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CHEMICAL ENGINEERING JOURNAL · 2025 · IF 13.2

Solar-driven Mn-Co3O4/NF dual-function evaporator integrating hydrovoltaic–galvanic effects for enhanced desalination and power generation

Ziyi Wang,Yuqian Zhang,Chengping Li,Liang Wang,Ting Bian,Shitan Yan,Kuzmin Anton,Liuting Zhang

Incorporating solar steam generation with the hydrovoltaic effect presents a promising approach to concurrently addressing water scarcity and energy challenges. However, realizing a high water evaporation rate while simultaneously maintaining substantial electrical output in a single device remains a formidable obstacle. Here, this study presents a novel hydrovoltaic and galvanic effects-coupled evaporation platform (HGEP) for dual-function applications in freshwater production and electricity generation from seawater. Coating urchin-like Mn-doped Co 3 O 4 on inclined nickel foam (NF), the system achieves a stable evaporation rate of 1.77 kg m −2 h −1 in 3.5 wt% brine under 1 kW m −2 irradiation with a 30° tilt angle. The inclined structure facilitates unidirectional ion transport by establishing a salinity gradient, effectively preventing salt deposition for up to 8 h. Moreover, integrating Zr-Al electrodes effectively combines the hydrovoltaic and galvanic effects, enabling the HGEP to deliver a stable open-circuit voltage of 1.0 V and a short-circuit current of 1.5 mA—over an order of magnitude higher than the pure hydrovoltaic effect (0.49 V, 0.15 mA)—and achieve a maximum power density of 0.8 W m −2 . This study presents an innovative solar-powered water treatment technology that simultaneously achieves water production and power generation

研究领域: 材料科学 · 能源技术 · 环境工程
✓ 已验证 DOI 高影响因子
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ENVIRONMENTAL POLLUTION · 2025 · IF 7.3

6-PPD triggered lipid metabolism disorder and inflammatory response in larval zebrafish (Danio rerio) by regulating PPARγ/NF-κB pathway

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 · 分子生物学 · 发育生物学 · 免疫学
✓ 已验证 DOI PubMed 高影响因子
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JOURNAL OF ETHNOPHARMACOLOGY · 2023 · IF 5.4

Mongolian medicine Wenguanmu ointment treats eczema by inhibiting the CKLF-1/NF-κB pathway

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 · 药理学 · 免疫学 · 分子生物学 · 中医药
✓ 已验证 DOI PubMed 高影响因子
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ACTA PHARMACOLOGICA SINICA · 2020 ·Vol. 41 ·期 9 ·1208-1222 · IF 5.064

Cinnamaldehyde protects against rat intestinal ischemia/reperfusion injuries by synergistic inhibition of NF-κB and p53

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.

CAS / MDL: 104-55-2
研究领域: 药理学 · 分子生物学 · 细胞生物学 · 病理生理学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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PULMONARY PHARMACOLOGY & THERAPEUTICS · 2020 · IF 2.681

Bergenin-activated SIRT1 inhibits TNF-α-induced proinflammatory response by blocking the NF-κB signaling pathway

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.

CAS / MDL: 477-90-7
研究领域: 药理学 · 免疫学 · 细胞生物学 · 呼吸医学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES · 2022 ·Vol. 23 ·期 22 ·14024 · IF 6.208

Methyl Gallate Alleviates Acute Ulcerative Colitis by Modulating Gut Microbiota and Inhibiting TLR4/NF-κB Pathway

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

CAS / MDL: 7439-95-4
研究领域: 药理学 · 免疫学 · 微生物学 · 胃肠病学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Experimental and Therapeutic Medicine · 2017 ·Vol. 14 ·期 6 ·5445-5451 · IF 1.261

Paeoniflorin inhibits proliferation of endometrial cancer cells via activating MAPK and NF‑κB signaling pathways

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.

