MOLECULES
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2025
·Vol. 30
·期 22
·
IF 4.6
Bingxin Zhang,Ning Wang,Xiaoxu Chen,Nan Yang,Ying Zhao,Xiaoshu Zhang
Alcoholic liver disease (ALD) caused by excessive alcohol consumption poses a serious threat to human health.Callistephus chinensis(L.) Nees is an herb of the Asteraceae family that has good results in the prevention and treatment of a variety of liver diseases, including multifactorial liver injury, non-alcoholic fatty liver disease/non-alcoholic steatohepatitis, liver fibrosis. Sesquiterpenes are thought to be biologically active components that typically have anti-inflammatory, immunomodulatory, and cardioprotective effects. Callistephus A (CA) is a sesquiterpene compound with a rare 6/7 ring skeleton, which has been isolated only from theCallistephus chinensisNees. However, the mechanism of action of CA on alcoholic liver disease remains unclear. In this study, alcoholic liver mice were fed with 20 and 40 mg/kg CA, respectively, for 11 days. This study showed that CA improved hepatic steatosis and oxidative stress associated with alcohol consumption. CA alleviated liver inflammation by inhibiting the TLR4/MYD88/NF-κB pathway, ameliorating gut imbalance by restoring the abundance ofAkkermansia, and restoring short-chain fatty acids in the gut. Transcriptome analysis revealed that CA primarily affects genes involved in lipid metabolism and inflammation. In vitro, by adding inhibitors of TLR4 (TAK-242) and AMPK (Dorsomorphin), it was confirmed that CA alleviates ALD by inhibiting TLR4 and activating AMPK. This study is the first to demonstrate that CA protects against alcoholic liver disease through the regulation of the gut flora and modulation of the AMPK/NF-κB pathway. In conclusion, CA can effectively improve alcoholic liver disease and can be used as an effective candidate drug with liver-protective effects.
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Artificial Cells Nanomedicine and Biotechnology
·
2018
·
IF 3.026
Shuai Mao,Lei Wang,Peipei Chen,Yong Lan,Rui Guo,Minzhou Zhang
Our previous works have shown that tanshinone IIA inhibited maladaptive extracellular matrix remodeling in cardiac fibroblasts implicating its potential role in treating of pathologic cardiac remodeling. However, the intrinsically poor solubility and bioavailability of tanshinone IIA hindered its clinical application. Here we develop monomethoxy-poly (ethylene glycol)-poly (lactic acid)-D-α-Tocopheryl polyethylene glycol 1000 succinate (mPEG-PLA-TPGS) nanoparticle incorporating tanshinone IIA (tanshinone IIA-NPs) and study its efficacy in post-infarction left ventricular (LV) remodeling. Male C57BL/6 mice underwent left coronary artery ligation followed by subsequent intravenously injected tanshinone IIA-NPs therapy for 5 consecutive days. Treatment with tanshinone IIA-NP improved cardiac function, limited infarct expansion, and prevented left ventricle dilation at 4 weeks post-MI. Furthermore, cardiomyocytes inflammation, apoptosis and myocardial fibrosis were significantly attenuated in tanshinone IIA-NP treated mice. These effects also correlated with inhibition of IκB protein phosphorylation and NF-κB activation, leading to suppression of proinflammatory cytokine expression. Together, these results demonstrate tanshinone IIA-NP attenuated adverse cardiac remodeling and dysfunction mediated through prevention of IκB phosphorylation and NF-κB activation. Tanshinone IIA-NP is a novel approach to treat myocardial IR injury in patients with MI.
