse transcription quantitative polymerase chain reaction (RT-qPCR), respectively.Results:HPLC analysis revealed that MDA samples from Guizhou harvested in 2019 contained the highest PA content (0.1117 mg/g). Network analysis predicted the NF-κB signaling pathway as a candidate mechanism underlying PA’s potential anti-inflammatory effects. Molecular docking showed that PA stably bound to IKKβ, p65, and IκBα, while ADMET prediction indicated favorable intestinal absorption, low drug–drug interaction risk, and good genetic safety, albeit with potential hepatotoxicity and reproductive toxicity risks. In the TNF-α-induced RA-HFLS model, PA dose-dependently inhibited abnormal cell proliferation and significantly reduced the secretion of pro-inflammatory cytokines TNF-α and interleukin-6 (IL-6). Mechanistic studies indicated that PA suppressed the activation of the NF-κB signaling pathway, thereby downregulating the mRNA expression of inflammatory genes such as IL-6, TNF-α, and interleukin-1β (IL-1β).Conclusions:PA, a bioactive metabolite of the Dong botanical drug MDA, may inhibit NF-κB signaling pathway activation, thereby downregulating TNF-α-induced inflammatory cytokine expression in RA-HFLS, demonstrating its in vitro anti-inflammatory potential.
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DESALINATION
·
2023
·
IF 9.9
Qingyi Wang,Yongping Dong,Junmei Ma,Huimin Wang,Xuping Xue,Chaojie Bai,Mingjie Lin,Lingping Luo,Congjie Gao,Lixin Xue
Polyamide/polyethylene thin film composite (PA/PE-TFC) NF membranes were prepared from reverse-phase interface polymerization (RIP) for improved Mg(II)/Li(I) separation. RIP processes between 1,3,5-benzenetricarbonyl chloride (TMC) in bottom organic phase and piperazine (PIP) in upper aqueous phase were developed to form continuous and intact surface PA separation layers on PE porous substrates thinner than traditional polysulfone (PSF) based substrates. After activation with isopropyl alcohol (IPA), PA/PE-TFC-IPA NF membranes were formed, whose NF performance could be tuned by adjusting the preparation conditions. When TMC concentration was kept at 0.15 % w/v, RIP with low PIP concentration (0.025 wt%) yield PA/PE-TFC-IPA NF membranes with negatively charged surfaces , high Na 2 SO 4 rejection rate (95 % ± 3 %) and water permeance (13–19 L·m −2 ·h −1 ·bar −1 ). RIP with high PIP concentration (0.3 wt%) formed PA/PE-TFC-IPA NF membranes with less negative surfaces, high MgCl 2 rejection rate (94.3 ± 0.7 %), low water permeance (4.8 ± 0.3 L·m −2 ·h −1 ·bar −1 ), and high Mg(II)/Li(I) separation coefficient S Li/Mg (18 ± 1) for 1000 ppm LiCl and MgCl 2 mixed solution. PA/PE-TFC-IPA NF membranes also showed good long-term stability and improved anti-fouling performance for positively charged pollutants, bearing high potential for applications in the lithium extraction processes.
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JOURNAL OF MEMBRANE SCIENCE
·
2023
·
IF 9.5
Haojie Zeng,Feiyun Sun,Jianjun Zhang,Ying Wang,Songwen Yang,Dingyu Xing
Polyvinyl alcohol (PVA) has been employed and crosslinked as the selective layer of NF membranes with enhanced hydrophilicity. However, the influences of different crosslinking methods and agents on the reaction mechanism and membrane performance still need to be comprehensively studied. In this study, NF membranes were prepared by coating crosslinking (CC-membrane) and gradient crosslinking (GC-membrane) methods. Compared with CC-membrane, the GC-membrane possessed a 65% higher flux with Na 2 SO 4 rejection around 90%, under the optimal preparation conditions with PVA content of 0.10%, curing at 80 °C for 10 min. Crosslinking agents including 1,3,5-benzenetricarboxylic acid (TMA), 4,4′-(hexafluoroisopropylidene) diphthalic anhydride (6FDA) and pyromellitic dianhydride (PMDA) with different spatial structure were used to optimize the GC-membrane. As confirmed by SEM, XPS, FTIR and contact angle tests, the 6FDA-GC membrane showed a thinner, smoother and more hydrophilic selective layer, and kept an excellent balance between the water flux (88.6 L/m 2 h) and Na 2 SO 4 rejection (88.7%). This is because the 6FDA with a large molecule and flexible spatial structure could form a more integrated crosslinking structure compared to PMDA. Meanwhile, the 6FDA-GC membrane showed rejections of over 80% towards the endocrine-disrupting compound 17α-Ethinylestradiol and exhibited stable antifouling ability and durability. Overall, this work studied systematically the influences of various crosslinking agents on the GC-membrane, and verified the potential of hydrophilic PVA membranes for nanofiltration.
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BMC Complementary Medicine and Therapies
·
2023
·Vol. 23
·期 1
·1-11
·
IF 3.9
Yi Zhirong,Jia Qingling,Wang Yujiao,Zhang Yuqin,Xie Tianyi,Ling Jianghong
Background Precancerous lesions of gastric cancer (PLGC) refer to a kind of histopathological changes in the gastric mucosa that can progress to gastric cancer. Elian granules (ELG), a Chinese medicinal prescription, have achieved satisfactory results in the treatment of PLGC. However, the exact mechanism underlying the therapeutic effect of ELG remains unclear. Here, this study aims to explore the mechanism of ELG alleviating PLGC in rats.Methods The chemical ingredients of ELG were analyzed using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS). Specific Pathogen Free SD rats were randomly assigned to 3 groups: the control, model, and ELG groups. The 1-Methyl-3-nitro-1-nitrosoguanidine (MNNG) integrated modeling method was adopted to construct the PLGC rat model in groups except for the control group. Meanwhile, normal saline was used as an intervention for the control and model groups, and ELG aqueous solution for the ELG group, lasting 40 weeks. Subsequently, the stomach of rats was harvested for further analysis. Hematoxylin-eosin staining of the gastric tissue was conducted to assess the pathological changes. Immunofluorescence was carried out for the expression of CD68, and CD206 proteins. Real-time quantitative PCR combined with Western blot was conducted to analyze the expression of arginase-1(Arg-1), inducible nitric oxide synthase (iNOS), p65, p-p65, nuclear factor inhibitor protein-α (IκBα), and p-IκBα in gastric antrum tissue.Results Five chemical ingredients including Curcumol, Curzerenone, Berberine, Ferulic Acid, and 2-Hydroxy-3-Methylanthraquine were identified in ELG. The gastric mucosal glands of rats treated with ELG were orderly arranged, with no intestinal metaplasia and no dysplasia. Furthermore, ELG decreased the percentage of M2-type TAMs marked with CD68 and CD206 proteins, and the ratio of Arg-1 to iNOS in the gastric antrum tissue of rats with PLGC. In addition, ELG could also down-regulate the protein and mRNA expression of p-p65, p65, and p-IκBα, but up-regulate the expression of IκBα mRNA in rats with PLGC.Conclusion sThe results showed that ELG attenuates PLGC in rats by suppressing the M2-type polarization of tumor-associated macrophages (TAMs) through NF-κB signaling pathway.
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