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Chinese Journal of Integrative Medicine 2024年第2期30卷 171-180页

作者： ZHAO Wen-xiao WANG Tong ZHANG Ya-nan CHEN Qian WANG Yuan XING Yan-qing ZHENG Jun DUAN Chen-chen CHEN Lijun ZHAO Hai-jun WANG Shijun School of Nursing Shandong University of Traditional Chinese MedicineShandong University of Traditional Chinese MedicineJi'nan(250355)China Shandong Co-innovation Center of Classic Traditional Chinese Medicine Formula Shandong University of Traditional Chinese MedicineJi'nan(250355)China College of Traditional Chinese Medicine Shandong University of Traditional Chinese MedicineJinan(250355)China

The accumulating evidence revealed that gut microbiota plays an important role in pathological process of disease including obesity,type 2 diabetes mellitus,heart failure,and non-alcoholic fatty liver disease.Polysaccharides extracted from Chinese medicine(CM)can not only alleviate pathological status but also promote health by anti-inflammatory,regulating immunity,lowering blood glucose and lipids,anti-cancer,and anti-oxidation.The alterations of gut microbiota composition and metabolism pathways are the potential mechanisms of CM polysaccharides treatment.In addition,they exert functions through gut-organ axis or play an indirect role by synergistic actions with other drugs or components mediated by gut microbiota.This review summarizes the molecular mechanisms of CM polysaccharides interacted with intestinal microbial inhabitants as potential prebiotics forpromoting health.

关键词： Chinese medicine polysaccharides gut microbiota short-chain fatty acids lipopolysaccharides gut-organaxis synergistic actions

Galacto-oligosaccharides improve barrier function and relieve colonic inflammation via modulating mucosa-associated microbiota composition in lipopolysaccharides-challenged piglets

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Journal of Animal Science and Biotechnology 2022年第1期13卷 240-255页

作者： Ren Gao Shiyi Tian Jing Wang Weiyun Zhu National Center for International Research on Animal Gut Nutrition Jiangsu Key Laboratory of Gastrointestinal Nutrition and Animal HealthNational Experimental Teaching Demonstration Center of Animal ScienceLaboratory of Gastrointestinal MicrobiologyCollege of Animal Science and TechnologyNanjing Agricultural UniversityNanjing 210095China

Background:Galacto-oligosaccharides(GOS)have been shown to modulate the intestinal microbiota of suckling piglets to exert beneficial effects on intestinal function.However,the modulation of intestinal microbiota and intestinal function by GOS in intestinal inflammation injury models has rarely been reported.In this study,we investigated the effects of GOS on the colonic mucosal microbiota composition,barrier function and inflammatory response of lipopolysaccharides(LPS)-challenged suckling piglets.Methods:A total of 18 newborn suckling piglets were divided into three groups,the CON group,the LPS-CON group and the LPS-GOS group.Piglets in the LPS-GOS group were orally fed with 1 g/kg body weight of GOS solution every day.On the d 14,piglets in the LPS-CON and LPS-GOS group were challenged intraperitoneally with LPS solution.All piglets were slaughtered 2 h after intraperitoneal injection and sampled.Results:We found that the colonic mucosa of LPS-challenged piglets was significantly injured and shedding,while the colonic mucosa of the LPS-GOS group piglets maintained its structure.Moreover,GOS significantly reduced the concentration of malondialdehyde(MDA)and the activity of reactive oxygen species(ROS)in the LPS-challenged suckling piglets,and significantly increased the activity of total antioxidant capacity(T-AOC).GOS significantly increased the relative abundance of norank_f_Muribaculaceae and Romboutsia,and significantly decreased the relative abundance of Alloprevotella,Campylobacter and Helicobacter in the colonic mucosa of LPS-challenged suckling piglets.In addition,GOS increased the concentrations of acetate,butyrate and total short chain fatty acids(SCFAs)in the colonic digesta of LPS-challenged suckling piglets.GOS significantly reduced the concentrations of interleukin 1β(IL-1β),interleukin 6(IL-6),tumor necrosis factor-α(TNF-α)and cluster of differentiation 14(CD14),and the relative mRNA expression of Toll-like receptor 4(TLR4)and myeloid differentiation primary response 88(MyD88)in the LPS-challenge

