NEUROSCIENCE LETTERS
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2024
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IF 2.5
Jinyun Long,Xiukuan Li,Chunyan Yao,Xiaoling Liu,Na Li,Yumeng Zhou,Dawei Li,Shengquan Su,Liangmei Wang,Hao Liu,Ying Xiang,Long Yi,Yao Tan,Peng Luo,Tongjian Cai
Lipopolysaccharide (LPS) is an important neurotoxin that can cause inflammatory activation of microglia. ZC3H12D is a novel immunomodulator, which plays a remarkable role in neurological pathologies. It has not been characterized whether ZC3H12D is involved in the regulation of microglial activation. The aim of this study was to investigate the role of ZC3H12D in LPS-induced pro-inflammatory microglial activation and its potential mechanism. To elucidate this, we established animal models of inflammatory injury by intraperitoneal injection of LPS (10 mg/kg). The results of the open-field test showed that LPS caused impaired motor function in mice. Meanwhile, LPS caused pro-inflammatory activation of microglia in the mice cerebral cortex and inhibited the expression of ZC3H12D. We also constructed in vitro inflammatory injury models by treating BV-2 microglia with LPS (0.5 μg/mL). The results showed that down-regulated ZC3H12D expression was associated with LPS-induced pro-inflammatory microglial activation, and further intervention of ZC3H12D expression could inhibited LPS-induced pro-inflammatory activation of microglia. In addition, LPS activated the TLR4-NF-κB signaling pathway, and this process can also be reversed by promoting ZC3H12D expression. At the same time, the addition of resveratrol, a nutrient previously proven to inhibit pro-inflammatory microglial activation, can also reverse this process by increasing the expression of ZC3H12D. Summarized, our data elucidated that ZC3H12D in LPS-induced pro-inflammatory activation of brain microglia via restraining the TLR4-NF-κB pathway. This study may provide a valuable clue for potential therapeutic targets for neuroinflammation-related injuries.
研究领域:
神经科学
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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
Experimental and Therapeutic Medicine
·
2017
·Vol. 14
·期 5
·4174-4180
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IF 1.261
Chuan‑Feng Huang,Wei‑Na Wang,Cheng‑Cao Sun,Yu‑Qing Wang,Ling Li,Yin Li,De‑Jia Li
The present study investigated the role of echinocystic acid (EA) on the expression of nuclear factor (NF)‑κB and cytochrome P450 1A1 (CYP1A1), and aortic morphology, in a rat model of hyperhomocysteinemia (Hhcy). A total of 50 Sprague Dawley rats were randomly divided into five groups as follows: Normal control (NC), model control (MC), vitamin control (VC; folic acid 1 mg/kg + vitamin B2 2 mg/kg + vitamin B12 10u g/kg), EA1 (20 mg/kg EA) and EA2 (40 mg/kg EA). Plasma homocysteine (Hcy) levels were determined via high performance liquid chromatography, and the morphology of the aorta was investigated using hematoxylin and eosin staining. Furthermore, aortic mRNA and protein levels of NF‑κB and CYP1A1 were measured using reverse transcription‑quantitative polymerase chain reaction analysis and western blotting, respectively. Plasma Hcy levels, and aortic mRNA and protein levels of NF‑κB and CYP1A1, were significantly lower in the EA‑treated group compared with the MC group (all P<0.05). However, the aortic morphology remained normal, including the endothelial cells of the inner layer, and smooth muscle cells of the media layer and adventitia. In conclusion, the results of the present study indicate that EA has a protective role on vascular endothelial cells in Hhcy through decreasing plasma Hcy, and thus NF‑κB and CYP1A1 expression.
