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Activation of primary human monocytes by the oxidized form of α1-antitrypsin

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第11期275卷 7693-7700页

作者： Moraga, F Janciauskiene, S Malmo Univ Hosp Dept Med Gastroenterol Hepatol Sect S-20502 Malmo Sweden

The oxidation of methionine residues in many proteins, including the serine proteinase inhibitor alpha 1-antitrypsin (AAT), can result in functional inactivation. In this study we investigated the pro-inflammatory properties of oxidized AAT (oxAAT), specifically its ability to activate human monocytes in culture. Monocytes stimulated with oxAAT at concentrations up to 0.2 mg/ml for 24 h showed significant elevation in monocyte tractant;tractant protein-1, cytokine interleukin-6, and tumor necrosis factor-a expression and increased NADPH oxidase activity. Monocytes activated with oxAAT showed surprising effects on lipid metabolism. Expression of low density lipoprotein (LDL) receptors increased by up to 76% compared with controls but was not accompanied by any changes in I-125-labeled LDL binding and, paradoxically, decreased LDL uptake, degradation, and intracellular cholesterol synthesis. oxAAT also down-regulated the scavenger receptor CD36, which takes up and is up-regulated by oxidized LDL and is down-regulated by cholesterol efflux, As a by-product of oxidative events accompanying inflammation, oxAAT has multiple effects on cytokine expression, generation of reactive oxygen species,and on intracellular lipid metabolism. The up-regulation of monocyte-derived reactive oxygen by oxAAT could potentially result in self-amplification of AAT oxidation and, thereby, the other effects deriving from it. This implies that there are as yet unidentified regulatory processes that control this cycle.

关键词：趋化因子CCL2/生物合成胆固醇/生物合成减量调节酶激活炎症介导素类/代谢白细胞介素6/生物合成脂蛋白类 LDL/代谢膜蛋白质类单核细胞/药物作用氧化还原受体免疫/生物合成受体 LDL/生物合成受体脂蛋白受体清道夫清道夫受体 B类肿瘤坏死因子α/生物合成 α1抗胰蛋白酶/化学 α1抗胰蛋白酶/药理学人类

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ESE-1 is a novel transcriptional mediator of inflammation that interacts with NF-κB to regulate the inducible nitric-oxide synthase gene

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第5期276卷 3302-3309页

作者： Rudders, S Gaspar, J Madore, R Voland, C Grall, F Patel, A Pellacani, A Perrella, MK Libermann, TA Oettgen, P Harvard Univ Sch Med Inst Med Boston MA 02115 USA Beth Israel Deaconess Med Ctr New England Baptist Bone & Joint Inst Boston MA 02115 USA Beth Israel Deaconess Med Ctr Div Cardiol Boston MA 02115 USA Brigham & Womens Hosp Dept Med Boston MA 02115 USA

Inflammation is a hallmark of several vascular diseases. The nuclear factor kappaB (NF-kappaB) transcription factors are dimeric proteins involved in the activation of a large number of genes in response to inflammatory stimuli. We report the involvement of a novel member of the ETS transcription factor, ESE-1, in mediating vascular inflammation. ESE-1 is induced in response to inflammatory cytokines and lipopolysaccharide in vascular smooth muscle cells, endothelial cells, and cells of the monocyte-macrophage lineage. This induction occurs within hours of stimulation and is mediated by NF-kappaB transactivation of the ESE-1 promoter. We have identified the inducible form of nitric-oxide synthase (NOS2) as a putative target for ESE-1, ESE-1 can bind to the p50 subunit of NF-kappaB, and cotransfection of ESE-1 with the p50 and p65 subunits of NF-kappaB synergistically enhances transactivation of the NOS2 promoter by ESE-1, An ESE-1-binding site within the NOS2 promoter has been identified, the site-directed mutagenesis of which completely abolishes the ability of ESE-1 to transactivate the NOS2 promoter. Finally, in a mouse model of endotoxemia, associated with acute vascular inflammation, ESE-1 is strongly expressed in vascular endothelium and smooth muscle cells. In summary, ESE-1 represents a novel mediator of vascular inflammation.

