JOURNAL OF PERIODONTAL RESEARCH
·
2023
·
IF 3.5
Yifan Ma,Yi Qian,Yuteng Chen,Xiaoxu Ruan,Xiaoya Peng,Yi Sun,Jue Zhang,Jingjing Luo,Songlin Zhou,Chao Deng
Objective The purpose of this study was to investigate resveratrol's specific role as an anti-inflammatory and osteogenic differentiation of hPDLSCs in periodontitis and to reveal the mechanisms involved. Background Numerous studies have shown that inhibiting the inflammatory response of periodontal tissues and promoting the regeneration of alveolar bone are crucial treatments for periodontitis. Resveratrol has been found to have certain anti-inflammatory property. However, the anti-inflammatory mechanism and osteogenic effect of resveratrol in periodontitis are poorly understood. Materials and Methods We constructed an in vitro periodontitis model by LPS stimulation of hPDLSCs and performed WB, RT-qPCR, and immunofluorescence to analyze inflammatory factors and related pathways. In addition, we explored the osteogenic ability of resveratrol in in vitro models. Results In vitro, resveratrol ameliorated the inflammatory response associated with activation of the NF-κB pathway through activation of the NRF2/HO-1 pathway, characterized by inhibition of p65/p50 nuclear translocation and the proinflammatory cytokines interleukin-1β levels. Resveratrol also has a positive effect on osteogenic differentiation. Conclusions Observations suggest that resveratrol modulates the inflammatory response in hPDLSCs via the NRF2/HO-1 and NF-κB pathways and promotes osteogenic differentiation.
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高影响因子
CRYSTENGCOMM
·
2023
·Vol. 25
·期 38
·5452-5460
·
IF 3.1
Huimin Du,Yunhao Liang,Xingzuo Liu,Yue Deng,Jie Yang,Jun Yang,Shanshan Hu
Yb2(MoO4)3:Ln3+ (Ln = Ho, Tm, Er) phosphors were synthesized by a hydrothermal method with further calcination. The crystal structure and morphology of the samples were characterized by X-ray diffraction and scanning electron microscopy. The effects of rare earth ion interaction in the Yb2(MoO4)3:Ln3+ phosphors on the upconversion (UC) luminescence properties and energy transfer process at different doping concentrations were discussed. It is concluded that by doping Ho3+, Tm3+, and Er3+ in the Yb2(MoO4)3 host, the phosphors emit orange-yellow, blue and green light, respectively, and the energy transfer from Yb3+ → Ho3+/Er3+ and Yb3+ → Tm3+ is a two and three photon process, respectively. Under the excitation of a 980 nm laser, by changing the Ho3+/Tm3+ ratio in doped Yb2(MoO4)3, we have realized the transition of phosphors from cold white light to warm white light. The temperature sensitivity of the 2H11/2 and 4S3/2 energy levels of Yb2(MoO4)3:Er3+ in the range of 323–573 K was studied by the FIR technology. The experimental results show that the maximum absolute sensitivity was 0.0081 K−1 at 573 K and the maximum relative sensitivity was 0.01 K−1 at 323 K. Compared with other materials, the Er3+ doped Yb2(MoO4)3 phosphor is an excellent optical temperature sensing material.
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PLoS One
·
2016
·Vol. 11
·期 2
·e0149032
·
IF 3.057
Zhao Gao,Yu Han,Yunhui Hu,Xiaoyan Wu,Yongbin Wang,Xiaoqun Zhang,Jinjuan Fu,Xue Zou,Jun Zhang,Xiongwen Chen,Pedro A. Jose,Xi Lu,Chunyu Zeng
Both oxidative stress and inflammation are involved in the pathogenesis of contrast-induced nephropathy (CIN). Epigallocatechin-3-gallate (EGCG), a purified catechin from green tea, has antioxidant and anti-inflammatory effects. However, it is unknown whether or not EGCG is effective in treating CIN. Our present study found that intravenous administration of EGCG, either before or just after the establishment of CIN, had a protective effect, determined by normalization of serum creatinine and blood urea nitrogen levels, improvement in renal histopathological scoring and alleviation of apoptosis, accompanied by decreased oxidative stress and inflammation. Because EGCG is a potent inducer of the antioxidant heme oxygenase-1 (HO-1), we studied HO-1 signaling in CIN. HO-1 levels were increased in CIN; treatment with EGCG further increased HO-1 levels, accompanied by an increase in Nrf2, a regulator of antioxidant proteins. Interestingly, blockade of HO-1 with protoporphyrin IX zinc(II) (ZnPP) prevented the protective effect of EGCG on CIN. ZnPP also blocked the ability of EGCG to increase the activity of an antioxidant (superoxide dismutase), and decrease markers of oxidative stress (myeloperoxidase and malondialdehyde) and inflammation (myeloperoxidase and IL-1β), indicating that HO-1 is the upstream molecule that regulates the EGCG-mediated protection. To determine further the role of HO-1 on the EGCG-mediated inhibition of inflammation, we studied the effect of EGCG on the NLRP3 inflammasome, an upstream signaling of IL-1β. EGCG down-regulated NLRP3 expression, which was blocked by ZnPP, indicating that HO-1 links EGCG with NLRP3. Therefore, EGCG, via up-regulation of HO-1, protects against CIN by amelioration of oxidative stress and inflammation.
