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Effects of Total Saponins from Dioscorea Nipponica Makino on Monosodium Urate-Induced M1-Polarized Macrophages through arachidonic acid Signaling Pathway:An in vitro Study

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Chinese Journal of Integrative Medicine 2023年第1期29卷 44-51页

作者： ZHOU qi SUN Hui-juan LIU Shu-min Research Institute of Chinese Medicine Heilongjiang University of Chinese MedicineHarbin150040China Graduate School Heilongjiang University of Chinese MedicineHarbin150040China Technological Innovation Team of Basic Theory Study Research of Institution of Higher Education in Heilongjiang Province Heilongjiang University of Chinese MedicineHarbin150040China

Objective To investigate and reveal the underlying mechanism of the effect of total saponins from Dioscoreae nipponica Makino(TSDN)on the arachidonic acid pathway in monosodium urate(MSU)crystal-induced M1-polarized macrophages.Methods M1 polarization of RAW264.7 cells were induced by 1µg/mL lipopolysaccharide(LPS).The methylthiazolyldiphenyl-tetrazolium bromide method was then used to screen the concentration of TSDN.MSU(500µg/mL)was used to induce the gouty arthritis model.Afterwards,10µg/L TSDN and 8µmol/L celecoxib,which was used as a positive control,were added to the above LPS and MSU-induced cells for 24 h.The mRNA and protein expressions of cyclooxygenase(COX)2,5-lipoxygenase(5-LOX),microsomal prostaglandin E synthase derived eicosanoids(mPGES)-1,leukotriene B(LTB)4,cytochrome P450(CYP)4A,and prostaglandin E_(2)(PGE_(2))were tested by real-time polymerase chain reaction and Western blotting,respectively.The enzyme-linked immunosorbent assay was used to test the contents of M1 markers,including inducible nitric oxid synthase(NOS)2,CD80,and CD86.Results TSDN inhibited the proliferation of M1 macrophages and decreased both the mRNA and protein expressions of COX2,5-LOX,CYP4A,LTB4,and PGE_(2)(Parachidonic acid signaling pathway.

关键词： gouty arthritis Dioscorea nipponica Makino arachidonic acid signaling pathway M1/M2 polarization

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Role of arachidonic acid in hyposmotic membrane stretch-induced increase in calcium-activated potassium currents in gastric myocytes

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Acta Pharmacologica Sinica 2005年第10期26卷 1233-1242页

作者： Meng YANG~2, Xing-lan LI~3, Hui-ying XU~3, Jia-bin SUN~3, Bin MEI~4, Hai-feng ZHENG~3, Lian-hua PIAO~3, De-gang XING~3 Zhai-liu LI~3, Wen-xie XU~(2,5) ~2 Department of Physiology, Shanghai Jiaotong University School of Medicine, Shanghai 200030 ~3 Department of Physiology Yanbian University College of Medicine Yanji 133000 ~4 East China Normal University School of Life Science, Shanghai 200062, China Department of Physiology Shanghai Jiaotong University School of Medicine Shanghai China Department of Physiology Yanbian University College of Medicine Yanji China East China Normal University School of Life Science Shanghai China

Aim: To study effects of arachidonic acid （AA） and its metabolites on the hyposmotic membrane stretch-induced increase in calcium-activated potassium currents (IKCa) in gastric myocytes. Methods: Membrane currents were recorded by using a conventional whole cell patch-clamp technique in gastric myocytes isolated with collagenase. Results: Hyposmotic membrane stretch and AA increased both IK（Ca）and spontaneous transient outward currents significantly. Exogenous AA could potentiate the hyposmotic membrane stretch-induced increase in IK（Ca）The hyposmotic membrane stretch-induced increase inK（Ca）was significantly suppressed by dimethyleicosadienoic acid （100 μmol/L in pipette solution）, an inhibitor of phospholipase A2. Nordihydroguaiaretic acid, a lipoxygenase inhibitor, significantly suppressed AA and hyposmotic membrane stretch-induced increases in IK（Ca）. External calcium-free or gadolinium chloride, a blocker of stretch-activated channels, blocked the AA-induced increase in IK（Ca）significantly, but it was not blocked by nicardipine, an L-type calcium channel blocker. Ryanodine, a calcium-induced calcium release agonist, completely blocked the AA-induced increase inK（Ca）; however, heparin, a potent inhibitor of inositol triphosphate receptor, did not block the AA-induced increase in IK（Ca）. Conclusion: Hyposmotic membrane stretch may activate phospholipase A2, which hydrolyzes membrane phospholipids to ultimately produce AA; AA as a second messenger mediates Ca2+influx, which triggers Ca2+-induced Ca2+release and elicits activation of IK（Ca）in gastric antral circular myocytes of the guinea pig.

关键词： gastric myocyte arachidonic acid hyposmotic membrane stretch calcium-activated potassium current.

