Foods
·
2025
·Vol. 14
·期 7
·1270
·
IF 5.1
Jiali Tang,Mengyao Zhang,Jiaying Wang,Haijing Zhang,Zhong Wang,Ziteng Lei,Chengtao Wang,Wei Chen
Inflammatory bowel disease (IBD) is a chronic disease influenced by a complex interplay of factors, including genetics, environmental, and gut microbiota. This study aimed to explore the therapeutic potential of the natural polyphenolic compound hydroxytyrosol (HT) in modulating dextran sodium sulfate (DSS)-induced colitis in mice. The findings demonstrate that oral administration of HT significantly alleviated colitis symptoms, as evidenced by a reduction in the disease activity index and improvements in colonic pathology. HT was found to inhibit the release of pro-inflammatory cytokines, enhance antioxidant status, and mitigate oxidative stress. Furthermore, HT contributed to the restoration of the gut barrier by reinstating tight junction proteins, reducing the inflammatory marker lipopolysaccharide (LPS), and suppressing inflammation-related genes. This compound also modulated the NLRP3-Cas-1-GSDMD-IL-1β inflammatory pathway and inhibited the NF-κB (nuclear factor kappa B) pathway, thereby alleviating colitis. Gut microbial analysis revealed that HT enriched the abundance of Bacteroidota and altered the balance between Bacteroidota and Firmicutes in mice. Correlation analysis between bacterial microbiota and inflammatory factors suggested that HT may alleviate colitis by modulating the relative abundance of Alistipes , Bacteroides , and unclassified_f__ Muribaculaceae . These findings underscore the potential of HT as a therapeutic agent in the treatment of colitis.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Antioxidants
·
2021
·Vol. 10
·期 6
·976
·
IF 6.313
Chongshan Dai,Hui Li,Yang Wang,Shusheng Tang,Tony Velkov,Jianzhong Shen
This study investigates the protective effect of baicalein on carbon tetrachloride (CCl4)-induced acute liver injury and the underlying molecular mechanisms. Mice were orally administrated baicalein at 25 and 100 mg/kg/day for 7 consecutive days or ferrostatin-1 (Fer-1) at 10 mg/kg was i.p. injected in mice at 2 and 24 h prior to CCl4injection or the vehicle. Our results showed that baicalein or Fer-1 supplementation significantly attenuated CCl4exposure-induced elevations of serum alanine aminotransferase and aspartate aminotransferase, and malondialdehyde levels in the liver tissues and unregulated glutathione levels. Baicalein treatment inhibited the nuclear factor kappa-B (NF-κB) pathway, activated the erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway in liver tissues, and markedly improved CCl4-induced apoptosis, inflammation and ferroptosis in liver tissues exposed with CCl4. In vitro, baicalein treatment improved CCl4-induced decreases of cell viabilities and knockdown ofNrf2and arachidonate 12-lipoxygenase (ALOX12) genes partly abolished the protective effect of baicalein on CCl4-induced cytotoxicity in HepG2 cells. In conclusion, our results reveal that baicalein supplementation ameliorates CCl4-induced acute liver injury in mice by upregulating the antioxidant defense pathways and downregulating oxidative stress, apoptosis, inflammation and ferroptosis, which involved the activation of Nrf2 pathway and the inhibition of ALOX12 and NF-κB pathways.Keywords:baicalein;oxidative stress;ferroptosis;acute liver injury;ALOX12 pathway;Nrf2 pathway
✓ 已验证
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2017
·
IF 2.956
Zhixin Peng,Xiaobao Gong,You Yang,Ligua Huang,Qingyan Zhang,Peng Zhang,Rongzhen Wan,Baoshun Zhang
Quercetin is regarded as a potential hepatoprotective agent in the treatment of acute liver injury. However, the underlying mechanism of how quercetin to protect against lipopolysaccharides/ d -galactosamine (LPS/ d -GalN) induced acute liver injury remains unclear. To investigate the mechanism, the antioxidative, anti-inflammatory and antiapoptotic responses were performed. The results showed that quercetin pretreatment improved the survival rate and substantially reduced the liver histopathological changes in mice. It also alleviated the hepatic damage and reduced the productions of oxidative markers induced by LPS/ d -GalN. In addition, quercetin pretreatment significantly diminished the production of inflammatory cytokines, including TNF-α, IL-6 and IL-1β, and inhibited the activation of the NF-κB and MAPK signaling pathways as well as the expression of apoptotic-related proteins induced by LPS/ d -GalN. We found that the potential mechanism of this quercetin-induced protection is mainly mediated through its powerful antioxidative capacity, inhibition of hepatocyte apoptosis and suppression of inflammatory cytokines through the IKK/NF-κB and MAPK signaling pathways. Thus, quercetin shows a promising therapeutic effect on acute liver injury in mice.
