JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2024
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IF 5.7
Liuming Xie,Ting Chen,Hong Li,Jindan Xiao,Linchun Wang,Soo-Ki Kim,Zhibing Huang,Jianhua Xie
Inflammatory bowel disease is a major health problem that can lead to prolonged damage to the digestive system. This study investigated the effects of an exopolysaccharide from genistein-stimulated Monascus purpureus (G-EMP) in a mouse model of colitis to clarify its molecular mechanisms and identified its structures. G-EMP (Mw = 56.4 kDa) was primarily consisted of → 4)-α-D-Galp-(1 →, → 2,6)-α-D-Glcp-(1→ and →2)-β-D-Manp-(1 → , with one of the branches being α-D-Manp-(1 →. G-EMP intervention reduced the loss of body weight, degree of colonic damage and shortening, disease activity index scores, and histopathology scores, while restoring goblet cell production and oxidative homeostasis, repairing colonic functions, and regulating inflammatory cytokines. RNA sequencing and Western blot analysis indicated that G-EMP exerts anti-inflammatory properties by suppressing the TLR4/MAPK/NF-κB inflammatory signaling pathway. G-EMP modulated the gut microbiota by improving its diversities, elevating the relative abundances of beneficial bacteria, declining the Firmicutes/Bacteroidota value, and regulating the level of short-chain fatty acids (SCFAs). Correlation analysis demonstrated strong links between SCFAs, gut microbiota, and the inflammatory response, indicating the potential of G-EMP to prevent colitis.
研究领域:
药理学
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微生物学
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免疫学
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胃肠病学
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DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2022
·
IF 5.988
Minjun Yao,Caihua Zhang,Lingzhi Ni,Xiaoxiao Ji,Jianqiao Hong,Yazhou Chen,Jie Wang,Congsun Li,Jiyan Lin,Tingting Lu,Yihao Sheng,Menghao Sun,Mingmin Shi,Chenhe Zhou,Xunzi Cai
Osteoarthritis is a worldwide joint disease caused by abnormal chondrocytic metabolism. However, traditional therapeutic methods aimed at anti-inflammation for early-stage disease are palliative. In the present study, we demonstrated that cepharanthine (CEP), extracted from the plant Stephania cepharantha , exerted protective medicinal efficacy on osteoarthritis for the first time. In our in vitro study, CEP suppressed the elevated expression of matrix metalloproteinases (MMPs), a disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) and inducible nitric oxide synthase (iNOS) stimulated by IL-1β or TNF-α by inhibiting the activation of MAPK and NF-κB signaling pathways, and upregulated the protein expression of aggrecan, collagen II, and Sox9. Also, CEP could reverse the reduced level of cellular autophagy in IL-1β or TNF-α–induced chondrocytes, indicating that the protective effect of CEP on osteoarthritis was achieved by restoring MAPK/NF-κB-mediated autophagy. Furthermore, in a murine OA model, CEP mitigated cartilage degradation and prevented osteoarthritis in the CEP-treated groups versus the OA group. Hence, our results revealed the therapeutic prospect of CEP for anti-osteoarthritic treatment.
