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Ganoderma lucidum polysaccharide inhibits LPS-induced inflammatory injury to mammary epithelial cells

未来食品学报(英文) 2023年第1期3卷 49-54页

作者： Yi Fan Wei Wang Xuefang Wang Liqin Yu Yue Wei Lei Wei Xiaoyang Xie Xiao Li Key Laboratory of Natural Products Henan Academy of SciencesZhengzhou 450002China Henan Natural Products Biotechnology Co.Ltd. Zhengzhou 450002China Center for Quality Inspection and Testing Henan Academy of SciencesZhengzhou 450002China

This study sought to investigate whether Ganoderma lucidum polysaccharide(GLP)has a protective effect on lipopolysaccharide(LPS)-induced inflammatory injury to mammary epithelial HC-11 cells and to characterize the mechanism *** viability was assessed using the cell counting kit 8(CCK-8)method,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and IL-1βlevels were measured by enzyme linked immunosorbent assay(ELISA),and IκBa,p65 NF-κB and STAT3 mRNA were determined using quantitative reverse transcription PCR(qRT-PCR),p65 and STAT3 protein expression were determined using Western blotting,*** was shown to inhibit LPS-induced TNF-α,IL-6,and IL-1βproduction(Pinflammatory cell injury.

关键词： Ganoderma lucidum polysaccharide Lipopolysaccharide Mouse mammary epithelial cells inflammatory injury

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Passive cigarette smoking induces inflammatory injury in human arterial walls

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Chinese Medical Journal 2009年第4期122卷 444-448页

作者： ZOU Ni HONG Jiang DAI Qiu-yan Department of Geriatric Shanghai Jiao Tong University Affiliated First People's Hospital Shanghai 200080 China Department of Cardiology Shanghai Jiao Tong University Affiliated First People's Hospital Shanghai 200080 China

Background Epidemiological studies have shown that both active and passive cigarette smoking increase the risk of atherosclerosis. But very little is known about the biological processes induced by passive cigarette smoking that contribute to atherosclerosis. We observe the expression of a few of biological and inflammatory markers in human arterial walls in vitro which were treated with the second-hand smoke solution （sidestream whole, SSW）, and discuss the possible mechanism of inflammatory injury induced by second-hand smoke. Methods The biological markers （platelet endothelial cell adhesion molecule-I, PECAM-1; a-smooth muscle actin, a-SMA; collagen IV, Col IV） and inflammatory markers （vascular cell adhesion molecule-1, VCAM-1; monocyte chemoattractant protein-1, MCP-1 ; interleukin-8, IL-8） of human aortat wall were tested by immunofluorescence staining. The levels of MCP-1 and IL-8 mRNA expression were detected by reverse transcription-polymerase chain reaction （RT-PCR）. Results No distinct difference was observed between SSW and the control group on the expression of biological markers as assessed by the light microscope. But the inflammatory markers VCAM-1, MCP-1 and IL-8 on the subendothelial layer and smooth muscle cell layers, which are near the endothelium of arterial wall, were strongly stained in the SSW group compared with the control group. Their fluorescence intensities in the 1：40 SSW group （VCAM-1： 0.35±0.04, MCP-1： 0.34±0.05, IL-8： 0.37±0.05） and the 1：20 SSW group （VCAM-I： 0.40±0.04, MCP-1： 0.52±0.09, IL-8： 0.51±0.07） were significantly stronger than the control group （VCAM-1： 0.12±0.04, MCP-1： 0.06±0.02, IL-8： 0.24±0.03） by semi-quantitative analysis of immunofluorescence （P 〈0.001 vs control）. MCP-1 mRNA expression in the 1：40 SSW （0.15±0.04） and the 1：20 SSW （0.19±0.06） group was significantly higher than in the control group （0.09±0.03）（P 〈0.05, P 〈0.01 vs control）; IL-8 mRNA expression in the 1：40 SSW （0.64±0.12） and 1：20 SSW （0.72±0.

关键词： passive cigarette smoking atherosclerosis inflammatory injury vascular cell adhesion molecule-I monocyte chemoattractant protein-l interleukin-8

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Long non-coding RNA Coro Marker regulates oxidized LDL-induced inflammatory injury via NF-κB/NLRP3 signaling pathway

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South China Journal of Cardiology 2022年第3期23卷 205-214页

作者：刘岗胡洵李怡龙明 Department of Cardiology the First Affiliated HospitalSun Yat-Sen Universityand NHC Key Laboratory ofAssisted Circulation(Sun Yat-Sen University)Guangzhou 510080China