研究领域:
药理学
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肾病学
·
氧化应激与炎症
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Pharmaceuticals
·
2022
·Vol. 15
·期 12
·1548
·
IF 5.215
Fei Yang,Cuizhen Shen
On the basis of the mice pressure ulcers (PU) model, the protective effect and potential mechanism of sodium Danshensu (SDSS) cream against PU were investigated. The mice were randomly divided into three groups: the negative control group (cream without 0.5 g SDSS), the SDSS group (cream containing 0.5 g SDSS), and the positive group (0.5 g Hirudoid®). After 7 and 14 days of ointment application, the wound-healing rate of the SDSS and positive groups was significantly higher than that of the control group (p< 0.05). The results of hematoxylin–eosin staining also indicated that SDSS has the potential to promote the healing of PU. In addition, the serum IL-6, IL-1β, TNF-α, and MDA levels decreased significantly (p< 0.01) after 14 days of SDSS treatment, while the SOD, CAT, and GSH-Px activities increased significantly (p< 0.01). In addition, SDSS cream was able to significantly increase the expression of Nrf2, HO-1, GCLM, NQO1, NF-κB p65, NF-κB p50, IKKα, and IKKβ while decreasing the expression of Keap1 and IκBαin the Nrf2/HO-1 and NF-κB pathways. Our research will provide a foundation for the future clinical prevention and treatment of PU with SDSS cream.Keywords:pressure ulcers;sodium Danshensu cream;ischemia/reperfusion injury;Nrf2/HO-1 pathway;NF-κB pathway
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INORGANIC CHEMISTRY
·
2022
·
IF 5.436
Min Chen,Zhengli Liang,Xiaoxiao Wang,Jiehua Li,Xingguo Chen,Xingxing Jiang,Zheshuai Lin,Zhen Ma,Hongming Liu
A series of lanthanide-containing water-resistant nitrates, namely RE(OH)2NO3 (RE = Tb(1), Dy(2), Ho(3), and Er(4)), was obtained through the hydrothermal process. As possible nonlinear optical materials, they feature a layered isomorph composed of an [REO3(OH)6] polyhedron and an [NO3] triangle, and the synergistic arrangement of the [REO3(OH)6] and [NO3] groups in their structures leads to their obvious second-order nonlinear optical effect. Nevertheless, the unique optical absorption caused by the electronic transitions on 4f–4f orbitals of lanthanides results in their second harmonic generation responses of different strengths, with 1 exhibiting 5.07 times that of KDP, but 2–4 showing less than half of KDP. In addition, 1 possesses an outstanding water-resistant capacity and a transparent cut-off edge around 300 nm, foreshadowing its potential value as a nonlinear optical crystal. Moreover, 1 is found to emit characteristic green fluorescence due to the typical 5D4 → 7F5 transitions of the excited Tb3+ ions
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FEBS Open Bio
·
2021
·Vol. 11
·期 8
·2118-2126
·
IF 2.693
Na Wei,Tan Lu,Libin Yang,Yonghan Dong,Xiaotan Liu
Ferroptosis is an iron-dependent programmed cell death, which participates in the pathogenesis of spinal cord injury (SCI). Our previous study has revealed that Lipoxin A4 (LXA4) exerts a protective role in SCI. Here, we investigated whether LXA4 can protect SCI through inhibiting neuronal ferroptosis. We treated primary spinal cord neurons with Erastin (ferroptosis activator) to induce ferroptosis. Erastin treatment reduced cell viability and enhanced cell death of primary spinal cord neurons, which was rescued by ferrostatin-1 (ferroptosis inhibitor). Moreover, Erastin repressed glutathione peroxidase 4 (GPX4) expression and the levels of glutathione and cysteine in primary spinal cord neurons. Erastin also enhanced the expression of ferroptosis biomarkers (PTGS2 and ACSL4) and the levels of reactive oxygen species (ROS) in primary spinal cord neurons. The influence conferred by Erastin was effectively abolished by LXA4 treatment. Furthermore, LXA4 enhanced the protein expression of p-AKT, nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and haem-oxygenase-1 (HO-1) in primary spinal cord neurons. LXA4-mediated inhibition of ferroptosis of primary spinal cord neurons was prohibited by LY294002 (AKT inhibitor), brusatol (Nrf2 inhibitor) or zinc protoporphyrin (HO-1 inhibitor). In conclusion, this work demonstrated that LXA4 exerted a neuroprotective effect in Erastin-induced ferroptosis of primary spinal cord neurons by activating the Akt / Nrf2 / HO-1 signaling pathway. Thus, this work provides novel insights into the mechanisms of action of LXA4 in ferroptosis of primary spinal cord neurons and indicates that LXA4 may be a potential therapeutic agent for SCI.