研究领域:
药理学
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风湿病学
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细胞生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Antioxidants
·
2021
·Vol. 11
·期 1
·65
·
IF 6.313
Zhi-Yuan Chen,Hui-Wen Xiao,Jia-Li Dong,Yuan Li,Bin Wang,Sai-Jun Fan,Ming Cui
Radiation pneumonia is a common and intractable side effect associated with radiotherapy for chest cancer and involves oxidative stress damage and inflammation, prematurely halting the remedy and reducing the life quality of patients. However, the therapeutic options for the complication have yielded disappointing results in clinical application. Here, we report an effective avenue for fighting against radiation pneumonia. Faecal microbiota transplantation (FMT) reduced radiation pneumonia, scavenged oxidative stress and improved lung function in mouse models. Local chest irradiation shifted the gut bacterial taxonomic proportions, which were preserved by FMT. The level of gut microbiota-derived PGF2α decreased following irradiation but increased after FMT. Experimental mice with PGF2α replenishment, via an oral route, exhibited accumulated PGF2α in faecal pellets, peripheral blood and lung tissues, resulting in the attenuation of inflammatory status of the lung and amelioration of lung respiratory function following local chest irradiation. PGF2α activated the FP/MAPK/NF-κB axis to promote cell proliferation and inhibit apoptosis with radiation challenge; silencing MAPK attenuated the protective effect of PGF2α on radiation-challenged lung cells. Together, our findings pave the way for the clinical treatment of radiotherapy-associated complications and underpin PGF2α as a gut microbiota-produced metabolite.Keywords:radiation pneumonia;gut microbiota;gut-lung axis;gut microbiota metabolites;PGF2α
研究领域:
肿瘤学
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微生物学
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免疫学
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药理学
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DOI
PubMed
高影响因子
Pharmaceuticals
·
2026
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IF 5.7
Xiaoyi Qiu,Lisha Chen,Ting Han,Hongji Wang,Juping Xing,Jiayi Zheng,Changshui Xu
Background/Objectives:Diabetic neuropathic pain (DNP) is a common complication of diabetes characterized by sensory abnormalities, including mechanical allodynia and thermal hyperalgesia. This study aimed to investigate the effects of naringin on experimental DNP and evaluate its association with dorsal root ganglion (DRG) neuronal injury, TRPV1-related calcium imbalance, and inflammatory signaling.Methods:Primary rat DRG neurons were exposed to high-glucose/high-free-fatty-acid (HGHF) conditions (50 mM glucose and 0.60 mM free fatty acids) and treated with naringin (40 or 80 μM). Cell viability, apoptosis, intracellular Ca2+levels, gene/protein expression, and signaling changes were assessed using CCK-8 assay, Annexin V-FITC/PI flow cytometry, Fluo-4 AM imaging, qRT-PCR, and Western blotting. Male Sprague–Dawley rats were fed a high-fat/high-sucrose diet for 4 weeks, injected with streptozotocin (35 mg kg−1), and treated with naringin (50 mg kg−1day−1) by gavage for 2 weeks.Results:HGHF exposure increased neuronal injury, TRPV1 expression, intracellular Ca2+accumulation, and p38 MAPK/NF-κB signaling activation. Naringin attenuated these changes in vitro, with stronger effects observed at 80 μM. In DNP rats, naringin improved pain-related behaviors, partially alleviated metabolic abnormalities, reduced TRPV1 expression and serum IL-1β/TNF-α levels, and decreased phosphorylation of p38 MAPK, NF-κB p65, and ERK in DRGs.Conclusions:Naringin alleviated experimental DNP-associated behavioral and molecular abnormalities, suggesting potential protective effects involving neuronal injury, calcium regulation, and inflammatory responses.
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DOI
高影响因子
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
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2021
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IF 3.228
Jianqing Chen,Bing Shao,Jinliang Wang,Zhiqiang Shen,Honggui Liu,Shu Li
Chlorpyrifos (CPF) is an organophosphate insecticide and can cause cell death of animals. In the study, the common carp were exposed to CPF at 0 μg/L (the control group), 1.16 μg/L (the low dose group), 11.6 μg/L (the medium dose group), and 116 μg/L (the high dose group), respectively. The carp were euthanized at the 30th day and gills were collected immediately. The ultrastructural and histopathological observations showed obvious necrosis characteristics and inflammatory injury in the CPF-treated groups. CPF exposure activated the MAPK pathway, in which the mRNA and protein expressions of extracellular signal-regulated (ERK), p38 MAP kinase (p38), and c-Jun N-terminal kinase (JNK) were increased; the mRNAs and proteins of NF-κB and TNF-α were activated; and the mRNAs and proteins of necroptosis related genes were changed (the mRNA and protein expression of RIPK1 , RIPK3 , MLKL, and FADD were increased and caspase-8 was decreased) with concentration dependency. Taken together, we concluded that CPF exposure activated the MAPK/NF-κB/TNF-α pathway, promoted inflammatory injure and evoked necroptosis in common carp gills. In addition, CPF-induced inflammation and necroptosis was concentration dependency. The toxic effects of CPF on gills provided data for both aquaculture and toxicological studies.