关键词： Barrier function Galacto-oligosaccharides Intestinal microbiota lipopolysaccharides Suckling piglets

Enhanced Expression of Aquaporin-9 in Rat Brain Edema Induced by Bacterial lipopolysaccharides

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2009年第2期29卷 150-155页

作者：王怀立金润铭田培超禚志红 Department of Pediatrics Union HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Pediatrics the First Affiliated Hospital of Zhengzhou University

To investigate the role of AQP9 in brain edema, the expression of AQP9 in an infectious rat brain edema model induced by the injection of lipopolysaccharide （LPS） was examined. Immuno- histochemistry and reverse transcription-polymerase chain reaction （RT-PCR） analysis demonstrated that the expressions of AQP9 mRNA and protein at all observed intervals were significantly increased in LPS-treated animals in comparison with the control animals. Time-course analysis showed that the first signs of blood-brain barrier disruption and the increase of brain water content in LPS-treated animals were evident 6 h after LPS injection, with maximum value appearing at 12 h, which coincided with the expression profiles of AQP9 mRNA and protein in LPS-treated animals. The further correlation analysis revealed strong positive correlations among the brain water content, the disruption of the blood-brain barrier and the enhanced expressions of AQP9 mRNA and protein in LPS-treated animals. These results suggested that the regulation of AQP9 expression may play im- portant roles in water movement and in brain metabolic homeostasis associated with the pathophysi- ology of brain edema induced by LPS injection.

关键词： aquaporins aquaporin-9 lipopolysaccharides infectious brain edema water channels

The effect of lipopolysaccharides on the expression of CD14 and TLR4 in rat Kupffer cells

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Hepatobiliary & Pancreatic Diseases International 2003年第2期2卷 581-585页

作者： Jun-Ming Feng Jing-Quan Shi You-Sheng Liu the Research Institute of Pathology Southwestern Hospital, Third Military Medical University, Chongqing 400038, China Research Institute of Pathology Southwestern Hospital Third Military Medical University Chongqing 400038 China. fjmds@***

OBJECTIVE: To assess the effect of lipopolysaccharides (LPS) on the expression of CD14 and TLR4 in rat Kupffer cells (KCs). METHODS: In rat KCs induced by LPS, the changes of CD14 and TLR4 expression were measured by RT-PCR and immunohistochemistry, and the expressions of TNF-αmRNA, IL-6mRNA or the concentrations of TNF-α, IL-6 were estimated by in situ hybridization, radioimmunoassay, and others. RESULTS: The expressions of CD14 and TLR4 in KCs induced by LPS were markedly increased in a dose-dependent manner (10 mg/L-1μg/L) or in a time-dependent manner (0.5 h-24 h), with the peaked expression of CD14 at 3-6 hours. The expressions of CD14 and TLR4 in KCs stimulated by the active mediators from KCs which had been exposed to LPS for 1 hour were obviously increased. CONCLUSIONS: There is a close relationship between LPS or the active mediators from KCs induced by LPS and the expressions of CD14, TLR4. It is implied that the increase of TLR4, CD14 expression may be induced by LPS within 1--3 hours, and further increase of TLR4, CD14 expression may be correlated with the cytokines produced bv KCs.

关键词： lipopolysaccharides Toll-like receptor TNF interleukin mediator cytokines Kupffer cell

Yajieshaba prevents lipopolysaccharide-induced intestinal barrier injury via anti-inflammatory and anti-apoptosis

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Journal of Traditional Chinese Medicine 2022年第5期42卷 707-714页

作者： YANG Liping YU Xinglin ZHANG Chao CHEN Pu DUAN Xiaohua Yunnan Key Laboratory of Dai and Yi Medicines Yunnan University of Chinese MedicineKunming 650500China