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Food & Function
·
2020
·Vol. 11
·期 12
·10852-10863
·
IF 4.171
Mingbao Gu,Jie Jin,Chenghao Ren,Ximiao Chen,Weiyang Gao,Xiangyang Wang,Yaosen Wu,Naifeng Tian,Zongyou Pan,Aimin Wu,Yifei Zhou,Xiaolei Zhang
As an ordinary joint vestigial disease, osteoarthritis (OA) contributes to a considerable proportion of disability cases worldwide. Inflammation, as the main pathological factor, mediates the occurrence and development of OA. Akebia Saponin D (ASD), also known as Asperosaponin VI, is one of the active components extracted from Dipsaci Radix and is rich in Dipsacus loose tea. It has shown sound therapeutic effects on various diseases; nevertheless, its role in OA therapy is not completely understood. This study demonstrated the anti-inflammatory activity of ASD in OA through a series of in vivo and in vitro experiments. In vitro experiments revealed that ASD might prohibit the production of inflammatory mediators in IL-1β treated chondrocytes such as COX-2, iNOS, NO, PGE2, IL-6, and TNF-α. Meanwhile, it may also inhibit the production of ADAMTS-5 and MMP13 and promote the production of Aggrecan and Collagen II. The mechanism study demonstrated that ASD exerted an anti-inflammatory effect by activating the NRF2 target, upregulating the expression of HO-1, and preventing P65 from binding to DNA. In vivo experiments demonstrated that ASD might improve the progression of OA in a DMM mouse model. These research results provide evidence for the potential application of ASD in OA therapy.
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Journal of Neuroinflammation
·
2020
·Vol. 17
·期 1
·1-13
·
IF 5.793
Bian Hetao,Wang Gaohua,Huang Junjie,Liang Liang,Zheng Yage,Wei Yanyan,Wang Hui,Xiao Ling,Wang Huiling
Background Recently, depression has been identified as a prevalent and severe mental disorder. However, the mechanisms underlying the depression risk remain elusive. The neuroinflammation and NLRP3 inflammasome activation are known to be involved in the pathology of depression. Dihydrolipoic acid (DHLA) has been reported as a strong antioxidant and exhibits anti-inflammatory properties in various diseases, albeit the direct relevance between DHLA and depression is yet unknown. The present study aimed to investigate the preventive effect and potential mechanism of DHLA in the lipopolysaccharide (LPS)-induced sickness behavior in rats. Methods Adult male Sprague–Dawley rats were utilized. LPS and DHLA were injected intraperitoneally every 2 days and daily, respectively. Fluoxetine (Flu) was injected intraperitoneally daily. PD98059, an inhibitor of ERK, was injected intraperitoneally 1 h before DHLA injection daily. Small interfering ribonucleic acid (siRNA) for nuclear factor erythroid 2-like (Nrf2) was injected into the bilateral hippocampus 14 days before the DHLA injection. Depression-like behavior tests were performed. Western blot and immunofluorescence staining detected the ERK/Nrf2/HO-1/ROS/NLRP3 pathway-related proteins. Results The DHLA and fluoxetine treatment exerted preventive effects in LPS-induced sickness behavior rats. The DHLA treatment increased the expression of ERK, Nrf2, and HO-1 but decreased the ROS generation levels and reduced the expression of NLRP3, caspase-1, and IL-1β in LPS-induced sickness behavior rats. PD98059 abolished the effects of DHLA on preventive effect as well as the levels of Nrf2 and HO-1 proteins. Similarly, Nrf2 siRNA reversed the preventive effect of DHLA administration via the decreased expression of HO-1. Conclusions These findings suggested that DHLA exerted a preventive effect via ERK/Nrf2/HO-1/ROS/NLRP3 pathway in LPS-induced sickness behavior rats. Thus, DHLA may serve as a potential therapeutic strategy for depression.