研究领域:
药理学
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分子生物学
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心血管疾病
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DOI
PubMed
高影响因子
Immunity Inflammation and Disease
·
2023
·Vol. 11
·期 5
·e879
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IF 3.2
Xiuping Zhang,Yuanjing Hu,Zhiping Zhang,Xueluo Zhang,Lixia Liang,Xiangrong Cui,Yuanxia Wu,Fen Hu,Xueqing Wu
Introduction Approximately 50% of cases with recurrent spontaneous abortion (RSA) have unexplained etiology. Aberrant expression of transmembrane and ubiquitin-like domain containing 1 (TMUB1) is closely related to a series of diseases, including RSA. However, the function and underlying mechanism of TMUB1 in the occurrence of RSA has not been described. Methods TMUB1 expression was detected in the placental villous tissues of 30 women with normal miscarriages and 12 women with RSA. The pregnant mice were injected intraperitoneally with lipopolysaccharide (LPS) to induce abortion. Human chorionic trophoblast cells were treated with LPS. Pathological analysis of placental tissues was performed by hematoxylin and eosin staining. Results TMUB1 was highly expressed in the placental villous tissues of RSA patients compared to the patients who underwent induced abortions. After LPS administration, the mice exhibited high embryo absorption and pathological alterations, as well as presented an increase in inflammation and apoptosis (the etiology of RSA induction) in placental tissues. Moreover, the upregulated expression of TMUB1 was also found in placental tissues of LPS-induced mice, and further investigation showed that TMUB1 deficiency blocked embryo loss as well as inhibited apoptotic rate and inflammation after LPS activation. Furthermore, we found that the loss of TMUB1 suppressed the phosphorylation of IkappaB kinase (IKK) α/β and attenuated cytoplasmic-nuclear translocation of nuclear factor-κB (NF-κB) p65 in LPS-induced cells. Conclusion Our results indicate that TMUB1 may involve in the modulation of apoptosis and NF-κB pathway-mediated inflammation in RSA. Therefore, TMUB1 may develop as a potential biomarker for RSA treatment.
研究领域:
妇产科学
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分子生物学
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免疫学
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病理学
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DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Yan Zhou,Tian Wen,Shan Yang,Binru Meng,Jing Wei,Jing Zhang,Lun Wang,Xiaofei Shen
Ethnopharmacological relevance Cichorium intybus is a traditional medicinal herb for hepatitis treatment in China and Europe. Sesquiterpene lactones are the main active ingredients in C. intybus . However, their structure-activity relationship (SAR) and molecular mechanisms of anti-inflammatory and hepatoprotective effects require further elucidation. Aim of the study To identify new sesquiterpene lactones from C. intybus , and further evaluate their anti-inflammatory effects, SAR, and mechanisms of anti-inflammatory and hepatoprotective properties. Methods Identification of sesquiterpene lactones from C. intybus using chromatographic fractionation, NMR, and mass spectrometry. The repression of inflammation was evaluated in RAW264.7 macrophages incubated with LPS. Western blotting was employed to investigate the anti-inflammatory mechanisms. The hepatoprotective effect was measured in LPS/D-galactosamine (D-GalN)-induced acute hepatitis in mice. Results We identified 3 new sesquiterpene lactones and 15 known analogues from C. intybus . SAR analysis showed that the α-methylene-γ-lactone moiety was essential for their anti-inflammatory properties. Furthermore, 8-deoxylactucin was identified as the most potent anti-inflammatory component in LPS-induced RAW264.7 macrophages by reduction of nitric oxide production via inhibiting iNOS expression, and suppression of IL-1β, IL-6, and TNF-α expression. Mechanistically, 8-deoxylactucin not only blocked LPS-induced IKKα/β phosphorylation, IκBα phosphorylation and degradation, and NF-κB nuclear accumulation, but also enhanced NRF2 expression and nuclear translocation, HO-1 and NQO1 expression, and reduced ROS generation in vitro . In vivo , 8-deoxylactucin mitigated LPS/D-GalN-induced acute hepatitis, which manifested as reduction in inflammatory infiltration, live injury, serum levels of AST and ALT, and production of pro-inflammatory cytokines and 4-hydroxynonenal. Conclusion 8-Deoxylactucin, the sesquiterpene lactone isolated from C. intybus , exerted anti-inflammatory and hepatoprotective effects by blocking NF-κB activation and enhancing NRF2 activation.