OBJECTIVE: To investigate the protective effect of Yajieshaba(YJSB) on the intestinal barrier dysfunction induced by lipopolysaccharide(LPS).METHODS: C57BL/6 mice and rat intestinal epithelial cells were treated with LPS. Thiazolyl Blue Tetrazolium Bromide assay were used to detect cell viability. DLactate, diamine oxidase and myeloperoxidase and cytokines were determined by enzyme-linked immunosorbent assay. Western blot was used to detect apoptosis-related proteins and tight junction(TJ) proteins. Real-time quantitative polymerase chain reaction was used to quantify the levels of m RNA expression of cytokines. Histological analysis was performed by hematoxylin and eosin staining. An immunofluorescence staining assay was performed to determine the expression level of TJ protein. RESULTS: YJSB increased cell viability and decreased apoptosis, maintained intestinal permeability after LPSinduced. YJSB inhibited LPS-induced decrease of TJ protein expression, pro-inflammatory cytokine levels and neutrophil infiltration. CONCLUSION: YJSB protect against LPS-induced intestinal barrier dysfunction via anti-inflammatory and anti-apoptosis, suggesting its therapeutic potential against intestinal barrier injury-related diseases.

关键词： inflammation apoptosis lipopolysaccharides Yajieshaba intestinal barrier function

Activating transcription factor 4 protects mice against sepsis-induced intestinal injury by regulating gut-resident macrophages differentiation

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Chinese Medical Journal 2022年第21期135卷 2585-2595页

作者： Zhenliang Wen Xi Xiong Dechang Chen Lujing Shao Xiaomeng Tang Xuan Shen Sheng Zhang Sisi Huang Lidi Zhang Yizhu Chen Yucai Zhang Chunxia Wang Jiao Liu Department of Critical Care Medicine Ruijin HospitalShanghai Jiao Tong University School of MedicineShanghai 200025China Department of Critical Care Medicine Shanghai Children’s HospitalShanghai Jiao Tong University School of MedicineShanghai 200062China Institute of Pediatric Infection Immunityand Critical Care MedicineShanghai Children’s HospitalShanghai Jiao Tong University School of MedicineShanghai 200062China Institute of Pediatric Critical Care Shanghai Jiao Tong UniversityShanghai 200062China

Background: Gut-resident macrophages (gMacs) supplemented by monocytes-to-gMacs differentiation play a critical role in maintaining intestinal homeostasis. Activating transcription factor 4 (ATF4) is involved in immune cell differentiation. We therefore set out to investigate the role of ATF4-regulated monocytes-to-gMacs differentiation in sepsis-induced intestinal injury.Methods: Sepsis was induced in C57BL/6 wild type (WT) mice andAtf4-knockdown (Atf4+/-) mice by cecal ligation and puncture or administration of lipopolysaccharide (LPS). Colon, peripheral blood mononuclear cells, sera, lung, liver, and mesenteric lymph nodes were collected for flow cytometry, hematoxylin and eosin staining, immunohistochemistry, quantitative reverse transcription polymerase chain reaction, and enzyme-linked immunosorbent assay, respectively.Results: CD64, CD11b, Ly6C, major histocompatibility complex-II (MHC-II), CX3CR1, Ly6G, and SSC were identified as optimal primary markers for detecting the process of monocytes-to-gMacs differentiation in the colon of WT mice. Monocytes-to-gMacs differentiation was impaired in the colon during sepsis and was associated with decreased expression of ATF4 in P1 (Ly6Chi monocytes), the precursor cells of gMacs.Atf4 knockdown exacerbated the impairment of monocytes-to-gMacs differentiation in response to LPS, resulting in a significant reduction of gMacs in the colon. Furthermore, compared with WT mice,Atf4+/- mice exhibited higher pathology scores, increased expression of inflammatory factor genes (TNF-α, IL-1β), suppressed expression of CD31 and vascular endothelial-cadherin in the colon, and increased translocation of intestinal bacteria to lymph nodes and lungs following exposure to LPS. However, the aggravation of sepsis-induced intestinal injury resulting fromAtf4 knockdown was not caused by the enhanced inflammatory effect of Ly6Chi monocytes and gMacs.Conclusion: ATF4, as a novel regulator of monocytes-to-gMacs differentiation, plays a critical role in protecting mice against sepsis-induc

