Bioactive Materials
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2025
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IF 20.3
Jieying Liu,Fuze Liu,Cairong Li,Zhengyao Li,Tianle Li,Yuanhao Wu,Di Wu,Yue Huang,Hui Chen,Hai Wang,Yuxiao Lai,Zhihong Wu
Background Iron oxide nanoparticles (IONPs)-based bone scaffolds have attracted increasing attention because of their potential to enhance osteogenesis and angiogenesis. However, the underlying mechanisms remain incompletely understood. Methods We fabricated a biocompatible bone scaffold by incorporating γ-Fe 2 O 3 magnetic nanoparticles into a PLGA matrix using 3D printing technology. The biosafety and effectiveness of the scaffold was validated through in vitro cell assays and in vivo implantation studies. To evaluate osteogenesis and neovascularization, we employed micro-CT imaging with a vascular contrast agent. In-depth mechanistic investigations were conducted via label-free proteomic profiling and pathway enrichment analysis. Results The PLGA/Fe 2 O 3 scaffolds demonstrated excellent biocompatibility and promoted both bone formation and angiogenesis in vitro and in vivo . Micro-CT analysis revealed enhanced new bone and vessel formation in the presence of magnetic scaffolds. Proteomic analysis revealed that alpha-B crystallin (CRYAB) is a key regulatory protein upregulated under a static magnetic field, thereby activating the PI3K/AKT signaling cascade and promoting osteogenic differentiation. In endothelial cells, we observed the upregulation of nuclear NF-κB and HIF-1α, leading to VEGF expression and angiogenic activation. Conclusion Our findings provide direct evidence that 3D-printed PLGA/Fe 2 O 3 scaffolds promote osteogenesis and angiogenesis both in vitro and in vivo . Importantly, we report for the first time that CRYAB-mediated stabilization of β-catenin plays a central role in magnetic scaffold-induced bone regeneration, offering new insights into the design of functional bone substitutes.
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JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Song-Xue Yang,Wei-Lie Xiao,Xing-Jie Zhang
Ethnopharmacological relevance The root of Saposhnikovia divaricata has been traditionally used in Chinese medicine to treat inflammation and immune related skin diseases, such as skin allergy and itchy rash. However, scientific research supporting its efficacy, particularly in curing inflammation from acne, is still scarce. Aim of the study To evaluate the therapeutic effects of essential oil of Saposhnikovia divaricata (EOSD) on Cutibacterium acnes ( C. acnes )-induced acne and investigate its mechanisms. Materials and Methods An acute acne model was established by injecting C. acnes into mouse ears, followed by topical EOSD treatment (0.25 %, 0.5 % and 1 %). Ear tissues were analyzed 24 hours post-treatment. In vitro, C. acnes -stimulated J774A.1 macrophages were treated with EOSD (3, 10 and 30 μg/ml) to assess mitochondrial damage, oxidative stress, and inflammatory responses. Key markers were analyzed using electron microscopy, real-time PCR, immunoblotting, ELISA, and immunofluorescence. Nrf2 knockdown was achieved via siRNA transfection. Results C. acnes suppressed Nrf2 activation, increased ROS levels, and triggered NLRP3 inflammasome activation, leading to inflammation. EOSD restored Nrf2 activity, reduced ROS levels, and inhibited NLRP3 activation. In vitro, EOSD disrupted Nrf2/Keap1 interaction, enhanced Nrf2 nuclear translocation, reduced mitochondrial damage, and suppressed pyroptosis by downregulating IL-1β, Caspase-1, GSDMD, and NF-κB signaling. These effects were reversed by Nrf2 knockdown. Conclusion EOSD alleviates oxidative stress and modulates NLRP3 inflammasome activation through upregulating Nrf2 pathway and inhibiting NF-κB pathway, as well as improving mitochondrial homeostasis and inflammatory responses in acne. These findings suggest that EOSD may be a promising therapeutic agent for the treatment of acne vulgaris.