研究领域:
药理学
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植物化学
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PubMed
高影响因子
Oncology Letters
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2023
·Vol. 25
·期 6
·1-12
·
IF 2.9
Boya Deng,Ailin Li,Ying Zhu,Yingying Zhou,Jing Fei,Yuan Miao
Cervical cancer (CC) is the most common human papillomavirus‑related disease. Continuous activation of the NF‑κB signaling pathway has been observed in CC. SHC binding and spindle associated 1 (SHCBP1) contributes to tumorigenesis and activation of the NF‑κB pathway in multiple cancer types, while its function in CC remains unclear. In the present study, three Gene Expression Omnibus datasets were used to identify differentially expressed genes (DEGs) in CC. Loss‑ and gain‑of‑function experiments were performed using stable SHCBP1‑silenced and SHCBP1‑overexpressing CC cells. To further explore the molecular mechanism of SHCBP1 in CC, small interfering RNA targeting eukaryotic translation initiation factor 5A (EIF5A) was transfected into stable SHCBP1‑overexpressing CC cells. The results demonstrated that SHCBP1 was an upregulated DEG in CC tissues compared with healthy control cervical tissues. Functional experiments revealed the pro‑proliferative and pro‑stemness role of SHCBP1 in CC cells (CaSki and SiHa cells), in vitro. Furthermore, the NF‑κB signaling pathway in CC cells was activated by SHCBP1. Increases in cell proliferation, stemness and activation of NF‑κB, induced by SHCBP1 overexpression in CC cells, were reversed by EIF5A knockdown. Taken together, the results indicated that SHCBP1 serves an important role in regulation of CC cell proliferation, self‑renewal and activation of NF‑κB via EIF5A. The present study demonstrated a potential molecular mechanism underlying the progression of CC.
研究领域:
肿瘤学
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分子生物学
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细胞生物学
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2023
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IF 5.4
Li Zhu,Xiao-jia Li,Chao Gu,Yuan Gao,Chun-sheng Zhang,Lu-yu Wang,Nai-hong Chen,Gang Li
Ethnopharmacological relevance The main clinical manifestations of eczema include itching, erythema, swelling and pain. Currently, allergies and TH1/TH2 cytokine imbalances are significant causes of eczema. TCM believes that eczema is mainly caused by incongruity between dry and wet. Wenguanmu ointment is a classic Mongolian medicine, which mainly composed of Xanthoceras sorbifolia Bunge , Coptis chinensis Franch and Bezoar. These ingredients can clear heat and dampness, dispel wind and dehumidification, anti-inflammatoryad analgesic. In this study, it was found that Wenguanmu ointment can treat eczema with anti-inflammatory, analgesic and antipruritic. Aim of the study In this study, the content of main components in Wenguanmu ointment was tested. Moreover, the therapeutic effect and mechanism of Wenguanmu ointment on eczema model mice were studied. Materials and methods Kunming mice (25 ± 2 g) were randomly divided into 6 groups: Control group; Model group; Vehicle group; Wenguanmu ointment group; Compound dexamethasone acetate cream group; Chushizhiyang ointment group. The eczema mouse model was established by DNCB. HPLC and TLC tests were used to determine the content of the main components in Wenguanmu ointment. HE staining was used to assess skin damage in mice. In order to detect the anti-inflammatory effect of Wenguanmu ointment on eczema, The levels of IgE, TNF-α, IFN-γ, COX-2 and IL-4 in serum was measured by ELISA. Genecards and Online Mendelian Inheritance in Man databases were used to analyze potential target gene predictions, and it was speculated that Wenguanmu ointment was associated with NF−κB signaling pathway and chemokine signaling pathway. To detect this inference, RT-qPCR and western blotting were used to detect protein and mRNA levels of CKLF-1, IκB-α, and NF-κB. Results Wenguanmu ointment can repress the symptoms of eczema caused by 2, 4-dinitrochlorobenzene, and inhibit the level of serum immunoglobulin E. Simultaneously it restrain the elevation of miscellaneous pro-inflammatory cytokines and chemokines, as well as reducing the expression of CKLF-1 and NF-κB protein in the nucleus, and increasing the protein expression of IκB to improve eczema. Conclusions The ameliorating effect of Wenguanmu ointment on eczema lesions can play a importment role by inhibiting the CKLF-1/NF-κB pathway.