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Inhibition of protein kinase B by Palmitate in the insulin signaling of HepG2 cells and the preventive effect of arachidonic acid on insulin resistance

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Frontiers of Medicine 2007年第2期1卷 200-206页

作者： XIA Yanzhi WAN Xuedong DUAN Qiuhong HE Shansu WANG Ximing Department of Medical Biology Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Biochemistry and Molecular Biology Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

Elevated plasma levels of free fatty acids(FFAs)may contribute to insulin resistance(IR)that is characteristic of type 2 diabetes mellitus.In this study,we investigated the effects of two fatty acids,palmitate(PA)and arachidonic acid(AA)on glycogenesis under insulin signaling in HepG2cells,a transformed hepatic carcinoma cell line.In the presence of 200μmol of palmitate,insulin(10−7 mol/L)stimulation of glycogenesis was inhibited,as evidenced by increased glucose in the medium and decreased intracellular glycogen.Wortmannin(WM),a specific inhibitor of PI3K,dramatically decreased the amount of intracellular glycogen in cells without PA incubation.However,glycogen in PA treated cells was not significantly changed by WM,indicating that PA may also act on PI3K.Interestingly,AA restored the effects of WM inhibition on glycogenesis in PA cells.Western blot analysis demonstrated that PA in the absence of WM increased phosphorylated glycogen synthase(inactive form of GS)and decreased phosphorylated protein kinase B(active form of PKB),causing a reduction of intracellular glycogen.AA,however,reversed the effects of PA on GS and PKB.Furthermore,inhibition of protein kinase C(PKC)by a specific inhibitor chelerythrine chloride(CC)abolished the inhibitory effect of PA on glycogen synthesis by decreasing phosphorylated GS and increasing phosphorylated PKB.However,the effect of CC in the presence of PA disappeared when AA was also present.Our results suggest that there is a disruption of the insulin signaling pathway between PKB and GS when the cells were exposed to PA,contributing to IR.PA may also interrupt the PKC signaling pathway.In contrast,AA could rescue glycogenesis impaired by PA.

关键词： insulin resistance palmitate protein kinase B glycogen synthase arachidonic acid

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Involvement of Oxidative Stress and Down-Regulation of Bcl-2 in arachidonic acid-Induced Apoptosis in HUVECs

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Wuhan University Journal of Natural Sciences 2005年第6期10卷 1057-1062页

作者： WANG Bing-hua WANG Yun CHEN Li-da CAO Jin-xiu ZHOU Wen-jing School of Medicine Wuhan University Wuhan 430071 HubeiChina

Human umbilical vein endothelial cells （HU VECs） were treated with arachidonic acid （AA）. After 24 h exposure to AA, typical morphological changes of apoptosis were observed by Giemsa stain and transmission electron microscopy. The apoptotic ratio in HUVECs treated with 50μmol/L, 100μmol/L and 150μmol/L AA were （20.7±3.6）%, （38.6±4.3）% and （52.5±7.5） % respectively. Contrarily, low concentration of AA （425μmol/L） exerted no influence on cell viability by MTT assay. Intracellular malondialdehyde increased significantly in a dose-dependent manner upon AA treatment and for the reduced glutathione. the opposite tendency was found Western Blots show that apoplosis triggered by AA was associated with the down-regulation of Bcl-2 expression, but not with Bax and p53. Pretreatment with 50μmol/L α-tocopherol reduced AA-induced oxidative stress and apoptosis, also inhibited the dowwregulation of Bcl-2/Bax ratio. These results suggested that high concentration of free AA could induce apoptosis in HUVECs probably via oxidative stress and down-regulation of Bcl-2.

关键词： arachidonic acid apoptosis oxidative stress endothelial cell Bcl-2

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Synthesis of symmetrical medium-and long-chain triacylglycerols rich in arachidonic acid at sn-2 position for infant formula

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Food Bioscience 2022年第1期45卷 386-392页

作者： Xuan Jiang Jianhua Huang Yaru Li Ye Wen Shibin Wu Xiuli Xu Zhonghao Chao Hong Zhang Xiaoqiang Zou National Engineering Research Center for Functional Food Collaborative Innovation Center of Food Safety and Quality Control in Jiangsu ProvinceNational Engineering Laboratory for Cereal Fermentation TechnologyState Key Laboratory of Food Science and TechnologySchool of Food Science and TechnologyJiangnan University1800 Lihu RoadWuxi214122JiangsuPR China Joint Laboratory of Functional Food for Healthy Body Fat Loss Chengdu Tianyi Cuisine Nutritious Food Co.Ltd.360 Tianhui RoadHigh-tech ZoneChengduSichuanChina Wilmar(Shanghai)Biotechnology Research&Development Center Co. No.118 Gaodong RoadPudong New DistrictShanghai200137China