关键词： Activating transcription factor 4 Mice lipopolysaccharides Monocytes Leukocytes,mononuclear Cell differentiation Macrophages Sepsis Homeostasis gMacs Intestinal injury

Protective mechanisms of Tuina therapy against lipopolysaccharide-induced fever in young rabbits based on untargeted metabolomics analysis

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中医杂志:英文版 2023年第4期43卷 725-733页

作者： LIU Di ZHANG Yingqi YU Tianyuan LIU Zhifeng JIAO Yi WANG Hourong XU Yajing GUAN Qian CHEN Lulu HU Hui School of Acupuncture-Moxibustion and Tuina Beijing University of Chinese MedicineBeijing 102401China Department of Acupuncture-Moxibustion Beijing Massage HospitalBeijing 100035China Department of Acupuncture-Moxibustion Dongfang HospitalBeijing University of Chinese MedicineBeijing 100078China

OBJECTIVE:To investigate the effect of Tuina on the plasma metabolites of lipopolysaccharide-induced febrile in infant rabbits.METHODS:Twenty-four infant New Zealand rabbits were selected and randomly divided into three groups:saline,model,and Tuina.The fever model was established by injecting LPS intravenously through the ear margin vein in the model group and Tuina group,respectively.The modeling was considered successful when the anal temperature increased by 0.5℃or above within 1 h.In the Tuina group,six Tuina techniques(i.e.,opening Tianmen/the heaven gate,pushing Kangong/the superciliary arch,kneading Taiyang and the prominent bone behind the ears,clearing Tianheshui,spine pinching)that alleviate fever were performed on the young rabbits 1 h after the modeling,whereas the model and saline groups were not given Tuina treatment,with the real-time anal temperature monitored during the experiment.The plasma was taken 3 h after the modeling for liquid chromatography-mass spectrometry(LC-MS)untargeted metabolomics study.RESULTS:Our results showed a fever-reducing effects of Tuina therapy on lipopolysaccharide-induced fever in young rabbits,as indicated by a significantly lower anal temperature,maximum rise in body temperature,and body response index at 2 and 3 h after modeling in the Tuina group compared to the model group,with reductions in the PGE2 expression observed in the blood and hypothalamus.The differential metabolites including riboflavin,nicotinamide N-oxide,porphobilinogen,5-hydroxyindoleacetic acid,gamma-aminobutyric acid,and lysoPC(16:1(9Z)/0:0)were found following the Tuina intervention.Tuina primarily involves glycine-serinethreonine,arginine-proline,porphyrin-chlorophyll,pyrimidine,primary bile acid biosynthesis,and cyanoamino acid metabolic pathways.CONCLUSION:Tuina therapy has proven to be effective in reducing body temperature and down-regulating PGE2 expression in LPS-induced febrile young rabbits,with its mechanism of fever-reducing action possibly associated with the changes in plasma metab

关键词： fever pediatrics metabolomics lipopolysaccharides riboflavin glycine Tuina therapy

Baicalin inhibits inflammation of lipopolysaccharide-induced acute lung injury via toll like receptor-4/myeloid differentiation primary response 88/nuclear factor-kappa B signaling pathway

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Journal of Traditional Chinese Medicine 2022年第2期42卷 200-212页

作者： ZHU Changle FENG Cuiling FENG Feng Yao Xiaoqin WANG Guishu SHI Liangtian ZHENG Jiakun Department of respiration Dongzhimen Hospital Affiliated to Beijing University of Chinese MedicineBeijing 100000China Department of traditional Chinese Medicine Peking University People's HospitalBeijing100000China Department of Traditional Chinese Medicine Peking University International HospitalBeijing 100000China