研究领域:
民族药理学
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药理学
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免疫学
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分子生物学
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中医药
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DOI
PubMed
高影响因子
ACTA PHARMACOLOGICA SINICA
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2020
·Vol. 41
·期 9
·1208-1222
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IF 5.064
Almoiliqy Marwan,Wen Jin,Xu Bin,Sun Yu-chao,Lian Meng-qiao,Li Yan-li,Qaed Eskandar,Al-Azab Mahmoud,Chen Da-peng,Shopit Abdullah,Wang Li,Sun Peng-yuan,Lin Yuan
Our preliminary study shows that cinnamaldehyde (CA) could protect against intestinal ischemia/reperfusion (I/R) injuries, in which p53 and NF-κB p65 play a synergistic role. In this study, we conducted in vivo and in vitro experiments to verify this proposal. SD rats were pretreated with CA (10 or 40 mg · kg −1 · d −1 , ig) for 3 days, then subjected to 1 h mesenteric ischemia followed by 2 h reperfusion. CA pretreatment dose-dependently ameliorated morphological damage and reduced inflammation evidenced by decreased TNF-α, IL-1β, and IL-6 levels and MPO activity in I/R-treated intestinal tissues. CA pretreatment also attenuated oxidative stress through restoring SOD, GSH, LDH, and MDA levels in I/R-treated intestinal tissues. Furthermore, CA pretreatment significantly reduced the expression of inflammation/apoptosis-related NF-κB p65, IKKβ, IK-α, and NF-κB p50, and downregulated apoptotic protein expression including p53, Bax, caspase-9 and caspase-3, and restoring Bcl-2, in I/R-treated intestinal tissues. We pretreated IEC-6 cells in vitro with CA for 24 h, followed by 4 h hypoxia and 3 h reoxygenation (H/R) incubation. Pretreatment with CA (3.125, 6.25, and 12.5 μmol · L −1 ) significantly reversed H/R-induced reduction of IEC-6 cell viability. CA pretreatment significantly suppressed oxidative stress, NF-κB activation and apoptosis in H/R-treated IEC-6 cells. Moreover, CA pretreatment significantly reversed mitochondrial dysfunction in H/R-treated IEC-6 cells. CA pretreatment inhibited the nuclear translocation of p53 and NF-κB p65 in H/R-treated IEC-6 cells. Double knockdown or overexpression of p53 and NF-κB p65 caused a synergistic reduction or elevation of p53 compared with knockdown or overexpression of p53 or NF-κB p65 alone. In H/R-treated IEC-6 cells with double knockdown or overexpression of NF-κB p65 and p53, CA pretreatment caused neither further decrease nor increase of NF-κB p65 or p53 expression, suggesting that CA-induced synergistic inhibition on both NF-κB and p53 played a key role in ameliorating intestinal I/R injuries. Finally, we used immunoprecipitation assay to demonstrate an interaction between p53 and NF-κB p65, showing the basis for CA-induced synergistic inhibition. Our results provide valuable information for further studies.