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ACS Applied Materials & Interfaces
·
2023
·
IF 9.5
Fengxian Luo,Beiwei Zhu,Di Wu,Yu Xu,Tao Chen,Yanfei Li,Jiangning Hu
Acute liver injury (ALI) is a severe health condition with limited treatment options. Phlorotannin (PT), a natural compound extracted from seaweeds, has shown potential in improving liver function. However, its poor stability and bioavailability have limited its applications in vivo. In this study, we developed PT-based nanoparticles (NPs) through a Mannich reaction with glycine, which exhibited good biocompatibility and prolonged circulation time in vivo. Our results revealed that the PT NPs possess strong free radical scavenging ability, effectively reducing reactive oxygen species (ROS) and alleviating oxidative stress and proinflammatory responses in the H2O2-induced oxidative damage model of HepG2 cells. Furthermore, the PT NPs effectively attenuated oxidative stress and inflammation in the liver tissue of carbon tetrachloride (CCl4)-induced liver injury mice by regulating the Nrf2/HO-1 signaling pathway. In summary, our results suggested that the PT NPs could serve as a promising nano-therapeutic strategy for alleviating ALI.
研究领域:
药理学
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纳米技术
·
肝病学
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高影响因子
JOURNAL OF VIROLOGY
·
2025
·
IF 3.8
Xiaohan Chen,Yipeng Pang,Fructueux Modeste Amona,Zilu Liu,Fang Wang,Yuan Liang,Jiachen Yang,Wanhan Zhang,Xingtang Fang,Xi Chen
Porcine reproductive and respiratory syndrome virus (PRRSV) is a highly contagious pathogen that causes substantial economic losses in the global swine industry, primarily by impairing reproductive performance and respiratory health. However, current therapeutic approaches remain limited in effectively controlling PRRSV infection. Here, we present self-assembled cyanidin-3-O-glucoside (C3G)-based nanoparticles (C3G-Cs-SeNPs) as a promising antiviral agent against PRRSV infection. These nanoparticles demonstrated excellent stability and biocompatibility, with minimal cytotoxicity in Marc-145 cells. C3G-Cs-SeNPs significantly reduced ROS levels in PRRSV-infected cells, enhancing the antioxidant capacity and mitigating oxidative stress. In addition, they effectively inhibited key stages of the PRRSV lifecycle, including viral internalization and replication, leading to a marked decrease in viral proliferation. Moreover, C3G-Cs-SeNPs alleviated ferroptosis by restoring redox homeostasis through enhanced antioxidant enzyme activity. Mechanistically, these nanoparticles potentially activate the SIRT1/Nrf2/HO-1 signaling pathway, which plays a critical role in regulating inflammation and ferroptosis in PRRSV-infected cells. These findings suggest that C3G-Cs-SeNPs could serve as a novel therapeutic approach to modulate inflammation, ferroptosis, and viral replication in respiratory viral infections. Our study highlights the therapeutic potential of C3G-Cs-SeNPs in combating PRRSV infection, with important implications for viral infection management and respiratory disease treatment.