OBJECTIVE:To explore the effect and mechanism of baicalin in the treatment of acute lung injury(ALI)by in vivo and in vitro experiments.METHODS:ALI was induced by instilling 10 mg/m L lipopolysaccharide(LPS)into the airway of rats.Different doses of baicalin(50 and 100 mg·kg^(-1)·d^(-1 ))were administered by gavage one day before modeling.RESULTS:Baicalin significantly reduced the permeability of the alveolocapillary membrane,alleviated tissue injury and inflammatory infiltration,and inhibited the secretion of inflammatory factors and the infiltration of neutrophils.The decline in these inflammations was related to the inhibition of the toll like receptor-4(TLR4)/myeloid differentiation factor 88(My D88)/nuclear factor-kappa B(NF-κB)/nod-like receptor pyrin containing 3(NLRP3)signaling pathway and the mitogen-activated protein kinase(MAPK)signaling pathway.CONCLUSIONS:Baicalin inhibits the secretion of inflammatory factors by inhibiting the TLR4-My D88-NF-κB/NLRP3 pathway and the MAPK signaling pathway.Thus,it reduces lung bronchial epithelial layer,alveolar damage,and pulmonary edema as detected in the in vivo and in vitro experiments.Therefore,baicalin may be a potential preventive and therapeutic drug for ALI.

关键词： baicalin acute lung injury epithelial cells lipopolysaccharides inflammation

Relationship between the Increase of Secretion of sTNF_α Induced by lipopolysaccharides and the Enhanced Expression of TACE mRNA in HL-60 Cells and Adhesive Cells from Human Spleen

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Journal of Tongji Medical University 2001年第4期21卷 265-268页

作者：丁廷波李凌波朱孔黎黄巍杨渝珍 Department of Molecular Biology Research Center of Experimental Medicine Tongji Medical College Huazhong University of Science and Technology Wuhan

In order to find out the potential modulators which influence the secretion of TNF α , the relationship between the amount of secreted TNF α (sTNF α ) and the level of TNF α converting enzyme (TACE) gene expression was studied before and after the stimulation by lipopolysaccharides (LPS) to HL 60 cells and adhered cells isolated from human spleen using cytological and molecular biology techniques and methods (RT PCR, Dot blot hybridization, etc.). The experimental results showed that: (1) LPS could induce the increase of expression of TNF α mRNA and TACE mRNA, reaching the peak value at 6 h and 10 h respectively after addition of LPS into cell culture medium; (2) The anti sense oligodeoxyribonucleotide (A ODN) complementary to TACE mRNA sequence really inhibited the secretion of TNF α as a result of blocked translation of TACE gene; (3) Furthermore, it was also observed that RDQ, a kind of injection derived from Chinese traditional herb, had strongly inhibitory effects on the expression of TACE mRNA and secretion of sTNF α stimulated by LPS. The above results suggested that the TACE indeed involved in delivering and processing of pro TNF α during the period of LPS stimulation and the study about the regulator/inhibitors of TACE gene expression would be very important to develop new types of therapy agents against toxic and side effects of sTNFα during the peroid of infection/inflammation to human body.

关键词： TNF α TNF α converting enzyme lipopolysaccharides anti sense oligodeoxyribonucleotide

Targeting Gut Microbiota for the Treatment of Primary Biliary Cholangitis:From Bench to Bedside

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Journal of Clinical and Translational Hepatology 2023年第4期11卷 958-966页

作者： Li Zhang Ling Yang Huikuan Chu Division of Gastroenterology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanHubeiChina

Primary biliary cholangitis(PBC)is a complex cholestatic liver disease with an unresolved etiology.The gut microbiota is composed of a dynamic community of bacteria,archaea,fungi,and viruses that have a key role in physiological processes related to nutrition,immunity,and host defense responses.A number of recent studies found that the composition of the gut microbiota of PBC patients was significantly altered,and reported that gut dysbiosis might arise during PBC development because of the close interactions of the liver and the gut.In light of the growing interest in this topic,the focus of this review is to characterize PBC gut microbiota alterations,the correlation between PBC pathology and the gut microbiota,and prospective therapies that target the altered gut microbiota,such as probiotics and fecal microbiota transplantation.

关键词： Primary biliary cholangitis Gut microbiota lipopolysaccharides Bile acids Probiotics Fecal microbiota transplantation