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WORLD JOURNAL OF GASTROENTEROLOGY
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2025
·Vol. 31
·期 34
·109825
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IF 5.4
Peng-Tuo Xiao,Chang-Feng Li,Yuan-Da Liu,Jing Zhong,Xi-Lun Cui,Chang Liu,Wei Yang
BACKGROUND Colorectal cancer (CRC) is a major global health burden. B cell CLL/lymphoma 10 (BCL10), a key component of the caspase recruitment domain protein-BCL10-mucosa-associated lymphoid tissue lymphoma paracaspase complexes, is upregulated in CRC and associated with poor patient prognosis, suggesting its potential role in CRC development and progression. Cuproptosis, a novel form of programmed cell death, has emerged as a promising therapeutic strategy for cancer. AIM To explore the role of BCL10 in regulating the sensitivity of CRC cells to cuproptosis. METHODS A series of in vitro and in vivo experiments were conducted using CRC cell lines and CRC mouse models to evaluate the effects of BCL10 on CRC cell proliferation, migration, invasion, and sensitivity to copper-induced cell death. Mechanistic studies were performed to elucidate the underlying molecular pathways. RESULTS BCL10 promoted CRC cell proliferation, migration, and invasion, while its knockdown had the opposite effects. BCL10 also influenced the sensitivity of CRC cells to cuproptosis, with BCL10 overexpression enhancing resistance and its knockdown increasing sensitivity. The mechanism involved BCL10 modulating the expression of DLAT, a key protein in the copper-induced cell death pathway, through activation of the nuclear factor kappa-B (NF-κB) signaling pathway. CONCLUSION BCL10 promotes CRC growth and regulates the sensitivity of CRC cells to cuproptosis by activating the NF-κB signaling pathway and modulating DLAT expression. These findings provide a molecular basis for developing BCL10-targeted therapies for CRC.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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IF 8.5
Wen-Jing Xiao,Su Dong,Yue Xuan,Xiao-Jie Huang,Jing-Rui Feng,Hong-Jing You,Yang Chen
Existing studies lack systematic investigation of the polysaccharide components in Citri Reticulatae Pericarpium (CRP), despite established anti-inflammatory and cardioprotective effects of its bioactive constituents. This study isolated and characterized CRP-derived polysaccharides, focusing on CP-0's protective role against Lactobacillus casei cell wall extract (LCWE)-induced endothelial barrier dysfunction. Structural characterization identified CP-0 and CP-1 as novel triple-helical heteropolysaccharides (MW 81,404 and 83,540 Da; glucose, ribose, mannose). Following isolation and physicochemical screening, CP-0 exhibited low cytotoxicity and high anti-inflammatory activity. Mechanistic analyses revealed that CP-0 attenuated LCWE-induced endothelial injury by reducing inflammatory infiltration, IL-1β levels, and adhesion molecules (VCAM-1/ICAM-1) while upregulating tight junction proteins ZO-1/2 in mouse microvascular endothelial cells (MVECs). CP-0 suppressed NLRP3 inflammasome activation via decreased colocalization of NLRP3/Caspase-1/ASC, and competitive binding assays confirmed its interaction with TLR2, which blocked NF-κB nuclear translocation. By targeting TLR2-mediated signaling pathways, CP-0 effectively mitigated LCWE-induced coronary arteritis in vitro, demonstrating potential as a therapeutic candidate for cardiovascular diseases through early-stage anti-inflammatory intervention.
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DALTON TRANSACTIONS
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2025
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IF 3.3
Li Zhang,Youwen Li,Yuying Feng,Jiahui Jiang,Ting Zhao,Guancheng Xu
A trimetallic selenide electrocatalyst (Co, Fe, Ni)Se2 supported on nickel foam (NF) has been successfully synthesized for the oxygen evolution reaction (OER) and urea oxidation reaction (UOR). The catalyst was fabricated through a two-step strategy involving the formation of metal-organic frameworks (MOFs) precursors followed by a selenization reaction. The optimized (Co, Fe, Ni)Se2/NF-3:1 exhibited remarkable OER activity with an overpotential as low as 170 mV to achieve 10 mA cm-2, along with excellent stability over 1000 cycles. Its superior UOR performance with even lower overpotential further demonstrates promise for urea-assisted energy-saving hydrogen production. The enhanced electrocatalytic performance originates from the synergistic electronic modulation between Co, Fe, and Ni, the rough surface morphology facilitating mass and charge transport, and the highly conductive NF substrate enabling efficient exposure of active sites. This work provides valuable insights into the design of efficient multimetallic selenide electrocatalysts for sustainable electrochemical energy conversion.