Medium-and long-chain triacylglycerols(MLCT)rich in arachidonic acid(ARA)at sn-2 position were synthesized by a two-step enzymatic method.Firstly,sn-2 monoacylglycerols(MAG)were synthesized at a temperature of 25℃ by enzymatic alcoholysis.The MAG with 69.42%ARA at sn-2 position were obtained by solvent extraction and low temperature solvent crystallization.Secondly,the MLCT rich in ARA at sn-2 position and capric acid(CA)at sn-1,3 positions were produced by enzymatic esterification.Under the optimal conditions(MAG:CA=1:3(mol/mol),0.05 MPa vacuum,8% Lipozyme RM IM,5 h,25℃),the content of triacylglycerol was up to 93.60%.The triacylglycerol in the form of C10:0-C20:4-C10:0(including isomers)was about 40.43%.The ARA contents in the total and sn-2 fatty acid composition of the final product were 32.35%and 51.12%,respectively.MLCT rich in ARA at sn-2 position were successfully produced and the product has the potential application for functional food and infant formula.

关键词： arachidonic acid sn-2 monoacylglycerol Lipase Medium-and long-chain triacylglycerol Infant formula

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The　Property　and　Application　of　arachidonic　acid

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Plasma Science and Technology 2002年第5期4卷 1505-1510页

作者：王相勤姚建铭袁成凌王纪余增亮 Key Laboratory of Ion Beam Bioengineering Institute of Plasma Physics Chinese Academy of Sciences Hefei 230031 China

arachidonic acid (AA) is one of the most important PUFAs (polyunsaturated fatty acids) in human body. A high-yield arachidonic acid-producing strain (mortierella alpina) was selected by ion implantation (the relative content of arachidonic acid is 70.2% among all fatty acids). This paper mainly introduced the structure, distribution, source, physiologic healthcare function and application of AA.

关键词： arachidonic acid property and application

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Metabolic flux analysis on arachidonic acid fermentation

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Frontiers of Chemical Science and Engineering 2007年第4期1卷 421-426页

作者： JIN Mingjie HUANG He ZHANG Kun YAN Jie GAO Zhen College of Life Science and Pharmaceutical Engineering Nanjing University of TechnologyNanjing 210009China

The analysis of flux distributions in metabolic networks has become an important approach for understand-ing the fermentation characteristics of the process.A model of metabolic flux analysis of arachidonic acid(AA)synthesis in Mortierella alpina ME-1 was established and carbon flux distributions were estimated in different fermentation phases with different concentrations of N-source.During the expo-nential,decelerating and stationary phase,carbon fluxes to AA were 3.28%,8.80%and 6.97%,respectively,with sufficient N-source broth based on the flux of glucose uptake,and those were increased to 3.95%,19.21%and 39.29%,respectively,by regulating the shifts of carbon fluxes via fermentation with limited N-source broth and adding 0.05% NaNO_(3) at 96 h.Eventually AA yield was increased from 1.3 to 3.5 g·L^(−1).These results suggest a way to improve AA fermentation,that is,fermentation with limited N-source broth and adding low concentration N-source during the stationary phase.

关键词： metabolic flux analysis arachidonic acid Mortierella alpina fermentation synthesis

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Long-term modifications of blood pressure in normotensive and spontane-ously hypertensive rats by gene delivery of rAAV-mediated cytochrome P450 arachidonic acid hydroxylase

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Cell Research 2005年第9期 42-49页

作者： Katherine CIANFLONE Montreal Mike Rosenbloom Laboratory for Cardiovascular Research Canada McGill University Health Center Quebec H3A 1A1

arachidonic acid cytochrome P-450 (CYP) hydroxylase 4A isoforms, including 4A1, 4A2, 4A3 and 4A8 in the rat kidney, catalyze arachidonic acid to produce 19/20-Hydroxyeicosatetraenoic acids (20-HETE), a biologically active metabolite, which plays an important role in the regulation of blood pressure. However, controversial results have been reported regarding the exact role of 20-HETE on blood pressure. In the present study, we used recombinant adeno- associated viral vector (rAAV) to deliver CYP 4A1 cDNA and antisense 4A1 cDNA into Sprague-Dawley (SD) rats and spontaneously hypertensive rats (SHR), respectively, to investigate the effects of long-term modifications of blood pressure and the potential for gene therapy of hypertension. The mean systolic pressure increased by 14.2±2.5 mm Hg in rAAV·4A1-treated SD rats and decreased by 13.7±2.2 mm Hg in rAAV·anti4A1-treated SHR rats 5 weeks after the injection compared with controls and these changes in blood pressure were maintained until the experiments ended at 24 weeks. In 4A1 treated animals CYP4A was overexpressed in various tissues, but preferentially in the kidney at both mRNA and protein levels. In anti-4A1-treated SHR, CYP4A mRNA in various tissues was probed, especially in kidneys, but 4A1 protein expression was almost completely inhibited. These results suggest that arachidonic acid CYP hydroxy- lases contribute not only to the maintenance of normal blood pressure but also to the development of hypertension. rAAV-mediated anti4A administration strategy has the potential to be used as targeted gene therapy in human hyperten- sion by blocking expression of CYP 4A in kidneys.