研究领域:
药理学
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分子生物学
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细胞生物学
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病理生理学
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PubMed
高影响因子
PULMONARY PHARMACOLOGY & THERAPEUTICS
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2020
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IF 2.681
Min Chen,Cuifen Chen,Yun Gao,Dongming Li,Dan Huang,Ziyu Chen,Xuanna Zhao,Qiu Huang,Dong Wu,Tianwen Lai,Guomei Su,Bin Wu,Beixian Zhou
Background Bergenin , a type of polyphenol compound, exhibits antiulcerogenic, anti-inflammatory, antitussive , and burn wound-healing properties. However, its therapeutic effect on tumor necrosis factor α (TNF-α)-induced proinflammatory responses in the airway and potential mechanisms of actions are still unclear. This study aimed to investigate the anti-inflammatory effects and mechanism of bergenin in TNF-α-stimulated human bronchial epithelial (16-HBE) cells. Methods Cell Counting Kit-8 was used to evaluate cytotoxicity. Cytokine expression was analyzed by reverse transcription-quantitative PCR (RT-qPCR) and enzyme-linked immunosorbent assay. Immunofluorescence, western blot , and sirtuin-1 (SIRT1) activity assays were employed to investigate potential molecular mechanisms. Results Bergenin obviously decreased both mRNA and protein expression levels of interleukins 6 and 8 (IL-6 and IL-8) in TNF-α-stimulated 16-HBE cells. Bergenin blocked TNF-α-mediated activation of nuclear factor κB (NF-κB) signaling and NF-κB nuclear translocation. Interestingly, RT-qPCR and western blotting results revealed that bergenin did not affect SIRT1 expression, but significantly increased its activity. Bergenin-mediated SIRT1 activation was further confirmed by results indicating decreased acetylation levels of NF-κB-p65 and p53. Moreover, the inhibitory effects of bergenin on mRNA and protein expression levels of IL-6 and IL-8 were reversed by a SIRT1 inhibitor. In addition, combining bergenin and dexamethasone (DEX) yielded additive effects on the reduction of IL-6 and IL-8 expression. Conclusions These findings demonstrate that bergenin could suppress TNF-α-induced proinflammatory responses by augmenting SIRT1 activity to block the NF-κB signaling pathway , which may provide beneficial effects for the treatment of airway inflammation associated with asthma.
研究领域:
药理学
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免疫学
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细胞生物学
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呼吸医学
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PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
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2022
·Vol. 23
·期 22
·14024
·
IF 6.208
Ping Zhou,Jia Lai,Yueyue Li,Junzhu Deng,Chunling Zhao,Qianqian Huang,Fei Yang,Shuo Yang,Yuesong Wu,Xiaoqin Tang,Feihong Huang,Long Wang,Xinwu Huang,Wenjun Zou,Jianming Wu
Ulcerative colitis (UC) is a complex immune-mediated inflammatory disease. In recent years, the incidence of UC has increased rapidly, however, its exact etiology and mechanism are still unclear. Based on the definite anti-inflammatory and antibacterial activities ofSanguisorba officinalisL., we studied its monomer, methyl gallate (MG). In this study, we employed flow cytometry and detected nitric oxide production, finding MG regulated macrophage polarization and inhibited the expression of proinflammatory cytokines in vitro. MG also exhibited anti-inflammatory activity accompanying with ameliorating body weight loss, improving colon length and histological damage in dextran sulfate sodium-induced UC mice. Meanwhile, transcription sequencing and 16S rRNA sequencing analyzed the key signaling pathways and changes in the gut microbiota of MG for UC treatment, proving that MG could alleviate inflammation by regulating the TLR4/NF-κB pathway in vivo and in vitro. Additionally, MG altered the diversity and composition of the gut microbiota and changed the abundance of metabolic products. In conclusion, our results are the first to demonstrate that MG has obvious therapeutic effects against acute UC, which is related to macrophage polarization, improved intestinal flora dysbiosis and inhibition of TLR4/NF-κB signaling pathway, and MG may be a promising therapeutic agent for UC treatment.Keywords:ulcerative colitis;methyl gallate;gut microbiota;gut immunity;TLR4/NF-κB
研究领域:
药理学
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免疫学
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微生物学