CAS / MDL: 51-21-8 23180-57-6
研究领域: 肿瘤学 · 药理学 · 细胞生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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EUROPEAN JOURNAL OF NUTRITION · 2024 ·Vol. 64 ·期 1 ·1-13 · IF 4.1

Xanthohumol ameliorates dextran sodium sulfate-induced colitis in mice by inhibiting of NF-κB signaling pathways and modulating intestinal microbiota

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

CAS / MDL: 6754-58-1
研究领域: 药理学 · 免疫学 · 胃肠病学 · 微生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE · 2024 · IF 3.3

Antioxidant synergistic anti-inflammatory effect in the MAPK/NF-κB pathway of peptide KGEYNK (KK-6) from giant salamander (Andrias davidianus)

Jun-qi Zhan,Jun-xin Wu,Jing-jing Fu,Gao-shang Li,Fang Wu,Yue-wen Chen

BACKGROUND Giant salamander protein peptide is a peptide with rich functional properties. Giant salamander protein peptide KGEYNK (KK-6) is a peptide with both antioxidant and anti-inflammatory properties. The antioxidant and anti-inflammatory mechanisms of KK-6 are still unclear. When we studied the functional mechanism of KK-6, we found that the antioxidant property of KK-6 has a synergistic and promoting effect on anti-inflammatory properties. RESULTS KK-6 enhances cellular resistance to LPS via the MAPK/NF-κB signaling pathway, leading to increased levels of inflammatory factors: interleukin-1β (764.81 ng mL −1 ), interleukin-6 (1.06 ng mL −1 ) and tumor necrosis factor-α (4440.45 ng mL −1 ). KK-6 demonstrates potent antioxidant properties by activating the Nrf2 signaling pathway, resulting in elevated levels of antioxidant enzymes (glutathione peroxidase: 0.03 μg mL −1 ; superoxide dismutase: 0.589 μg mL −1 ) and a reduction in the concentration of the oxidative product malondialdehyde (967.05 μg mL −1 ). CONCLUSION Our findings highlight the great potential of KK-6, a peptide extracted from giant salamander protein, as a remedy for intestinal inflammation. Through its dual role as an antioxidant and anti-inflammatory agent, KK-6 offers a promising avenue for alleviating inflammation-related damage and oxidative stress. This study lays the foundation for further exploration of giant salamander products and highlights their importance in health and novel food development. © 2024 Society of Chemical Industry.

CAS / MDL: 25126-32-3
研究领域: 生物化学 · 免疫学 · 营养学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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INORGANIC CHEMISTRY · 2024 · IF 4.3

Controlled Hierarchical Construction of Ultrahomogeneous Co9S8@CoAl-LDH/NF Layered Core–Shell Heterostructures for High-Performance Asymmetric Supercapacitors

Yue Yan,Wenrui Wu,Yang Yang,Tao Xu,Xianfu Li

The rational collocation and construction of multiphase composite electrode materials with ingenious structures is a key strategic to enhance the electrochemical performance of supercapacitors (SCs). Within this project, a unique Co9S8@CoAl-LDH/NF core–shell heterostructure consisting of CoAl-LDH/NF ultrathin nanosheets sturdily attached to Co9S8/NF needle-like nanorods is grown in situ on self-supported conductive substrate nickel foam (NF) by an effortless and productive multistep hydrothermal method. The construction of the core–shell structure can effectively enhance the capacitive properties as well as the mechanical strength of the material. Compared with the single-component materials Co9S8/NF (1769.6 mF cm–2 and 91.6%) and CoAl-LDH/NF (858 mF cm–2 and 85.2%), the Co9S8@CoAl-LDH/NF composites have excellent capacitance properties (5052.4 mF cm–2) along with exceptional capacitance retention (5000 cycles) 98.5% even after undergoing charging and discharging. Furthermore, the asymmetric SCs fabricated with Co9S8@CoAl-LDH/NF and AC/NF exhibit an energy density of 0.17 mWh cm–2 at 3.20 mW cm–2. Therefore, the innovative core–shell heterostructure of Co9S8@CoAl-LDH/NF presented in this study holds immense practical potential as a groundbreaking electrode material in the realm of SCs.