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INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
·
2018
·Vol. 42
·期 3
·1473-1483
·
IF 2.784
Jun Fu,Luhua Yu,Jie Luo,Rui Huo,Bing Zhu
The purpose of the present study was to analyze the association between paeonol and the known genes related to gastric cancer (GC) using bioinformatics methods, and to investigate the role of paeonol in the potential impact on the nuclear factor‑κB (NF‑κB) signaling pathway, in order to provide a theoretical basis for further elucidating the effect of paeonol on cancer cells. Cell viability, morphology and apoptosis were detected using an MTT assay, an inverted microscope, and flow cytometry, respectively. The correlation between drugs and genes was analyzed using the Search Tool for Interactions of Chemicals (STITCH) gene‑drug interaction network. The expression levels of related mRNA and proteins were determined using reverse transcription‑quantitative polymerase chain reaction analysis and enzyme‑linked immunosorbent assay. The changes in protein expression were examined using western blot analysis. The correlation network between target genes directly affected by paeonol and known GC genes was determined by analyzing the association between the compounds and genes recorded in the STITCH database. The GC‑related epidermal growth factor receptor 2 (ERBB2) gene was at the core position of the paeonol interaction network and may be an important potential target gene for the effect of paeonol on cancer cells. The effect of paeonol on the viability of the SGC‑7901 GC cell line was detected using an MTT assay, which showed that the inhibitory effect occurred in a time‑ and dose‑dependent manner. The observations of cell morphology demonstrated that the cells were floating, abnormal in shape, had unclear boundaries and were sparse in arrangement following paeonol treatment. Flow cytometry indicated that paeonol significantly accelerated the apoptotic rate of the SGC‑7901 GC cells. The examination of clinical samples suggested that ERBB2 was expressed at a high level in GC samples, and was significantly downregulated following the addition of paeonol. The western blot analysis revealed that downregulating ERBB2 affected the activation of the NF‑κB signaling pathway, thereby upregulating the pro‑apoptotic factor B‑cell lymphoma‑associated X protein. Taken together, paeonol significantly downregulated ERBB2 and inhibited the activation of the NF‑κB signaling pathway, thereby inhibiting the proliferation of SGC‑7901 cells and inducing apoptosis.
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JOURNAL OF ETHNOPHARMACOLOGY
·
2022
·
IF 5.195
Zhenhua Bian,Yuwen Qin,Lin Li,Lianlin Su,Chenghao Fei,Yu Li,Minmin Hu,Xiaowei Chen,Wei Zhang,Chunqin Mao,Xiaohang Yuan,Tulin Lu,De Ji
Ethnopharmacological relevance the fruit of Schisandra chinensis (Turcz.) Baill. (SC) is an important traditional Chinese herbal medicine, which has been widely used in traditional Chinese medicine (TCM) for treating intestinal diseases . It is also traditionally used as health product and medicine in Russia and other countries. However, the effect of SC ethanol extract on anti-ulcerative colitis (UC) has not been systematically studied yet. Aim of the study We investigated the protective effects and underlying action mechanisms of SC extract (SCE) for UC treatment. Materials and methods An animal model of UC induced by dextran sulfate sodium (DSS) was established. After oral administration of SCE, the Disease Activity Index (DAI) was calculated, the length of colon measured, levels of proinflammatory factors determined, and histopathology carried out to assess the therapeutic efficacy of SCE on UC. The effects of SCE on the toll-like receptor 4/nuclear factor-kappa B/nucleotide-binding and oligomerization domain-like receptor family pyrin domain containing 3 inflammasome (TLR4/NF-κB/NLRP3 inflammasome) signaling pathway were evaluated by western blotting . High-throughput sequencing was done to reveal the effect of SCE on the change of the gut microbiota (GM) in mice with DSS-induced colitis. Results SCE significantly reduced the DAI score, restored colon-length shortening, and ameliorated colonic histopathologic injury in mice with DSS-induced colitis. SCE inhibited the inflammatory response by regulating the TLR4/NF-κB/NLRP3 inflammasome pathway in mice with UC. SCE also maintained gut barrier function by increasing the levels of zonula occludens (ZO)-1 and occludin . 16S rRNA sequencing showed that SCE could reverse the GM imbalance caused by UC. Conclusions SCE can ameliorate DSS-induced colitis, and that its effects might be associated with suppression of the TLR4/NF-κB/NLRP3 inflammasome pathway and GM regulation, which may provide significant supports for the development of potential candidates for UC treatment.
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Journal of Essential Oil Bearing Plants
·
2020
·
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.