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ENVIRONMENTAL POLLUTION
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2025
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IF 7.3
Qiuhui Qian,Ji Wu,Cuizhen Wang,Zheng Yang,Ying Cheng,Yuansi Zheng,Xuedong Wang,Huili Wang
As a synthetic rubber antioxidant, the environmental monitoring concentrations of N-(1,3-Dimethylbutyl)-N′-phenyl-p-phenylenediamine (6-PPD) have exceeded the risk threshold, attracting widespread attention. Although investigations into the harmful effects on zebrafish have commenced, a comprehensive exploration of its toxicological impacts and underlying molecular mechanisms remains to be conducted. By using zebrafish as a model, this study systematically evaluated 6-PPD-induced lipid metabolism disorders and inflammation response following environmental exposure. Bioinformatics analysis revealed that 6-PPD target genes enriched in the hepatitis B pathway, indicating potential hepatic toxicity via inflammatory pathways. Therefore, we hypothesize that 6-PPD could trigger hepatotoxicity through the crosstalk between lipid metabolism and inflammation. Further experiments substantiated this hypothesis by showing lipid accumulation in the liver following 6-PPD exposure, along with elevated triglyceride (TG) and total cholesterol (TC) levels, and imbalanced expression of lipid metabolism-related marker genes. Additionally, 6-PPD exposure induced the accumulation of reactive oxygen species (ROS) and inhibited the differentiation and maturation of immune cells, resulting in immune evasion. Most of these abnormalities were exacerbated in a dose-dependent manner with increasing concentrations of 6-PPD. The addition of the PPARγ pathway agonist puerarin (PUE) or NF-κB pathway inhibitor quinazoline (QNZ) to 6-PPD exposure group mitigated these toxic effects, validating our conjecture that lipid metabolism disorder and inflammatory responses may result from the regulation of the PPARγ/NF-κB pathway.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2024
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IF 7.7
Jiqi Huang,Yifan Su,Qianyu Wang,Mingxiao Feng,Dawei Zhang,Qian Yu,Chunyan Yan
Ganoderma lucidum spores are tiny mature germ cells ejected from the abaxial side of the pileus and were responsible for multiple pharmacological properties. The defatted G. lucidum spores are the byproducts after the extraction of G. lucidum spores oil by supercritical fluid extraction technology, which have not been given sufficient attention. In order to fully utilize the resources of G. lucidum spores, a glucomannan (SGL90–1, 6.4 kDa) was isolated from the defatted G. lucidum spores. SGL90–1 was composed of mannose, glucose, galactose, and fucose in a molar ratio of 23.9:28.7:9.0:1.0. The backbone of SGL90–1 was consisted of →2,4)- α -D-Man p -(1→, →6)- β -D-Man p -(1→, →2,6)- α -D-Man p -(1→, →2)- α -D-Glc p -(1→, and →3,6)- β -D-Glc p -(1 → with seven side chains, and terminated with β -D-Man p -(1→, β -D-Glc p -(1→, α -L-Fuc p -(1→, and β -D-Gal f -(1→. Moreover, SGL90–1 could significantly elevate the phagocytic capability of RAW264.7 macrophages and promote the levels of nitric oxide (NO), tumor necrosis factor- α (TNF- α ), and interlrukin-6 (IL-6) through activating the TLR4/MyD88/NF-κB signaling pathway. Collectively, these findings demonstrated the potential of SGL90–1 as a natural functional food with strong immune-enhancing effect.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2025
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IF 6.2
Zuyue Li,Shasha Wang,Mahmoud Abou-Elsoud,Yijie Li,Houchuntai Wang,Meiyu Liu,Wei Hu,Dong Uk Ahn,Xi Huang
NVMEERKIK, a peptide derived from ovalbumin, exhibited remarkable immunomodulatory activity. This study investigated the effect of simulated gastrointestinal digestion on its structure and bioactivity. NVMEERKIK was found to be unstable against gastrointestinal enzymes and completely degraded into NVME, NVMEE, KIK, K, and R. Among these, NVME, which constituted 90.90% of the digest, was synthesized and demonstrated a superior immune-enhancing activity than NVMEERKIK. Specifically, NVME improved phagocytosis, NO production, and TNF-α content in RAW264.7 cells by 1.31–15.86%, 17.17–122.08%, and 0.36–16.76%, respectively. TLR4 inhibition and immunofluorescence assays revealed the strong TLR4 activation and recognition capacities of both peptides. Furthermore, the Western blot results showed that NVMEERKIK and NVME activated the MAPK/NF-κB pathway by upregulating ERK, JNK, p38, and p65, leading to enhanced activation of RAW264.7 cells. The improved immune-enhancing activity of NVMEERKIK after digestion highlighted its potential as an immunomodulatory peptide for functional food applications.