CAS / MDL: 7784-27-2
研究领域: 材料科学 · 电化学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES · 2023 ·Vol. 24 ·期 19 ·14771 · IF 5.6

Ursolic Acid Alleviates Neuroinflammation after Intracerebral Hemorrhage by Mediating Microglial Pyroptosis via the NF-κB/NLRP3/GSDMD Pathway

Pan Lei,Zhiyang Li,Qiuwei Hua,Ping Song,Lun Gao,Long Zhou,Qiang Cai

The neuroinflammatory response after intracerebral hemorrhage (ICH) causes a large amount of neuronal loss, and inhibiting the inflammatory response can improve the prognosis. In previous laboratory studies and clinical trials, ursolic acid (UA) inhibited the inflammatory response, but whether it can be administered to inhibit the neuroinflammatory response after cerebral hemorrhage is unknown. The aim of this study was to investigate the effects of ursolic acid after cerebral hemorrhage. Online databases were used to obtain potential therapeutic targets of ursolic acid for the treatment of cerebral hemorrhage, and possible mechanisms were analyzed by KEGG, GO, and molecular docking. A rat model of cerebral hemorrhage was established using collagenase, and an in vitro cerebral hemorrhage model was constructed by adding hemin to BV2 cell culture medium. Enzyme-linked immunosorbent assay (ELISA), Western blotting (WB), immunofluorescence, TUNEL staining, and calcein/PI staining were used to investigate the degree of microglial M1 polarization, changes in the levels of inflammatory factors, activation of the NF-κB pathway, and changes in the indicators of cellular death after ursolic acid treatment. In addition, phorbol 12-myristate 13-acetate (PMA) was used to activate the NF-κB pathway to verify that ursolic acid exerts its anti-neuroinflammatory effects by regulating the NF-κB/NLRP3/GSDMD pathway. Network pharmacology and bioinformatics analyses revealed that ursolic acid may exert its therapeutic effects on cerebral hemorrhage through multiple pathways. Together, in vivo and in vitro experiments showed that ursolic acid inhibited microglial M1 polarization and significantly reduced the levels of p-NF-κB, GSDMD-N, cleaved caspase-1, TNF-α, IL-6, and IL-1β, which were significantly inhibited by the use of PMA. Ursolic acid inhibits microglial pyroptosis via the NF-κB/NLRP3/GSDMD pathway to alleviate neuroinflammatory responses after cerebral hemorrhage.Keywords:ursolic acid;neuroinflammation;cerebral hemorrhage;microglial;pyroptosis

CAS / MDL: 8001-30-7 314-13-6
研究领域: 神经科学 · 药理学 · 分子生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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JOURNAL OF DRUG TARGETING · 2019 · IF 3.277

Artemisinin alleviates atherosclerotic lesion by reducing macrophage inflammation via regulation of AMPK/NF-κB/NLRP3 inflammasomes pathway

Yan Jiang,Hongjiao Du,Xue Liu,Xi Fu,Xiaodong Li,Qian Cao

There is increasing evidence that atherosclerosis is the significant risk factor for cardiovascular diseases, which are the leading causes of morbidity and mortality worldwide. Artemisinin is a natural endoperoxides quiterpene lactone compound in Artemisia annua L with vasculoprotective effects. The primary aim of this study was to investigate whether artemisinin could be conferred an anti-atherosclerotic effect in high-fat diet (HFD)-fed ApoE–/– mice and explore the possible mechanism. We found that treatment with artemisinin (50 and 100 mg/kg) effectively ameliorated atherosclerotic lesions, such as foam cell formation, hyperplasia and fibrosis in the aortic intima. Atherosclerotic mice treated with artemisinin showed reduced inflammation by up-regulating adenosine 5′-monophosphate (AMP) activated protein kinase (AMPK) activation and by down-regulating nuclear factor-κB (NF-κB) phosphorylation and nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome expression in the aortas. In addition, artemisinin was found to promote AMPK activity in macrophages and its anti-inflammatory effect was neutralised by AMPK silence using specific siRNA. In conclusion, we demonstrate that artemisinin may protect the aortas from atherosclerotic lesions by suppression of inflammatory reaction via AMPK/NF-κB/NLRP3 inflammasomes signalling in macrophages.

CAS / MDL: 63968-64-9
研究领域: 心血管疾病 · 药理学 · 分子生物学
✓ 已验证 产品关联 DOI PubMed 高影响因子
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