关键词：结合部位钙结合蛋白质类细胞培养的细胞因子类/药理学 DNA结合蛋白质类炎症/代谢炎症介导素类/代谢炎症介导素类/生理学膜糖蛋白类/代谢突变 NF-κB/代谢 NF-κB/生理学神经组织蛋白质类/代谢一氧化氮合酶/代谢一氧化氮合酶Ⅱ型蛋白质结构三级原癌基因蛋白质类突触结合蛋白质Ⅰ 突触结合蛋白质类反式激活因子类/遗传学反式激活因子类/代谢反式激活因子类/生理学转录因子血管疾病/代谢人类

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Inflammatory platelet-activating factor-like phospholipids in oxidized low density lipoproteins are fragmented alkyl phosphatidylcholines

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第40期274卷 28395-28404页

作者： Marathe, GK Davies, SS Harrison, KA Silva, AR Murphy, RC Castro-Faria-Neto, H Prescott, SM Zimmerman, GA McIntyre, TM Univ Utah Dept Pathol Salt Lake City UT 84112 USA Univ Utah Dept Internal Med Salt Lake City UT 84112 USA Univ Utah Huntsman Canc Inst Salt Lake City UT 84112 USA Natl Jewish Med & Res Ctr Dept Pediat Denver CO 80206 USA Fiocruz MS Dept Fisiol & Farmacodinam IOC BR-21045900 Rio De Janeiro Brazil

Oxidation of human low density lipoprotein (LDL) generates proinflammatory mediators and underlies early events in atherogenesis. We identified mediators in oxidized LDL that induced an inflammatory reaction in vivo, and activated polymorphonuclear leukocytes and cells ectopically expressing human platelet-activating factor (PAF) receptors, Oxidation of a synthetic phosphatidylcholine showed that an sn-l ether bond confers an 800-fold increase in potency. This suggests that rare ether-linked phospholipids in LDL are the likely source of PAF-like activity in oxidized LDL, Accordingly, treatment of oxidized LDL with phospholipase A, greatly reduced phospholipid mass, but did not decrease its PAF-like activity. Tandem mass spectrometry identified traces of PAF, and more abundant levels of 1-O-hexadecyl-2-(butanoyl or butenoyl)-sn-glycero-3-phosphocholines (C-4-PAF analogs) in oxidized LDL that comigrated with PAF-like activity. Synthesis showed that either C-4-PAF was just 10-fold less potent than PAF as a PAF receptor ligand and agonist. Quantitation by gas chromatography-mass spectrometry of pentafluorobenzoyl derivatives shows the C-4-PAF analogs were 100-fold more abundant in oxidized LDL than PAF, Oxidation of synthetic alkyl arachidonoyl phosphatidylcholine generated these C-4-PAFs in abundance. These results show that quite minor constituents of the LDL phosphatidylcholine pool are the exclusive precursors for PAF-like bioactivity in oxidized LDL.

关键词：色谱法高压液相炎症介导素类/化学炎症介导素类/代谢脂蛋白类 LDL/代谢质谱分析法氧化还原磷脂酰胆碱类/化学磷脂酰胆碱类/代谢血小板活化因子/化学血小板活化因子/代谢重组蛋白质类/化学重组蛋白质类/代谢人类

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Heparan sulfate proteoglycan isoforms of the CD44 hyaluronan receptor induced in human inflammatory macrophages can function as paracrine regulators of fibroblast growth factor action

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第11期275卷 7964-7974页

作者： Jones, M Tussey, L Athanasou, N Jackson, DG Univ Oxford Nuffield Dept Med MRC Human Immunol UnitInst Mol Med Oxford OX3 9DU England John Radcliffe Hosp Dept Cellular Sci Oxford OX3 9DU England Nuffield Orthopaed Ctr Oxford OX3 7LD England

The CD44 glycoprotein is expressed in multiple isoforms on a variety of cell types where it functions as a receptor for hyaluronan-mediated motility. Recently, interest has centered on CD44 heparan sulfate proteoglycan (HSPG) isoforms because of their potential to sequester heparin-binding growth factors and chemokines. Expression of these isoforms on ectodermal cells has recently been shown to regulate limb morphogenesis via presentation of fibroblast growth factor (FGF) 4/FGF 8 while expression on tumor cells was shown to sequester hepatocyte growth factor and promote tumor dissemination. To date, however, CD44 HSPG expression in tissue macrophages and lymphocytes has not been adequately investigated, despite the fact these cells actively synthesize growth factors and chemokines and indirect evidence that monocyte CD44 sequesters macrophage inflammatory-protein-Ip. Here we show primary human monocytes rather than lymphocytes express CD44 HSPGs, but only following in vitro differentiation to macrophages or activation with the proin-flammatory cytokine interleukin-1 alpha or bacterial lipopolysaccharide. Furthermore, we show these isoforms are preferentially modified with heparan rather than chondroitin sulfate, bind the macrophage-derived growth factors FGF-2, vascular endothelial growth factor, and heparin-binding epidermal growth factor with varying affinities (K-d 25-330 nM) and in the case of FGF-2, can stimulate productive binding to the high affinity tyrosine kinase FGF receptor 1 (FGFR1). In contrast, we find no evidence for significant binding to C-C chemokines. Last, we confirm by immunofluorescent antibody staining that inflamed synovial membrane macrophages express CD44 HSPGs and that expression is greatest in cells containing high FGF-2 levels. These results suggest a paracrine role for macrophage CD44 HSPG isoforms in the regulation of growth factor action during inflammation.