研究领域:
药理学
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植物化学
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炎症研究
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CELL BIOLOGY INTERNATIONAL
·
2026
·Vol. 50
·期 8
·e70195
·
IF 3.5
Cheng Zhang,Fei Lu,Ting Ye,Yueping Jin,Yunpeng Qin,Kairui Wu,Kai Liu,Xuncui Wang,Hang Song,Xuejun Li
Chronic atrophic gastritis (CAG) with intestinal metaplasia (IM) is a key precancerous lesion that may progress to intestinal‐type gastric adenocarcinoma. Piwei Peiyuan Pill (PPP) has shown significant clinical efficacy in ameliorating CAG with IM, but its active components and underlying mechanisms remain unclear. High‐performance liquid chromatography (HPLC) and ultra‐high performance liquid chromatography coupled with high‐resolution mass spectrometry (UHPLC‐HRMS) were used to identify the components of PPP and the active ingredients in PPP‐containing serum. The therapeutic efficacy and potential mechanisms of PPP were further investigated via transcriptomic sequencing and experimental validation. UHPLC‐HRMS analysis of PPP‐containing serum identified several bioactive components, including esculin, lithospermic acid, and atractylenolide III. In CAG rats, PPP significantly ameliorated gastric mucosal damage and reduced serum IL‐6 and TNF‐α levels. Transcriptomic results showed that IRAK1 was highly expressed in CAG patients with IM and associated with activation of the NF‐κB pathway. PPP intervention dose‐dependently suppressed hyperactivation of the Pellino1/IRAK1/NF‐κB axis and decreased the expression of intestinal metaplasia markers CDX1 and MUC2. Additionally, PPP improved immune function by increasing the proportion of CD4 + T cells and decreasing the proportion of CD8 + T cells in CAG model rats. Taken together, these findings suggest that PPP mitigates CAG and attenuates IM at least in part by suppressing the Pellino1/IRAK1/NF‐κB signaling pathway, indicating that it may serve as a promising therapeutic strategy for reducing inflammation‐associated gastric carcinogenesis.
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Pharmaceuticals
·
2026
·Vol. 19
·期 2
·275
·
IF 5.7
Zhongnan Hu,Hui Liu,Weihua Wu,Tayyab Ali,Adam Junka,Farukh S. Sharopov,Xuan Zou,Shisong Fang,Yanfang Sun
Background: Influenza A virus is an acute respiratory virus that spreads quickly, affects a broad range of populations, and can lead to many complications and mortality.ArtemisiaL. species are widely used in traditional medicine, but their antiviral potential against H1N1 remains uncertain.Methodology: Network pharmacology and molecular docking were used to computationally explore their potential function in this domain, and to investigate how their invasion mechanisms and adsorption occur. UPLC-MS/MS analysis identified the main components of the extracts. The anti-H1N1 mechanism ofArtemisiaL. extracts was studied in vitro.Results: Network pharmacology identified 95 key targets betweenArtemisiaL. and IAV, with quercetin and luteolin as core active compounds. Molecular docking predicted strong binding affinities between these compounds and influenza virus proteins. UPLC-MS/MS analysis identified 75, 100, and 64 chemical components inACBE,AALE, andACTE, respectively, mainly flavonoids and terpenoids.ArtemisiaL. extracts exhibited both preventive and therapeutic effects against H1N1, reducing progeny virus NP mRNA and protein levels. In vitro experiments showed that higher concentrations of the extracts prevent virus attachment to MDCK cells by denaturing the HA protein. NA plays an essential role in progeny virus release. We found that a high concentration of ACTE can inhibit NA up to 85%, and ACBE showed a low inhibitory effect on NA.Conclusions: In terms of therapeutic effects,ArtemisiaL. extracts can regulate intracellular inflammatory factors via the TLR4/NF-κB/MyD88 signaling pathways and reduce the expression of IL-1β, IL-6, TNF-α, TLR4, NF-κB, p65, and MyD88 at the mRNA level, thereby inhibiting H1N1 virus replication. These results suggest that bioactive components inArtemisiaL. extracts may inhibit H1N1, potentially leading to the development of natural-product-based anti-influenza agents.
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NATURAL PRODUCT RESEARCH
·
2026
·
IF 1.8
Lin Zhang,Guanke Liu,Bingyang Zhang,Shiqing Song,Xiao Liu,Tie Yao,Feng Qiu,Feng Zhao
Two new secoiridoid glycosides, gentscaside A (1) and gentscaside B (2), were isolated along with three known compounds gentiopicroside (3), rindoside (4), gentiotrifloroside (5), from the Rhizomes of Gentiana scabra. The structures of the new compounds were determined by comprehensive NMR analysis, and their absolute configurations were determined on the basis of detailed spectroscopic analyses and acidic hydrolysis. The five compounds were evaluated for their anti-inflammatory activity (NO inhibitory activity in LPS-stimulated macrophages). Compounds 1, 4 and 5 showed significant inhibitory effects on LPS-induced NO release in RAW 264.7 cells. The IC50 values are 2.15 μM, 3.02 μM and 6.87 μM, respectively. Additionally, the potential anti-inflammatory mechanism of the active new compound 1 was explored.