Background Long noncoding RNAs(lnc RNAs) are considered to be important for the development and progression of atherosclerosis. The lnc RNA AC100865.1(referred to as Coro Marker) has been recognized a novel and specific biomarker of coronary artery disease. However, its underlying molecular mechanisms remain ***: The aim of this study was to investigate the implication of Coro Marker in oxidized low-density lipoprotein(ox-LDL)-induced apoptosis and inflammation in THP-1 cells. The regulatory relationship between Coro Marker and the nuclear factor kappa B(NF-κB)/NOD-like receptor protein 3(NLRP3) pathway was also ***: THP-1 cells were stimulated with ox-LDL to induce inflammatory injury. The expression of Coro Marker was silenced by small interfering RNA. Cell apoptosis were assessed by flow cytometry. inflammatory response was determined by detecting levels of inflammatory cytokines using quantitative real-time polymerase chain reaction(q RT-PCR) and enzyme-linked immunosorbent assay(ELISA). Furthermore, western blot was used to assess the expression of NF-κB/NLRP3 signaling pathway-related proteins. Results: Ox-LDL markedly induced cell injury by promoting cell apoptosis, oxidative stress, and inflammation. Meanwhile, the expression of Coro Marker was also up-regulated in ox-LDL-injured THP-1 cells. The knockdown of Coro Marker reduced apoptosis rate and significantly changed the expression levels of apoptosis-related genes(Bax and BCL-2). In addition, knockdown of Coro Marker relieved oxidative stress by significant changes in the level of malondialdehyde, superoxide dismutase, and reactive oxygen species, and attenuated inflammatory injury by inhibit the production of interleukin-1β(IL-1β), IL-6 and tumor necrosis factor alpha(TNF-α). Importantly, the suppression of Coro Marker decreased the expression of NF-κB/NLRP3 signaling pathway-related proteins, including p-NF-κB, p-Ik Bα and ***: This study demonstrated that downreg

关键词： Long noncoding RNA inflammatory injury NF-κB/NLRP3 pathway Atherosclerosis

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Salt-inducible Kinases inhibitor HG-9-91-01 targets RIPK3 kinase activity to alleviate necroptosis-mediated inflammatory injury

Salt-inducible Kinases inhibitor HG-9-91-01 targets RIPK3 ki...

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第十四届全国免疫学学术大会

作者： Mengtao Cao Hanchao Gao Shenzhen Longhua District Central Hospital

Receptor-interacting protein kinase 3(RIPK3) functions as a central regulator of necroptosis,mediating signaling transduction to activate pseudokinase mixed lineage kinase domain-like protein(MLKL) *** evidences show that RIPK3 contributes to the pathologies of inflammatory diseases including multiple sclerosis,infection and ***,we identified a novel small molecular compound Salt-inducible Kinases(SIKs) inhibitor HG-9-91-01 inhibiting necroptosis by targeting RIPK3 kinase *** found that SIKs inhibitor HG-9-91-01 could block TNF-or Toll-like receptors(TLRs)-mediated necroptosis independent of *** revealed that HG-9-91-01 dramatically decreased cellular activation of RIPK3 and ***,HG-9-91-01 inhibited the association of RIPK3 with MLKL and oligomerization of downstream ***,we found that HG-9-91-01 also trigger RIPK3-RIPK1-caspase 8 dependent apoptosis,which activated cleavage of GSDME leading to its dependent *** studies revealed that SIKs inhibitor HG-9-91-01 directly inhibited RIPK3 kinase activity to block necroptosis and interacted with RIPK3 and recruited RIPK1 to activate caspase 8 leading to cleave ***,mice pretreated with HG-9-91-01 showed resistance to TNF-induced systemic inflammatory response ***,HG-9-91-01 treatment protected mice against Staphylococcus aureus-mediated lung damage through targeting RIPK3 kinase ***,our results revealed that SIKs inhibitor HG-9-91-01 is a novel inhibitor of RIPK3 kinase and a potential therapeutic target for the treatment of necroptosis-mediated inflammatory diseases.

关键词： RIPK3 SIKs Necroptosis inflammatory injury

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NF-κB: A novel therapeutic pathway for gastroesophageal reflux disease?

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World Journal of Clinical Cases 2022年第24期10卷 8436-8442页

作者： Mao-Lin Zhang Long-Qing Ran Meng-Jun Wu Qin-Chen Jia Zhi-Ming Qin Yong G Peng Department of Thoracic and Cardiovascular Surgery The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400042China Department of Anesthesia Chengdu Women's and Children's Central HospitalSchool of MedicineUniversity of Electronic Science and Technology of ChinaChengdu 610019China Thoracic and Cardiovascular Surgery The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400042China Department of Anesthesiology University of Florida College of MedicineGainesvilleFL 32610United States

Although gastroesophageal reflux disease(GERD),a common chronic disease in clinical practice,has been widely studied,its potential adverse impact on patients is still a significant clinical *** is necessary to understand the pathogenesis of the disease and choose appropriate treatment according to its *** pathogenesis of GERD is diverse and *** the traditional treatment methods are expensive and ineffective in alleviating symptoms in some patients,new treatment options need to be *** previous study suggested that the activation of nuclear factor-kappa beta(NF-κB)in esophageal mucosa may be related to the injury of epithelial barrier function caused by *** on the literature and our previous study results,it is speculated that inhibition of NF-κB activation may block the insult of GERD on the esophageal mucosal ***-κB may play an important role in the development of *** article reviews the pathogenesis of GERD and the relationship between NF-κB and GERD,in order to provide new strategies for the treatment of GERD.