✓ 已验证
DOI
PubMed
高影响因子
EXPERIMENTAL ANIMALS
·
2022
·
IF 1.798
Zhanchun SONG,Xiaozeng WANG,Lianqi HE,Liang CHEN,Zhichao REN,Siyu SONG
Myocardial infarction (MI) as the remarkable presentation of coronary artery disease is still a reason for morbidity and mortality in worldwide. Lysosomal-associated protein transmembrane 5 (LAPTM5) is a lysosomal-related protein found in hematopoietic tissues and has been confirmed as a positive regulator of pro-inflammatory pathways in macrophages. However, the role of LAPTM5 in MI remains unknown. In this study, we found that both mRNA and protein expression levels of LAPTM5 were significantly elevated in MI mice. Suppression of LAPTM5 in myocardial tissues decreased cardiac fibrosis and improved cardiac function after MI. At the molecular level, downregulated LAPTM5 dramatically suppressed the macrophage activation and inflammatory response via inhibiting the activation of the NF-κB pathway. Collectively, suppression of LAPTM5 in myocardial tissues inhibits the pro-inflammatory response and the cardiac dysfunction caused by MI. This study indicated that LAPTM5 as a pro-inflammatory factor plays a crucial role in MI disease.
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2020
·
IF 4.873
Liu Tang,Xiao-Lei Li,Zi-Xin Deng,Yao Xiao,Ya-Hong Cheng,Jing Li,Hong Ding
Conjugated linoleic acid (CLA), commonly found in beef, lamb and dairy products, has been reported to exhibit anti-inflammatory and antipruritus effects and to inhibit the release of chemical mediators such as histamine and eicosanoid in laboratory rodents. The chief objective of the study is to assess the efficacy of CLA on atopic dermatitis (AD) in mice and to explore possible mechanisms with CLA treatments . To develop a new therapy for AD, the anti-AD potential of CLA was investigated by inducing AD-like skin lesions in mice using 2,4-dinitrofluorobenzene. We evaluated dermatitis severity; histopathological changes; serum levels of T helper (Th) cytokines (interferon-γ, interleukin-4); changes in protein expression by western blotting and immunohistochemistry staining for cyclooxygenase-2 (COX-2), 5-lipoxygenase (5-LOX), toll like receptor 4 (TLR-4), myeloid differentiation factor 88 (MyD88), nuclear factor-κB (NF-κB) and tumor necrosis factor α (TNF-α); and production of the proinflammatory lipid mediators, such as prostaglandin E 2 and leukotriene B4 , in the skin lesions. Treatment with CLA ameliorated the development of AD-like clinical symptoms and effectively inhibited epidermal hyperplasia and infiltration of mast cells and CD4 + T cells in the AD mouse skin. Total serum immunoglobulin E levels and the expression levels of Th1/Th2 cytokines and lipid mediators in dorsal skin were dramatically suppressed by CLA. Furthermore, CLA down-regulated the expressions of COX-2, 5-LOX, TLR4, MyD88, NF-κB and TNF-α. Taken together, our findings demonstrate the potential usefulness of CLA as an anti-inflammatory dietary supplement or drug for the prevention and management of AD skin diseases by modulating the COX-2/5-LOX and TLR4/MyD88/NF-κB signaling pathways .
✓ 已验证
DOI
PubMed
高影响因子
Materials Science & Engineering C-Materials for Biological Applications
·
2021
·
IF 7.328
Rui Yang,Yurong Yan,Zheng Wu,Yong Wei,Hao Song,Lian Zhu,Chenchen Zhao,Na Xu,Jijiang Fu,Kaifu Huo
Although titanium and its alloys are widely used in bone surgeries, the implantation failures caused by sterile inflammation still occur. The excessive reactive oxygen species (ROS) in the peri-implant region are considered to cause inflammation and impede the osseointegration of titanium implants. In this study, a coating of resveratrol-loaded titania nanotube (TNT-Res) for eliminating ROS was fabricated on titanium surface through electrochemical anodization and following surface adsorption of resveratrol. The resveratrol concentration of released from TNT-Res coating was controlled by modulating the loading amount. The ROS production in macrophage cell lineage RAW 264.7 and bone mesenchymal stem cells (BMSCs) were significantly decreased when cultured on TNT-Res coatings. The pro-inflammatory factors, including tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), and NO produced by RAW 264.7 cells were reduced when cells were cultured on TNT-Res coatings. These results proved that the TNT-Res coating can effectively eliminate ROS and inhibit inflammation. Moreover, the osteogenic indicators, including alkaline phosphatase (ALP) production, extracellular calcium deposition, and osteogenesis-related gene expression, including collagen І (Col-І), osteocalcin (OCN), osteopontin (OPN), and runt-related transcription factor 2 (Runx2), were significantly promoted for TNT-Res groups, which demonstrated that the TNT-Res coating can enhance the osteogenic differentiation of BMSCs. Additionally, the phosphorylation of nuclear factor κ-B (NF-κB) were down-regulated both in RAW 264.7 cells and BMSCs, which indicated that the TNT-Res coating could inhibit inflammation and promote osteogenesis by inhibiting the activation of NF-κB signaling pathway. The TNT-Res coating could be an effective implant surface for improving osseointegration ability of titanium implants.