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EUROPEAN JOURNAL OF PHARMACOLOGY
·
2026
·
IF 5.7
Hui Zhang,Qimei Yun,Zezhou Xu,Yifan Wang,Xianzhi Zhou,Ling Deng,Binsheng He
Neuroinflammation plays an essential role in neurological dysfunction in cerebral ischemia and reperfusion injury. Understanding the molecular network associated with neuroinflammation will provide potential targets for the neuroprotective treatment of ischemic stroke. An ischemia/reperfusion (I/R) rat model was established by middle cerebral artery occlusion (MCAO) and verified by laser speckle imaging and neurological function scoring. The ipsilateral cortex was analyzed using transcriptomic sequencing. The resulting transcriptomic dataset was combined with the ischemic stroke-associated C0948008 dataset from DisGeNet to screen differentially expressed genes (DEGs). Protein‒protein interaction (PPI) analysis was performed on DEGs associated with the inflammatory response. The candidate genes were verified using Western blotting or ELISA. I/R rats were subsequently treated with the TLR4 inhibitor TAK-242 to investigate the role of the TLR4/SYK/NF-κB pathway in neuroinflammation during ischemic stroke. A total of 264 genes were identified, most of which were enriched in inflammatory response pathways. PPI analysis of the DEGs associated with the inflammatory response revealed a total of three mutually interacting gene clusters, with TLR4, SYK, and NF-κB serving as the hub genes. The expression of proteins in the TLR4/SYK/NF-κB pathway and inflammatory cytokines significantly upregulated the I/R rats, whereas the trends were dramatically reversed by TAK-242. In addition, TAK-242 efficiently decreased the infarct area, improved neurological function, alleviated poststroke cognitive impairment (PSCI), recovered neuronal viability, and inhibited the overactivation of microglia and astrocytes. These data suggest that the TLR4/SYK/NF-κB pathway plays an important role in neuroinflammation and provide potential targets for neuroprotective therapy for ischemic stroke.
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CARBOHYDRATE POLYMERS
·
2026
·
IF 13.2
Shengyu Li,Yuting Pan,Gang Wang,Jintao Fang,Jingwei Wang,Youqi Ji,Zhenhao Dong,Ping Ling,Xianghou Zheng,Yao Gao,Qing Xia,Xia Liu,Wei Zhang
Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease characterized by large-intestinal mucosal ulceration and persistent inflammation, which manifests as bloody diarrhea and abdominal pain and may elevate colorectal cancer risk. Polysaccharide-based hydrogels are attractive candidates for local rectal therapy of UC owing to favorable biocompatibility; however, their therapeutic performance is compromised by short lesion residence time caused by continuous intestinal peristalsis. Herein, we fabricated a muco-adaptive multifunctional hydrogel (B-ODT/CM@PF) constructed via dual-dynamic cross-linking of boronate-diol ester bonds and Schiff-base imine bonds for local treatment of UC. The carboxymethyl chitosan component contributes to rapid local hemostasis and epithelial barrier repair, whereas boron-complexed oxidized dextran confers broad-spectrum bactericidal capacity by disrupting bacterial membrane integrity. Benefiting from boronate-diol interactions, paeoniflorin (PF) is anchored within hydrogel networks to realize inflammation-triggered sustained release. The released PF targets the TLR4-NF-κB signaling axis to drive macrophage M2 polarization and mitigate excessive intestinal inflammatory responses. Moreover, B-ODT/CM@PF rescues the integrity of the intestinal mucosal barrier by inhibiting MLCK activation and preserving tight-junction proteins expression, further ameliorating colitis manifestations. Collectively, this dual-crosslinked bioadhesive hydrogel achieves synergistic functions including mucosal adhesion, hemostasis, antibacterial activity, immunomodulation and barrier reconstruction, providing a promising strategy for local treatment of UC.