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胃肠病学
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PubMed
高影响因子
Experimental and Therapeutic Medicine
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2017
·Vol. 14
·期 6
·5445-5451
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IF 1.261
Jianxin Zhang,Fengchun Wang,Huali Wang,Yanna Wang,Yan Wu,Hui Xu,Chen Su
Paeoniflorin (PAE), a principal bioactive component of Paeonia lactiflora Pall., appears to have antitumor properties. However, the pharmacological activity of PAE in endometrial cancer and the specific mechanisms have remained largely elusive. The present study aimed to determine the antitumor activity of PAE in the human endometrial cancer cell line RL95‑2 and explore the potential mechanisms. Cell proliferation was assessed to evaluate the antitumor effect of PAE towards RL95‑2 cells via a Cell Counting Kit‑8 assay. Protein expression was examined to investigate changes in the signaling pathways of p38 mitogen‑activated protein kinase (MAPK), c‑Jun N‑terminal kinase (JNK), extracellular signal‑regulated kinase (ERK) and nuclear factor (NF)‑κB in RL95‑2 cells during PAE treatment by western blot analysis. The results revealed that PAE significantly and dose‑ and time‑dependently inhibited the proliferation of RL95‑2 cells. In addition, PAE activated MAPK signaling pathways (p38, JNK and ERK) and the NF‑κB signaling pathway. Furthermore, p38 MAPK and NF‑κB inhibitors (SB203580 and MG‑132, respectively) prevented PAE‑induced proliferative inhibition in RL95‑2 cells. However, ERK and JNK inhibitors (PD98059 and BI‑78D3, respectively) did not produce such an inhibition. In conclusion, the present study demonstrated that PAE exerts its anti‑proliferative activity via activating p38 MAPK and NF‑κB signaling pathways in endometrial cancer cells, providing a potential new drug of choice for endometrial cancer therapy.
研究领域:
肿瘤学
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药理学
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细胞生物学
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DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
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.
研究领域:
环境毒理学
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分子生物学
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发育生物学
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免疫学
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DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF NUTRITION
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2024
·Vol. 64
·期 1
·1-13
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IF 4.1
Han Ning,Li Jie,Li Yangyang,Zhao Feiei,Wang Jun,Ye Peiyu,Zeng Zhenling
Ethnopharmacological relevance Xanthohumol (XN), an isoprenylated flavonoid natural product found only in hops, possesses a variety of biological activities such as anticancer, anti-inflammatory, hepatoprotective, and anti-obesity. Aim of the study The aim of this study was to investigate the effects and mechanisms of XN on the treatment of colitis. Materials and methods First, acute colitis was induced by using distilled water containing 3% DSS for 10 consecutive days. The therapeutic efficacy of XN was assessed by an established DSS-induced mouse colitis model. Subsequently, disease activity index (DAI) and colon length of mice were assessed. The health of the intestines was assessed by histopathological analysis. Inflammatory factors, IL-1β, IL-6, and TNF-α, were detected in colon tissues by ELISA.Finally, mouse intestinal contents were extracted and subjected to 16 S rRNA Sequencing, and the gut microbiota was analysed for Alpha-diversity and Beta-diversity. Results The results showed that XN ameliorated DSS-induced colitis. Furthermore, XN reduced pro-inflammatory cytokine levels such as IL-1β, IL-6, and TNF-α, as well as inhibited the activation of the TLR4/NF-κB pathway, all of which helped to mitigate the inflammatory response. Finally, we also found that XN alleviated intestinal dysbiosis in colitis mice. Conclusion In conclusion, our study demonstrated that XN provides protective effects against colitis, and has the potential to be further explored as a lead compound for the treatment of inflammatory bowel disease (IBD). Graphical
研究领域:
药理学
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免疫学
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胃肠病学
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微生物学
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PubMed
高影响因子
危险品化学品经营许可证（带存储）