研究领域:
环境毒理学
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鱼类生理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
ONCOLOGY REPORTS
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2016
·Vol. 36
·期 1
·315-323
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IF 2.486
Qiang Liu,Lei Dong,Hong Li,Jia Yuan,Yuping Peng,Shejiao Dai
Bone marrow (BM) suppression (also known as myelosuppression) is the most common and most severe side-effect of therarubicin (THP) and thereby limits the clinical application of this anticancer agent. Lentinan (LNT), a glucan extracted from dried shiitake mushrooms (Lentinula edodes), exhibits a variety of pharmacological activities. The objectives of the present study were to determine the effect of LNT on the myelosuppression of THP-treated mice and to examine the pharmacological mechanism of these effects. In vivo experiments indicated that non-cytotoxic levels of LNT strongly increased blood myeloperoxidase (MPO) activity; improved BM structural injuries; increased the numbers of leukocytes and neutrophils in the blood and BM; elevated the blood levels of granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF); and reduced the self-healing period in THP-treated mice. In vitro experiments indicated that LNT increased the viability of BM-derived macrophages (BMDMs) in a time- and dose-dependent manner without toxic side-effects and markedly increased the release of G-CSF, GM-CSF and M-CSF by BMDMs. Further analyses revealed that LNT activated the NF-κB and MAPK signalling pathways and promoted the nuclear import of p65 and that BAY 11-7082 (a specific inhibitor of NF-κB) suppressed the release of G-CSF, GM-CSF and M-CSF. Furthermore, we found that U0126, SB203580 and SP600125 (specific inhibitors of ERK, p38 and JNK, respectively) markedly inhibited the IKK/IκB/NF-κB-dependent release of G-CSF, GM-CSF and M-CSF. In conclusion, LNT induces the production of G-CSF, GM-CSF and M-CSF by activating the MAPK/NF-κB signalling pathway in BM cells, thereby mitigating THP-induced myelosuppression.
研究领域:
肿瘤学
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药理学
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免疫学
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细胞生物学
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2026
·
IF 5.4
Aoyu Zhang,Shuying Li,Jie Qiao,Chuanqi Zhong,Zhiwen Zhang,Xiguang Ye,Jun Jin,Shiyan Shang,Song Wu,Qing Zhang,Gongxu Yang
Ethnopharmacological relevance The therapeutic effect of Psoralea corylifolia L. on knee joint pain was recorded as early as the Ming Dynasty in the Compendium of Materia Medica, which notes its actions of tonifying the kidney, strengthening tendons, and bones. Isopsoralen (ISO), derived from the Psoralea corylifolia L., has shown efficacy in improving osteoarthritis (OA) in both traditional use and our previous screening, demonstrating effects in alleviating joint inflammation and protecting cartilage. Aim of the study OA is a common disabling disease. Its progression connects local joint pathology to systemic metabolic and inflammatory states, extending to gut microbiota and metabolites. This study examines the therapeutic mechanism of isopsoralen against OA using a DMM-induced model. Materials and methods ISO's targets were predicted by network pharmacology approaches. Therapeutic effects were evaluated through behavioral tests, micro-CT, histology, Western blot, and PCR, while safety was assessed via liver/kidney staining. 16S rDNA sequencing and targeted metabolomics were employed to analyze gut microbiota structure and short-chain fatty acids (SCFAs). Pseudo germ-free mice and fecal microbiota transplantation (FMT) were used to validate the role of gut microbiota. Results Network pharmacology indicated ISO's multi-target action against OA. ISO downregulated the MAPK/NF-κB pathway, attenuated subchondral bone abnormalities, and alleviated joint degeneration in DMM mice. It also modulated gut microbiota composition and SCFA levels. FMT confirmed the essential role of gut microbiota in ISO's efficacy. Furthermore, no hepatorenal toxicity was observed. Conclusion ISO alleviates OA by modulating gut microbiota/SCFAs and inhibiting the MAPK/NF-κB pathway, thereby reducing inflammation and improving bone abnormalities, without hepatorenal toxicity.