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Scientific Reports
·
2023
·Vol. 13
·期 1
·1-11
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IF 4.6
Lan Xiang,Qi Dongdong,Ren Hao,Liu Tao,Shao Hong,Zhang Jiantao
Damage to lamellar keratinocytes, an essential cellular component of the epidermal layer of hoof tissue, can have a detrimental effect on hoof health and the overall production value of dairy cows. We isolated and cultured cow lamellar keratinocytes using the Dispase II and collagenase methods. We purified them by differential digestion and differential velocity adherent methods at each passaging and identified them by keratin 14 immunofluorescence. We established an in vitro model of inflammation in laminar keratinocytes using LPS and investigated whether chicoric acid protects against inflammatory responses by inhibiting the activation of the TLR4/MAPK/NF-κB signaling pathway. The results showed that cow lamellar keratinocytes were successfully isolated and cultured by Dispase II combined with the collagenase method. In the in vitro inflammation model established by LPS, the Chicoric acid decreased the concentration of inflammatory mediators (TNF-α, IL-1β, and IL-6), down-regulated the mRNA expression of TLR4 and MyD88 (P < 0.01), down-regulated the expression of TLR4, MyD88, p-ERK, p-p38, IKKβ, p-p65, p-p50 (P < 0.05), and increased the IκBα protein expression (P < 0.05). In conclusion, Chicoric acid successfully protected cow lamellar keratinocytes from LPS-induced inflammatory responses by modulating the TLR4/MAPK/NF-κB signaling pathway and downregulating inflammatory mediators.
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Theranostics
·
2026
·Vol. 16
·期 16
·9295
·
IF 14.9
Jinli Li,Liyao Zhang,Yuanyuan Ren,Junxuan Wang,Pan Zhang,Qianran Shen,Yaqi Wang,Yi Yu,Zi Cheng,Qiang Wang,Haiying Wang,Yuyan Xiong
Rationale Age-associated osteoporosis (AAOP) is characterized by progressive bone loss that can be driven by impaired osteoblast function and increased cellular senescence. However, the molecular mechanisms driving osteoblast senescence during aging remain incompletely understood. In this study, we aim to investigate the role of arginase 2 (ARG2) and its underlying mechanisms in osteoblast senescence and AAOP. Methods AAOP were assessed in D-galactose-induced aging mice, naturally aged mice, and osteoblast-specific ARG2 knockout mice. In vitro , osteoblast senescence was induced by hydrogen peroxide exposure. Bone phenotypes, cellular senescence, mitochondrial function, and mitophagy were examined using histological, molecular, and imaging techniques. Luciferase reporter assays, co-immunoprecipitation (Co-IP), and pharmacological or genetic approaches were employed for molecular mechanistic investigations. Results We observed that ARG2 expression was markedly elevated in senescent osteoblasts and aged mice with osteoporosis. Osteoblast-specific deletion of ARG2 alleviated age-related bone loss, improved trabecular bone microarchitecture, and reduced osteoblast senescence in vivo . Mechanistically, ARG2 promoted mitochondrial oxidative stress and impaired mitophagy, as evidenced by inhibition of the PINK1/Parkin/LC3 pathway and accumulation of p62. Furthermore, we revealed that ARG2 activated IκBα/NF-κB signaling, leading to HDAC9-mediated transcriptional repression of thioredoxin 2 (TXN2), a key mitochondrial antioxidant. Restoration of TXN2 expression, antioxidant treatment, or blockade of NF-κB/HDAC9 signaling rescued mitophagy, attenuated osteoblast senescence, and restored osteogenic function. Moreover, pharmacological inhibition of ARG2 using S-(2-boronoethyl)-L-cysteine (BEC) significantly suppressed osteoblast senescence and protected against age-related osteoporosis. Conclusion ARG2 plays a pivotal role in osteoblast senescence and the development of AAOP by inducing mitochondrial oxidative stress and mitophagy dysfunction through the IκBα/NF-κB/HDAC9/TXN2 signaling axis. Targeting ARG2 may offer a promising therapeutic approach for AAOP prevention and treatment.