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF DAIRY SCIENCE
·
2026
·
IF 4.7
Yi Ma,Jiatao Zhang,Cheng Chen,Mengzhi Wang,Haifei Li,Yunfei Deng,Xingru Zhou,Jianhui Hu,Hao Zhang,Guohui Li,Jin Wang,Zhongjian Guo
Subacute ruminal acidosis, induced by high-concentrate diets, can trigger systemic inflammation and mastitis, a pathology linked to ruminal dysbiosis and disruption of the host's circadian rhythm. In this study, 32 mid-lactating Saanen goats (41.5 ± 1.79 kg BW) were randomly allocated to 4 treatment groups (n = 8/group): a low-concentrate diet (LC; 30:70 concentrate:forage ratio), a high-concentrate diet (HC; 70:30), and their respective counterparts supplemented with 200 mg/kg of DM thiamine (LCT and HCT). Results demonstrated that the HC diet decreased ruminal pH, induced microbial dysbiosis, and increased plasma LPS concentrations. This resulted in systemic and mammary inflammation, characterized by elevated cytokine expression and a significant decline in milk yield and quality. Thiamine supplementation in the high-concentrate diet (HCT group) effectively reversed these changes. It stabilized ruminal pH, modulated the microbiota by enriching beneficial taxa such as f_Ruminococcaceae , reduced inflammatory cytokine levels, and restored milk production. At the molecular level, goats receiving thiamine supplementation exhibited reduced activation of the NF-κB and NLRP3 inflammasome pathways and higher expression of core clock proteins (CLOCK, BMAL1) in the mammary tissue. In conclusion, thiamine alleviates SARA-induced mastitis by stabilizing the rumen microbiota and mitigating inflammation, and these protective effects are associated with concurrent changes in the NF-κB/NLRP3/CLOCK signaling axis in the mammary gland.
✓ 已验证
产品关联
DOI
高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2026
·
IF 6.5
Cheng Cao,Mubin Sun,Jiabao Li,Zhenyu Yuan,Yuwei Gu,Yufan Shao,Lisheng Wang,Xiaohua Jin,Yijie Cheng,Bo Fan
Urate transporter 1 (URAT1, encoded by SLC22A12 ) is a key mediator of renal urate reabsorption and an important pharmacological target for urate-related disorders. Sodium butyrate (BuNa), a gut microbiota derived short-chain fatty acid, has been implicated in host metabolic regulation, but its role in renal urate transport remains unclear. Here, using molecular docking, cellular thermal shift assays, immunoprecipitation-mass spectrometry and multi-omics analyses, we identified free fatty acid receptor 2 (FFAR2) as a direct target of BuNa in renal proximal tubular HK2 cells . BuNa binding upregulated FFAR2 and promoted URAT1 expression and urate uptake via an FFAR2-dependent pathway. Mechanistically, BuNa/FFAR2 signaling acts via GNAQ to activate PLCβ, generating diacylglycerol and engaging a PKC-dependent p38 MAPK/ELK1 cascade that upregulates arrestin beta 2 (ARRB2). ARRB2 directly binds to IκB, preventing its phosphorylation-dependent degradation, thereby stabilizing IκB and inhibiting NF-κB nuclear translocation. Within the SLC22A12 promoter, NF-κB (RELA/p50) and hepatocyte nuclear factor 1 beta (HNF1β) compete for overlapping binding sites. By blocking NF-κB nuclear entry, BuNa relieves this competition, permitting HNF1β-driven SLC22A12 transcription. Thus, BuNa enhances URAT1-mediated urate reabsorption in HK2 cells via an FFAR2/GNAQ/p38 MAPK/ELK1/ARRB2 axis that stabilizes IκB, suppresses NF-κB, and relieves the competitive binding between NF-κB and HNF1β on the SLC22A12 promoter. These findings establish a previously unrecognized gut microbiota–kidney axis linking microbial BuNa to renal urate homeostasis through a novel transcriptional regulatory circuit.