关键词： Gastroesophageal reflux disease NF-κB Pathogenesis Mechanism inflammatory injury Esophageal epithelial barrier

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The Three Main SCFAs Inhibit the inflammatory Response of A549 Cells Induced by Acinetobacter baumannii

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Journal of Biosciences and Medicines 2022年第4期10卷 114-125页

作者： Shixiang Fu Yue Xi Longkun Ding Man Yan Chang Sun Jun Zhao Yudong Jiao Liang Wu The Third People’s Hospital of Yangzhou Yangzhou China School of Medicine Jiangsu University Zhenjiang China

Objective: The objective is to explore the mechanism of inhibitory effect of three main SCFAs (acetate, propionate and butyrate) on inflammatory response of A549 cells. Methods: Human lung adenocarcinoma cells (A549 cells) were cultured, and were divided into normal control group (NC group), A. baumannii infection group (A. baumannii group), NF-κB inhibitor group (JSH group), A. baumannii infection + sodium acetate group (NaAc group), A. baumannii infection + sodium propionate group (NaPc group) and A. baumannii infection + sodium butyrate group (NaB group). Real-time quantitative PCR was used to detect the mRNA expression of NLRP3, Caspase-1, IL-1β, IL-6, and TGF-β in A549 cells. Western blotting assay was used to determine the expression of autophagy and “pyroptosis” related proteins of NRLP3, cleaved-Caspase-1 (P20), GSDMD (P30), LC-3 and Beclin-1. At the same time, the expression of NF-κB p65 protein in nucleus and cytoplasm of A549 cells was detected. The level of reactive oxygen species in A549 cells was detected by flow cytometry. Results: Compared with A. baumannii group, the mRNA expression of NLRP3, IL-1β and IL-6 in NaAc group, NaPc group and NaB group decreased significantly, the mRNA expression of Caspase-1 in NaPc group and NaB group decreased significantly, only the mRNA expression of TGF-β in NaB group increased significantly;LC3-II expression increased significantly in NaPc group and NaB group, only Beclin-1 expression increased and GSDMD (p30) expression decreased significantly in NaB group. All three kinds of SCFAs could significantly inhibit the expression of cleaved-Caspase-1 (p20) after A. baumannii infection, but there was no significant change in the protein expression of NLRP3. Compared with NC group, the production of reactive oxygen species in A. baumannii group increased significantly at 3 h after A. baumannii infection. Compared with A. baumannii group, NaB could significantly suppress the production of reactive oxygen species induced by

关键词： Acinetobacter baumannii SCFAs A549 Cells inflammatory injury

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NEFAs activate the oxidative stress-mediated NF-κB signaling pathway to induce inflammatory response in calf hepatocytes

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畜牧与饲料科学 2015年第Z1期 342-342页

作者： ZHAO Chenxu WANG Yazhou LIU Huan ZHANG Min LEI Lin DU Xiliang LIU Guowen LI Xinwei College of Veterinary Medicine Jilin University

Non-esterified fatty acids(NEFAs) are important induction factors of inflammatory responses in some metabolic *** plasma levels of NEFAs and oxidative stress exist in the dairy cows with *** aim of this study was to investigate whether high levels of NEFAs can induce inflammatory response and the specific molecular mechanism in the hepatocytes of dairy *** vitro,primary cultured bovine hepatocytes were treated with different concentrations of NEFAs,PDTC(an NF-κB inhibitor) and NAC(an antioxidant).NEFAs significantly activated NF-κB *** NF-κB upregulated the release of pro-inflammatory cytokines,thereby inducing inflammatory response in bovine *** PDTC was added,activation of NF-κBmediated inflammatory response induced by NEFAs was *** treatment results in the overproduction of the markers of oxidative stress,reactive oxygen species(ROS) and malondialdehyde(MDA),which were ameliorated by NAC *** increased ROS and MDA were caused by decreasing activity of antioxidant system,including glutathione peroxidase,superoxide dismutase and catalase,in bovine hepatocytes treated with *** also ameliorated NEFAs-mediated NF-κB activation and the release of pro-inflammatory *** results indicate that high concentrations of NEFAs can induce cattle hepatocytes inflammatory response through activating the oxidative stress-mediated NF-κB signaling pathway.

关键词： non-esterified fatty acids cow ketosis oxidative stress inflammatory injury bovine hepatocytes

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