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Human Cell
·
2025
·Vol. 39
·期 1
·20
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IF 3.1
Tian Tian,Luan Xiaona,Wang Lingzhi,Kong Yan,Huang Liying,Wang Yan
Ovarian cancer is one of the most lethal gynecologic malignancies contributing to cancer-related deaths among women. However, the mechanisms underlying its development remain poorly understood. This study aimed to investigate the role of STARD7 in tumorigenesis and its potential molecular mechanisms in ovarian cancer. Cell proliferation was assessed using the Cell Count Kit-8 and colony formation assays. The migration and invasion capabilities of ovarian cancer cells were evaluated through wound healing and Transwell invasion assays. A xenograft tumor model was established in nude mice to examine the role of STARD7 in tumor growth in vivo. The results demonstrated that the knockdown of STARD7 in A2780 and SK-OV-3 cells inhibited cell proliferation, invasion, and migration, while overexpression of STARD7 yielded opposing results. Furthermore, STARD7 was found to enhance the levels of phosphorylated p65 proteins and nuclear protein p65. Treatment with the NF-κB inhibitor PDTC inhibited STARD7 overexpression-induced cell proliferation, invasion, and migration. These results suggest that the activation of the NF-κB pathway is involved in STARD7-mediated ovarian cancer progression. Consistent with the in vitro findings, similar results were observed in in vivo ovarian cancer xenograft models. Additionally, dual luciferase reporter assays indicated that STARD7 was regulated by RUNX1-IT1, which acted as a sponge for miR-377-3p. Collectively, these findings suggest that STARD7 may serve as an independent prognostic indicator, promoting ovarian cancer development by activating the NF-κB pathway. This research expands the current understanding of NF-κB regulatory networks and positions STARD7 as a promising therapeutic target for developing pathway-specific interventions. Graphical abstract
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Journal of Cell Communication and Signaling
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2024
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IF 3.6
Le Cao,Weilu Gao,Haitao Yang,Ran Zeng,Zongsheng Yin
Inflammation promotes the degradation of the extracellular matrix, which contributes to the development of osteoarthritis (OA). Adipocyte enhancer binding protein 1 (AEBP1) participates in multiple pathological processes related to inflammatory diseases. However, the role of AEBP1 in OA development is unknown. We found a higher AEBP1 expression in articular cartilage of OA patients ( n = 20) compared to their normal controls ( n = 10). Thus, we inferred that AEBP1 might affect OA progression. Then mice with destabilization of the medial meniscus (DMM) surgery and chondrocytes with IL-1β treatment (10 ng/mL) were used to mimic OA. The increased AEBP1 expression was observed in models of OA. AEBP1 knockdown in chondrocytes reversed IL-1β-induced inflammation and extracellular matrix degradation, which was mediated by the inactivation of NF-κB signaling pathway and the increased IκBα activity. Co-immunoprecipitation assay indicated the interaction between AEBP1 and IκBα. Importantly, IκBα knockdown depleted the protective role of AEBP1 knockdown in OA. Moreover, AEBP1 knockdown in mice with OA showed similar results to those in chondrocytes. Collectively, our findings suggest that AEBP1 knockdown alleviates the development of OA, providing a novel strategy for OA treatment.
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