✓ 已验证
产品关联
DOI
高影响因子
Food Bioscience
·
2026
·
IF 6.2
Xiao Qiang,Mengyuan Gao,Zongshuo Li,Weidong Li
SQLE is a potential functional food for alleviating spleen deficiency syndrome. • SQLE contains diverse bioactive compounds with flavonoids as major components. • SQLE restores gut microbiota homeostasis and promotes SCFAs production. • SQLE improves spleen deficiency via the PI3K/Akt/NF-κB/AQP3 signaling pathway. Spleen deficiency syndrome (SDS) manifests as impaired digestive function, fatigue, and metabolic issues, which are closely associated with dysbiosis of the gut microbiota. Shen-Qi-Ling extract (SQLE) is a natural extract prepared from food-medicine homologous resources, primarily consisting of Codonopsis pilosula , Astragalus membranaceus , and Poria cocos . However, the bioactive constituents and mechanisms by which it alleviates SDS remain unclear. In this study, we systematically characterized the chemical constituents of SQLE and elucidated its potential mechanisms of action against SDS in mice. Using ultra-high-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) analysis, 137 compounds were identified in SQLE, with flavonoids being the most abundant, followed by coumarins, phenylpropanoids, and organic acids. Molecular docking analysis indicated that SQLE might have a spleen-strengthening effect. Treatment with SQLE, particularly SQLE-M, significantly enhanced intestinal absorption, exercise performance, tissue damage, and oxidative stress. Moreover, SQLE-M restored gut microbial homeostasis, increased the relative abundance of potentially beneficial bacteria, and promoted the production of short-chain fatty acids (SCFAs). Notably, SQLE-M normalized the intestinal barrier dysfunction and metabolic disorders by activating the PI3K/Akt signaling pathway, inhibiting NF-κB-mediated inflammatory responses, and upregulating aquaporin 3 (AQP3) expression. Collectively, SQLE mitigates SDS, which may be associated with alterations in the gut microbiota-metabolite axis and the PI3K/Akt/NF-κB/AQP3 signaling pathway, offering new perspectives for developing spleen-strengthening functional foods derived from food-medicine homologous resources. Download: Download high-res image (462KB) Download: Download full-size image
✓ 已验证
DOI
高影响因子
NEUROCHEMICAL RESEARCH
·
2026
·Vol. 51
·期 1
·73
·
IF 4.5
Zhou Juan,Li Haipeng,Wen Ying,He Lingli,He Yangli,Meng Heng
Neuromyelitis optica spectrum disorder (NMOSD) is a rare but serious inflammatory demyelinating disease. A key characteristic of NMOSD is the presence of a pathogenic autoantibody in serum called aquaporin-4 immunoglobulin G (AQP4-IgG). This study investigates the mechanism of astrocyte-derived small extracellular vesicles (EVs) carrying mitochondrial DNA (mtDNA) to promote AQP4-IgG-induced microglial activation in neuromyelitis optica (NMO) via the toll-like receptor 9 (TLR9)/myeloid differentiation primary response 88 (MyD88)/nuclear factor-kappa B (NF-κB) pathway. Serum IgG was isolated from NMOSD patients (AQP4-IgG) and healthy controls (Con-IgG). Astrocytes were treated with AQP4-IgG or Con-IgG. EVs were isolated via ultracentrifugation, characterized, and examined for internalization. Microglia were exposed to EVs, and mtDNA levels were assessed. An NMO mouse model was established, with neurological damage, mouse behaviors, tissue damage, and microglial characterization evaluated using modified neurological severity score, open-field test, rotarod test, luxol fast blue staining, and flow cytometry. Inflammatory cytokines, TLR9, MyD88, p65, IκBα, p-p65, and p-IκBα in BV2 cells and spinal cord tissues were analyzed via ELISA, RT-qPCR, and western blot. AQP4-IgG-induced astrocyte-derived EVs increased Iba1-high-expressing and CD86/tumor necrosis factor-α-high-expressing cells, reduced CD206/transforming growth factor-β-high-expressing cells, and boosted inflammatory responses. AQP4-IgG-induced EVs carried mtDNA to activate microglia via the TLR9/MyD88/NF-κB pathway. TLR9/MyD88/NF-κB pathway inhibition reversed AQP4-IgG-induced EVs’ promotion on microglial activation. In vivo, AQP4-IgG-induced EVs-mtDNA exacerbated microglial activation and NMO through the TLR9/MyD88/NF-κB pathway. AQP4-IgG-induced EVs carried mtDNA to upregulate TLR9, further activating the MyD88/NF-κB pathway, thereby promoting microglial activation and transition toward pro-inflammatory gene-high-expressing cells to drive NMO progression.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