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Frontiers in Immunology
·
2026
·
IF 7
Bingliang Zhou,Xiangshun Meng,Zhengying Yu,Bao Zhang,Wei Zhao,Lei Wang,Liang Peng,Jinhu Zou,Jingyu Chen,Xu Lin,Xuefeng Gao,Sheng-He Huang,Hong Cao
IntroductionIbeA is a critical virulence factor that is present in the GimA island in Escherichia coli (E. coli) K1, the most common cause of Gram-negative bacterial meningitis in newborns. IbeA has multiple virulence functions, including adhesion, invasion, and biofilm formation in the pathogenesis of E. coli K1 meningitis. However, it is unclear how IbeA coordinates its role in bacterial adhesion, invasion, and biofilm formation during crossing the blood-brain barrier (BBB).MethodsAn isogenic ibeA deletion mutant (ZD1) was generated from the neonatal meningitis–associated E. coli K1 strain E44. To define IbeA-mediated virulence, bacterial adhesion, invasion, and biofilm formation were quantified in human brain microvascular endothelial cells (HBMECs) using TEER, confocal imaging, and crystal violet assays. A neonatal rat meningitis model evaluated bacterial dissemination, BBB disruption, neuroinflammation, and neurological deficits. Mechanistic studies focused on Vimentin (VIM) dynamics using lipid-raft fractionation, cytoskeleton extraction, immunofluorescence, vimentin-knockout (Vim-KO) HBMEC and Co-immunoprecipitation to assess its redistribution, post-translational modifications, and interaction with NF-κB. The functional involvement of the IbeA–VIM–NF-κB signaling pathway was further examined by modulating VIM activity with glatiramer acetate (GA) in both in vitro and in vivo experiments.ResultsDeletion of ibeA and VIM significantly impaired bacterial adhesion, invasion, and biofilm formation both on HBMECs and on abiotic surfaces. In neonatal rats, infection with ZD1 resulted in higher survival rates, milder neurological symptoms, and a marked reduction of biofilm structures within the cerebral microvasculature compared with infection by the wild-type strain. IbeA-triggered post-translational modifications and cytoplasmic mobilization of VIM drive its nuclear translocation, which in turn activates NF-κB signaling. Pharmacological inhibition of VIM with GA disrupted IbeA-mediated virulence, lowering bacterial loads in the blood and alleviating neurological injury.ConclusionsIbeA is a key virulence factor that coordinates E. coli K1 adhesion, invasion, and biofilm formation by activating the VIM–NF-κB signaling pathway. Our study establishes for the first time a direct mechanistic link between IbeA’s multiple virulence functions through the above signaling pathway leading to acute BBB disruption and meningitis and identify GA as a potential drug development candidate for this disease.
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Antioxidants
·
2026
·Vol. 15
·期 8
·970
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IF 8.2
Xiaofen Li,Yinju Zhang,Wenxia Dai,Ming Xia,Lang Zhou
Acute myocardial ischemia (AMI) is a life-threatening cardiovascular disorder characterized by excessive oxidative stress and persistent inflammatory cascades, yet safe multi-target natural therapeutic agents remain scarce.Cinnamomum migaois a well-known Miao ethnic medicine used for cardiovascular conditions, yet its cardioprotective effects and mechanisms remain largely unclear. This study investigated the efficacy and underlying mechanism ofC. migaoethyl acetate extract (MGE) against AMI. MGE significantly improved the viability of H9c2 cardiomyocytes subjected to OGD/R injured. UPLC-MS/MS and molecular networking identified 30 constituents in MGE, among which sesquiterpenoids predominated. In ISO-induced AMI rats, MGE dose-dependently mitigated myocardial injury, as reflected by reduced ST-segment elevation, serum CK-MB and LDH levels, and alleviated histopathological damage. MGE enhanced SOD and CAT activities, decreased MDA content, and inhibited the secretion of TNF-α, IL-6 and IL-1β. Mechanistically, MGE downregulated the expression of NOX4, HIF-1α, p38 MAPK and NF-κB p65, while activating the Nrf2/HO-1 pathway. Oxyphyllenone A and magnodelavin C were identified as key active sesquiterpenoids that stably bound to IL-17 and TNF. Collectively, MGE alleviates AMI injury via anti-oxidative, anti-hypoxic, and anti-inflammatory effects through modulation of the HIF-1α/Nrf2/NF-κB/MAPK axis downstream of oxidative stress, with sesquiterpenoids serving as its key bioactive components. This work provides robust experimental evidence supportingC. migaoas a promising natural antioxidant candidate for the prevention and treatment of AMI.
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