研究领域:
病毒学
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纳米技术
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免疫学
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抗病毒治疗
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氧化应激研究
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高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
Mengxin Li,Jun Wang,Zihan Xu,Yue Lin,Jingquan Dong
Background Obstructive sleep apnea syndrome (OSAS), a chronic disorder affecting approximately 10% of adults worldwide with heightened prevalence in males and obese populations, induces irreversible neurocognitive impairment. Atraric Acid (AA), a natural depside compound derived from lichens, exhibits dual functional properties through its molecular groups capable of free radical scavenging and metal chelation. However, its therapeutic potential in OSAS-related pathologies remains unexplored. Objective This study aims to investigate the neuroprotective effects and molecular mechanisms of AA against CIH-induced neuronal damage. Methods CIH mouse models and hypoxic injury models in HT22 neurons were established. AA was administered to mice at doses of 5, 10, and 20 mg/kg (selected based on literature references and preliminary experiments), and to cells at an optimal concentration of 20 μM (determined by CCK-8 assays). Therapeutic efficacy was evaluated through behavioral tests including the Morris Water Maze, Elevated Plus Maze, and Open Field Test. Neuroprotective effects were assessed via histopathological examination (e.g., neuronal survival in hippocampal CA3 and DG sub-regions) and detection of oxidative stress/ferroptosis markers (e.g., MDA levels, GPX4 expression, and related biomarkers). Transcriptomic sequencing and molecular docking analyses were employed to investigate differentially expressed genes, pathway enrichment, and underlying mechanisms. Results In vivo and in vitro experiments demonstrated that AA significantly alleviated neuronal damage in CIH mice and enhanced HT22 cell viability. AA down-regulated oxidative stress- and ferroptosis-related gene expression. Transcriptomic sequencing identified AMPK signaling as a key target. Combined AMPK inhibitor (Compound C) and nuclear-cytoplasmic fractionation experiments confirmed that AA synergistically regulates dual antioxidant pathways (Nrf2/HO-1 and FoxO3a/SOD2) via AMPK activation. Conclusion AA mitigates CIH-induced neurocognitive impairment by AMPK-dependent activation of the Nrf2/HO-1 and FoxO3a/SOD2 axes, establishing a dual antioxidant-ferroptosis defense barrier. This study is the first to systematically elucidate AA's molecular mechanisms using transcriptomics data integrated with computational simulations, providing novel therapeutic targets and a translational paradigm for developing natural compound-based therapies for OSAS.
研究领域:
神经生物学
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睡眠医学
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分子药理学
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氧化应激
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信号转导
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转化医学
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天然产物药理学
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高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2025
·Vol. 26
·期 14
·6666
·
IF 4.9
Siqi Zhang,Fei Tang,Zhe Zhou,Linhui Li,Yang Tang,Kaiwen Fu,Yang Tan,Ling Li
Liver fibrosis remains a critical health concern with limited therapeutic options. Kaempferol (Kae) is a natural flavonoid widely present in natural plants, yet its role in modulating gut–liver axis interactions during fibrosis is unexplored. This study investigates the hepatoprotective effects of Kae on alleviating carbon tetrachloride (CCl4)-induced liver fibrosis, and its underlying mechanisms, focusing on oxidative stress, gut microbiota, and short-chain fatty acids (SCFAs), are revealed. A mouse model of hepatic fibrosis was built by the subcutaneous injection of CCl4. Meanwhile, Kae was administered by gavage at doses of 25, 50, and 100 mg/kg body weight. Serum biomarkers, liver histopathology, oxidative damage markers, and nuclear factor erythroid 2-related factor 2 (Nrf2)/kelch-like ECH-associated protein 1 (Keap1)/heme oxygenase 1 (HO-1) signaling were analyzed. AML12 hepatocytes were pretreated with Kae or SCFAs (acetate, propionate, butyrate) before H2O2-induced oxidative injury. The changes in gut microbiota and the levels of SCFAs were assessed via 16S rRNA sequencing and GC-MS, respectively. Kae effectively alleviated the destruction of the liver morphology and tissue structure, reduced the infiltration of inflammatory cells, collagen deposition in the liver, and the expression of fibrotic factors, and downregulated the oxidative stress level in the liver of mice with liver fibrosis by activating the Nrf2/Keap1/HO-1 pathway (p< 0.05 or 0.01). In vitro, Kae significantly mitigated H2O2-induced cytotoxicity and oxidative damage (p< 0.05 or 0.01). Furthermore, Kae restored gut microbiota diversity, increased beneficial genera (e.g.,Lactobacillus), and elevated both intestinal and hepatic SCFA levels (p< 0.01). The discrepant SCFA pretreatment similarly protected AML12 cells by activating Nrf2 signaling (p< 0.05 or 0.01). Our research suggests that Kae could inhibit CCl4-induced liver fibrosis by restoring the levels of intestinal metabolite SCFAs to reduce oxidative damage.
研究领域:
药理学
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肝脏病学
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微生物学
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生物化学
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分子生物学
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营养科学
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危险品化学品经营许可证（带存储）