POULTRY SCIENCE
·
2026
·
IF 4.5
Dan Shao,Longqing Hu,Wei Guo,Jinglong Chen,Xuming Guo,Hong Yao
This study aimed to investigate the protective effect and mechanism of dietary dimethylglycine (DMG) on jejunal injury in yellow-feathered broilers subjected to cyclic heat stress (HS). A total of 180 35-day-old male yellow-feathered broilers were randomly allocated into 3 groups: the thermoneutral condition with basal diet group (CON), the cycle heat stress with basal diet group (HS, 32-35°C), and the cycle heat stress with 0.1% DMG in basal diet group (HS_DMG, 32-35°C). The experiment included a 7-day heating period followed by a 14-day cyclic heat stress period. Growth performance, rectal temperature, jejunal morphology and ultrastructure, inflammatory cytokine levels, and protein expression related to the TLR4/NF-κB pathway and MUC2 were evaluated. Additionally, primary chicken jejunal epithelial cells were isolated and exposed to heat stress with or without DMG pretreatment to validate in vivo findings. Results showed that heat stress significantly increased rectal temperature ( P < 0.05), had a tendency to reduce body weight (BW, P = 0.058) and average daily gain (ADG, P = 0.050), and increase the feed-to-gain ratio (F/G, P = 0.053). Histologically, HS caused epithelial shedding, reduced villus height and villus height/crypt depth, and induced microvilli damage and mitochondrial swelling, all of which were attenuated by DMG supplementation. Heat stress also elevated jejunal mucosa levels of IL-6, IL-8, IL-1 β , and TNF- α ( P < 0.05), while DMG reduced IL-6, IL-8, and TNF- α ( P < 0.05). Immunohistochemistry and western blotting revealed that HS decreased MUC2 expression and increased TLR4 and p-NF-κB-p65 protein levels ( P < 0.05), whereas DMG reversed these changes ( P < 0.05). In vitro, DMG pretreatment alleviated HS-induced reduction in inflammatory cytokine release, and alterations in TLR4, NF-κB, and MUC2 protein expression. In conclusion, dietary DMG supplementation alleviates cyclic heat stress-induced jejunal injury in yellow-feathered broilers by suppressing the TLR4/NF-κB signaling pathway and restoring MUC2 expression.
✓ 已验证
DOI
PubMed
高影响因子
BIOLOGICAL TRACE ELEMENT RESEARCH
·
2026
·
IF 4.3
Yang Wenyan,Ma Lu,Hu Ting,Zhang Lei,Wu Kewei,Chen Hualin,Zhang Dandan,Luo Peng
Geochemical fluoride pollution is a global public health issue affecting a wide range and large population. The major health hazard from long-term fluoride exposure is skeletal fluorosis, a highly disabling and irreversible bone damage disease with no effective early interventions available to date. Given reactive oxygen species (ROS) accumulation is a key event in fluoride-induced bone damage, we established a sodium fluoride-exposed rat model. During the phase when fluoride induced ROS accumulation and mild bone damage in rat bone tissue, we administered Rosa roxburghii Tratt juice (RRTJ)—a natural food-medicinal homologous plant with antioxidant properties—to explore its intervention effect and potential mechanism against fluoride-induced bone damage. Results showed RRTJ inhibited fluoride-induced decreases in bone mineral density and trabecular number in male rats. Since enhanced bone resorption mediated by osteoclast overactivation is the initiating link of these fluoride-induced pathological changes, this study further found RRTJ suppressed fluoride-induced increases in osteoclast activity in male rat bone tissue, specifically reducing osteoclast numbers in bone tissue and lowering serum levels of bone resorption markers CTX and TRAP-5b. This effect is achieved by RRTJ scavenging fluoride-induced ROS accumulation in bone tissue, restoring ROS/TNF-α/NF-κB pathway homeostasis, and thereby inhibiting the overexpression of osteoclast activation-related genes tartrate-resistant acid phosphatase and cathepsin K. In conclusion, this study confirms RRT inhibits fluoride exposure-induced bone damage in male rats by regulating ROS/TNF-α/NF-κB pathway homeostasis. These findings provide new perspectives on the mechanism of fluoride-induced bone damage and, more importantly, reveal a potential novel intervention strategy.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）