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF FOOD BIOCHEMISTRY
·
2026
·Vol. 2026
·期 1
·8438287
·
IF 2.3
Shiying Mai,Liyan Li,Yinfeng Tan,Minghai Fu,Junqing Zhang,Fang Zhang,Yonghui Li,Qi Wang,Yuhuang Wu
Background Lihuabidouyan Tablet is a compound Chinese herb preparation used for the treatment of respiratory diseases. As the main active ingredient in it, Ficus pumila ( F . pumila ) contains polysaccharides that exert unique biological activity. In this study, polysaccharides in F . pumila were extracted and purified, and the protective effect and mechanism of action of F . pumila polysaccharide 1-1 (FPP1-1) in lipopolysaccharide (LPS)-induced acute lung injury (ALI) mice were discussed. Methods BALB/c mice were randomly divided into control, model, dexamethasone (DEX), and FPP-1-1 groups (50, 100, and 200 mg/kg), and the drug was administered by gavage for one week. Hematoxylin–eosin staining (H&E) and wet/dry ratio were used to evaluate lung injury and pulmonary edema. The ELISA was used to detect inflammatory factors. qRT-PCR was used to examine mRNA expression in tissues. Proteins related to inflammation were evaluated by western blotting. 16S rDNA sequencing was used to analyze the gut microbiota. Results FPP-1-1 significantly reduced lung injury in the ALI mice and significantly reduced levels of the proinflammatory factors interleukin (IL)-6 and tumor necrosis (TNF)- α and promoted the anti-inflammatory factor IL-10 in bronchoalveolar lavage fluid. FPP-1-1 inhibited the expression of phospho-ERK1/2, phospho-P38, and phospho-NF- κ B p65 proteins. FPP-1-1 also increased the diversity of the gut microbiota and increased the abundance of Lachnospiraceae in the ALI mice. Correlation analysis results showed that there was a significant correlation between the MAPK/NF- κ B pathway and inflammatory cytokines and gut microbiota in ALI mice. Conclusion The present study characterized the structure and molecular weight of a novel homogeneous polysaccharide, FPP-1-1, isolated from F. pumila . In addition, FPP-1-1 affected the expression of inflammatory factors by inhibiting the MAPK/NF- κ B pathway. FPP-1-1 also restored the diversity of gut microbiota and changed the relative abundance of key bacterial genera such as Lachnospiraceae and Alloprevotella , suggesting that the “gut–lung” axis may serve as a crucial pathway through which FPP-1-1 exerts its effect.
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产品关联
DOI
高影响因子
AQUATIC TOXICOLOGY
·
2022
·
IF 5.202
Xia Zhao,Xu Shi,Qingqing Liu,Xiaojing Li
Overuse of acetochlor pollutes soil and rivers, causing threats to the ecosystem. Studies found that acetochlor exposure could damage multiple organs and tissues in fish and mammal. Tea polyphenols (TP), a natural antioxidant that extracted from tea, has been widely used in food and feed additions. However, the mechanism by which acetochlor causes tissue damage is unclear, and its mitigating agent has yet to be developed. Therefore, we established acetochlor exposure and TP mitigation models by treating Ctenopharyngodon idellus kidney (CIK) cells with 20 μM acetochlor and/or 2.5 μg/mL TP for 24 h, and detected the programmed cell death and its related pathways. The results showed that acetochlor exposure modified antioxidant enzyme activities, induced oxidative stress, resulted in the decline of MMP and ATP levels, enhanced glycolysis and lactate accumulation, and triggered apoptosis and necroptosis in CIK cells. However, TP could inhibit CYP450s expression, activate Nrf2 pathway, enhance antioxidant capacity, further effectively alleviate acetochlor-induced CIK cell death. Overall, the present study proved that acetochlor exposure triggered mitochondrial damage and lactate accumulation-mediated apoptosis and necroptosis through CYP450s/ROS/MAPK/NF-κB pathway. Furthermore, TP could alleviate effectively cell death through relieving oxidative stress and lightening Warburg-like effect.
研究领域:
毒理学
·
细胞生物学
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环境科学
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水生生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2021
·
IF 5.279
Jinwen Yuan,Siyan Che,Li Zhang,Zheng Ruan
Luteolin, a dietary flavonoid, has gained increasing interest as an intestinal protectant. This study aimed to evaluate the reparative effect of luteolin against ethanol-induced intestinal barrier damage in a Caco-2 cell monolayer model and the potential mechanisms. Luteolin attenuated ethanol-induced intestinal barrier injury, by increasing transepithelial monolayer resistance (TEER, 27.75 ± 14.75% of the ethanol group, p < 0.01), reducing Lucifer yellow flux (13.21 ± 1.23% of ethanol group, p < 0.01), and upregulating the expression of tight junction (TJ) proteins zonulin occludin-1 (ZO-1), occludin, and claudin-1 (37.963 ± 8.62%, 17.69 ± 7.35%, and 29.40 ± 8.08% of the ethanol group, respectively, p < 0.01). Further mechanistic studies showed that luteolin suppressed myosin light chain 2 (MLC) phosphorylation, myosin light chain kinase (MLCK) activation, nuclear factor kappa-B (NF-κB) nuclear translocation, and mitogen-activated-protein-kinase (MAPK) phosphorylation. Moreover, luteolin also acted as antioxidants indirectly by upregulating antioxidant-responsive-element (ARE) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation to relieve ethanol-induced oxidative damage and TJ dysfunction. The results of the study indicate that luteolin may play an effective role in relieving intestinal barrier damage, and this effect is at least partially due to its indirect antioxidant capacity.