关键词： arachidonic acid cytochrome P450 4A1 hypertension recombinant adeno-associated virus 20- Hydroxyeicosatetraenoic acids spontaneously hypertensive rats.

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arachidonic　acid　Metabolism　in　Galactosamine／Endotoxin　Indudced　Acute　Liver　injury　in　Rats

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Journal of Huazhong University of Science and Technology(Medical Sciences) 1994年第3期14卷 169-172页

作者：蒙学军王家

The changes of the levels of LTC4, PGI2 and TXA2 in the liver tissue in SD rats with GaIN/LPS-induced acute liver injury was studied with radioimmunoassay (RIA). As a result,12h after the administration of GaIN/LPS, serum AST (398±37u), ALT (565 ±43u) increased (P0.05) and the inflammatory changes of the pathological findings were observed. The improvement of serum ALT (300±168u)(p 0. 05) levels and histopathology did not change with administration of indomethacin, a cyclooxygenase inhibitor, but the liver LTC4 (12166±13027) contents increased (Parachidonic acid metabolism in rats with acute liver injury are significantly abnormal. Leukotrienes and thromboxane are important inflammatory mediators in the liver injury.

关键词： arachidonic acid galactosamine endotoxin. liver injury

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Adipose-derived stem cells inhibit dermal fibroblast growth and induce apoptosis in keloids through the arachidonic acid-derived cyclooxygenase-2/prostaglandin E2 cascade by paracrine

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Burns & Trauma 2021年第1期9卷 288-298页

作者： Jinxiu Yang Shiyi Li Leren He Minliang Chen Department of Burn and Plastic Surgery the Fourth Medical CentreChinese People’s Liberation Army General HospitalNo.51 Fucheng RoadHaidian DistrictBeijing100038China Chinese People’s Liberation Army General Hospital No.28 Fuxing RoadHaidian DistrictBeijing100853China 7th Department of Plastic Surgery Plastic Surgery HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeNo.33 Ba Dachu RoadShi Jingshan DistrictBeijing100144China

Background:The clinical features of keloids consist of aberrant proliferation,secretion,differentiation and apoptosis of keloid dermis-derived fibroblasts(KFBs).Notably,the apoptosis rate of KFBs is lower than the proliferation rate.Though the anti-fibrotic effect of adipose-derived stem cells(ADSCs)on keloids has become a hot topic of research,the exact anti-fibrotic mechanism of the paracrine effect remains unclear.This study aimed to find out how the conditioned medium of ADSCs(ADSC-CM)exerts an anti-fibrotic effect in KFBs.Methods:KFBs and ADSCs were extracted and cultured.Then,ADSC-CM was prepared.Whether ADSC-CM could inhibit KFB growth and induce apoptosis was verified by the use of a cell counting kit-8,an 5-Ethynyl-2-deoxyuridine(Edu)kit and flow cytometry.The expressions of cyclooxygenase-1(COX-1),COX-2,caspase 3 and B-cell lymphoma-2(Bcl-2)in ADSC-CM-cultured KFBs were tested by real-time PCR and western blotting.To clarify the role of COX-2 in ADSC-CM-induced KFB apoptosis,a specific COX-2 inhibitor,celecoxib,was applied to KFBs cultured in ADSC-CM.Moreover,we tested the production of arachidonic acid(AA)and prostaglandin E2(PGE2)by ELISA.Then,we established a keloid transplantation model in a nude mouse to validate the therapeutic effect in vivo.Results:The proliferation ability of KFBs cultured in ADSC-CM was found to be weakened and apoptosis was significantly increased.Caspase 3 expression was significantly upregulated and Bcl-2 was downregulated in ADSC-CM-cultured KFBs.Furthermore,ADSC-CM strikingly elevated COX-2 mRNA and protein expressions,but COX-1 expression was unaltered.COX-2 inhibitors reduced ADSC-CM-induced apoptosis.Additionally,COX-2 inhibition blocked the elevation of caspase 3 and reversed the decrease in Bcl-2 expression.ADSC-CM increased PGE2 levels by 1.5-fold and this effect was restrained by COX-2 inhibition.In the nude mouse model,expressions of AA,COX-2 and PGE2 were higher in the translated keloid tissues after ADSC-CM injection than in the controls.Conclusions:We showed ac

关键词： Keloids Adipose-derived stem cells Fibroblasts Apoptosis Anti-fibrosis cyclooxygenase-2 arachidonic acid

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