关键词：细胞分化炎症趋化因子类/代谢内皮生长因子/代谢表皮生长因子/代谢成纤维细胞生长因子2/代谢类肝素硫酸蛋白聚糖类/代谢炎症/代谢炎症介导素类/代谢胞间信号肽类和蛋白质类白细胞介素1/代谢淋巴因子/代谢巨噬细胞/细胞学巨噬细胞/免疫学单核细胞/细胞学单核细胞/免疫学旁分泌细胞细胞间通讯蛋白质结合蛋白质亚型/代谢受体蛋白质酪氨酸激酶类/代谢受体成纤维细胞生长因子 1型受体成纤维细胞生长因子/代谢滑膜/免疫学滑膜/病理学血管内皮生长因子A 血管内皮生长因子类人类

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Neural modulation of inflammatory reactions in dental tissues incident to orthodontic tooth movement. A review of the literature

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EUROPEAN JOURNAL OF ORTHODONTICS 1999年第3期21卷 231-247页

作者： Vandevska-Radunovic, V Univ Bergen Dept Anat & Cell Biol N-5009 Bergen Norway

This article reviews the current knowledge of the biological aspects of dental tissue changes incident to orthodontic tooth movement. The inflammatory nature of these tissue changes was first recognized in the early 1970s, and since then a number of morphological and quantitative investigations have been published in support of this view. The studies dealing with vascular and cellular dental tissue changes, as well as those concerned with inflammatory mediators present at sites of orthodontic tooth movement are systematized and presented accordingly. Special emphasis is placed upon the role of the sensory nerve fibres and their neuropeptides in the control, and development of an inflammatory process, i.e, their role in tooth movement.

关键词：牙槽突/血液供给牙槽突/病理生理学骨重建去神经支配牙髓/血液供给炎症介导素类/代谢下颌神经/生理学下颌神经/外科学神经原性感染/病因学神经原性感染/病理生理学神经肽类/代谢牙周组织/血液供给牙周组织/神经支配动物人类

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Gene expression of inflammatory mediators in different chambers of the human heart

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ANNALS OF THORACIC SURGERY 2000年第2期70卷 562-567页

作者： Valen, G Paulsson, G Bennet, AM Hansson, GK Vaage, J Karolinska Hosp Dept Thorac Surg Ctr Mol Med S-17176 Stockholm Sweden Karolinska Hosp Cardiovasc Res Unit Ctr Mol Med S-17176 Stockholm Sweden

Background. Inflammatory genes may be unevenly expressed in different heart chambers. Methods. Biopsies were taken simultaneously from the right atrium (RA), left atrium (LA), and left ventricle (LV) of 19 patients before cardioplegic arrest during open heart surgery. The mRNA expression of tumor necrosis factor alpha (TNF alpha), interleukin 1 beta (IL-1 beta), inducible and endothelial nitric oxide synthase (iNOS and eNOS), endothelin-l (ET-1), E-selectin (CD62E), intercellular adhesion molecule-1 (ICAM-1) and its ligand CD18, and CD25 was evaluated with semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). Results. Expression of TNF alpha mRNA was higher in RA than LA and LV (p < 0.05), whereas IL-1 beta was more expressed in LA than RA (p < 0.05), which was higher than LV (p < 0.0001). There were no significant regional differences in the expression of ICAM-1, CD62E, CD25, iNOS, and eNOS. CD18 was higher in RA than LA (p < 0.05);ET-1 was more expressed in RA than LV (p < 0.04). Patients with stable angina had no expression of eNOS. Conclusions. Gene expression of inflammatory mediators was detected in the hearts of patients with different cardiovascular disorders, and was unevenly distributed in different heart chambers. Cardiac biopsies should be taken from the same site. (C) 2000 by The Society of Thoracic Surgeons.