研究领域:
药理学
·
细胞生物学
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胃肠病学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2024
·
IF 4.8
Ping Chen,Cheng Lin,Qi Jin,Baibai Ye,Xinxu Liu,Keke Wang,Han Zhang,Jiahui Liu,Runan Zhang,Hao Huang,Chenning Zhang,Linfu Li
Ethnopharmacological relevance In TCM opinion, most of pneumonia is related to "lung heat". Sophora davidii (Franch.) Skeels flower was first documented in "Guizhou Herbal Medicine", and was recorded as having functions of clearing heat, detoxifying, and cooling blood. It can be used to treat lung heat cough. Aim of the study To investigate main mechanisms of Sophora davidii flower extract (SDFE) in Treating LPS-induced acute Pneumonia. Materials and methods Acute pneumonia models on BEAS-2B cells and rats were established using LPS. The rat model was used to verified the protective effects of SDFE through HE staining, lung tissue W/D ratio assay, white blood cell count analysis, and ammonia-induced coughing test. Network pharmacology was applied to predict the active compounds, core targets and main pathways of SDFE in treating acute pneumonia. Western Blot and ELISA kits were employed to validate representative proteins in selected pathway in vivo and in vitro . Results HE staining, lung tissue W/D ratio assay, white blood cell count analysis, and ammonia-induced coughing test showed SDFE could improve pathological features (leukocyte infiltration, pulmonary edema, lung injury and cough). Network pharmacology indicated MAPK/NF-κB pathway was the most relevant pathway. SDFE could significantly inhibit the expression of Fos and Jun, and the phosphorylation levels of p38, ERK, JNK, NF-κB and IκB. It also down-regulated the expression of pro-inflammatory factors (TNF-α, IL-6 and IL-1β). Conclusions SDFE can exert protective effects against acute pneumonia through the MAPK/NF-κB signaling pathway.
研究领域:
药理学
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免疫学
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中医药
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分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MOLECULAR NEUROBIOLOGY
·
2025
·
IF 4.3
Wan Yu-hui,Cheng Zeng-jing,Fan Ling-xiang,Yang De-hong,Chen Bing-lin,Chen Xiang-xin,Zhu Qing
Subarachnoid hemorrhage (SAH) is associated with high mortality and morbidity rates. In its early stages, a substantial influx of blood into the subarachnoid space triggers excessive activation of microglia, which markedly contributes to early brain injury (EBI), a pivotal determinant of poor prognosis. Tremella fuciformis polysaccharides (TFPSs), as acidic heteropolysaccharides from the fruiting bodies of Tremella, exhibit robust anti-inflammatory characteristics and many biological properties. Nonetheless, the impact of TFPSs on EBI after SAH has yet to be reported, and the molecular mechanisms underlying these effects remain elusive. We used in vivo and in vitro models to study the effects of TFPSs on microglia post-SAH. Network pharmacology analysis was used to predict the targets of TFPSs and the pathways through which it exerts its therapeutic effects. These predictions were subsequently corroborated through flow cytometry, Western blotting, immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA), and quantitative real‑time polymerase chain reaction, both in vivo and in vitro. After 24 h post-SAH, TFPS-treated mice presented improved neurological function and reduced cerebral edema. TFPSs reversed microglial activation, enhanced phagocytic ability, and reduced neuronal apoptosis. Network pharmacology identified KDR as a potential target of TFPSs, with the P38 MAPK pathway as the downstream pathway. TFPSs attenuated KDR expression, inhibited the P38 MAPK/NF-κB pathway, reduced inflammatory cytokine expression, and increased microglial phagocytic capacity post-SAH. This investigation revealed that TFPSs may ameliorate EBI after SAH, potentially via the regulation of the KDR-mediated P38 MAPK/NF-κB pathway and phagocytic function.
研究领域:
神经科学
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药理学
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分子生物学
✓ 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）