关键词：抗原 CD18/代谢心脏外科手术 E选择素/代谢基因表达心房心脏病/代谢心室炎症介导素类/代谢一氧化氮合酶/代谢一氧化氮合酶Ⅱ型一氧化氮合酶Ⅲ型 RNA 信使/分析受体白细胞介素2/代谢肿瘤坏死因子α/代谢人类

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Tear and serum soluble leukocyte activation markers in conjunctival allergic diseases

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AMERICAN JOURNAL OF OPHTHALMOLOGY 2000年第2期129卷 151-158页

作者： Leonardi, A Borghesan, F Faggian, D Depaoli, M Secchi, AG Plebani, M Hosp & Univ Padua Inst Physiopathol Opt Padua Italy Hosp & Univ Padua Dept Lab Med Padua Italy

PURPOSE: To measure markers of leukocyte activation in patients with an exclusively ocular inflammatory or bacterial disease. METHODS: Neutrophil myeloperoxidase, eosinophil cationic protein, eosinophil neurotoxin, and soluble interleukin-2 receptor were measured in serum and tears of 17 patients with allergic vernal keratoconjunctivitis, seven with atopic keratoconjunctivitis, ii with seasonal allergic conjunctivitis, seven with giant papillary conjunctivitis, 13 with rosacea blepharokeratoconjunctivitis, seven with bacterial conjunctivitis, and 13 normal subjects as controls. RESULTS: In serum of patients with vernal and atopic keratoconjunctivitis, levels of eosinophil cationic protein, eosinophil neurotoxin, and interleukin-2 receptor were significantly increased compared with control subjects but were not correlated with the severity of ocular symptoms. In tears of patients with vernal and atopic keratoconjunctivitis and seasonal allergic conjunctivitis, as well as in the nonallergic diseases, rosacea blepharokeratoconjunctivitis and bacterial conjunctivitis, levels of eosinophil cationic protein, neurotoxin, and interleukin-2 receptor were significantly increased compared with control subjects. The highest values of these markers were found in vernal keratoconjunctivitis samples. Neutrophil myeloperoxidase was significantly increased in vernal and atopic keratoconjunctivitis, rosacea blepharokeratoconjunctivitis, and bacterial conjunctivitis. In vernal keratoconjunctivitis, tear markers were correlated to the clinical score of the disease, but not with cytology. CONCLUSIONS: Tear histamine was measured in 10 allergic patients after allergen challenge. Although none of the above markers can be considered specific to a single disease, their measurement may still be useful for the quantification of local cell activation in ocular inflammatory diseases. (Am J Ophthalmol 2000;129:151-158. (C) 2000 by Elsevier Science Inc. All rights reserved.)

关键词：生物学标记血蛋白质类/代谢结膜炎变应性/血液结膜炎细菌性/血液嗜酸细胞颗粒蛋白质类嗜酸细胞源神经毒素组胺/代谢炎症介导素类/代谢角结膜炎/血液白细胞/代谢嗜中性白细胞激活中性白细胞/酶学过氧化物酶/代谢蛋白质类/代谢受体白细胞介素2/代谢核糖核酸酶类眼泪/代谢青少年成年人女(雌)性人类男(雄)性

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Anti-inflammatory activity of macrolide antibiotics

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期292卷 156-163页

作者： Ianaro, A Ialenti, A Maffia, P Sautebin, L Rombolà, L Carnuccio, R Iuvone, T D'Acquisto, F Di Rosa, M Univ Naples Federico II Dept Expt Pharmacol I-80131 Naples Italy

The effect of four macrolide antibiotics (roxithromycin, clarithromycin, erythromycin, and azithromycin) on the generation of some mediators and cytokines involved in the inflammatory process has been studied both in vivo and in vitro. Rat carrageenin pleurisy was used as a model of acute inflammation, and the macrolides were administered (10, 20, and 40 mg/kg p.o.) 1 h before the carrageenin challenge. Exudate volume and leukocyte accumulation were both dose-dependently reduced by roxithromycin, clarithromycin and erythromycin in either normal or adrenalectomized animals. Furthermore, in normal rats, prostaglandin (PG) E-2, nitrate plus nitrite, and tumor necrosis factor-alpha levels in pleural exudate were significantly reduced by these macrolides. Roxithromycin appeared more effective than erythromycin and clarithromycin, whereas azithromycin only slightly affected the inflammatory reaction. None of the macrolides were able to modify leukotriene B-4 exudate levels. In vitro experiments have shown that the four macrolides (5-80 mu M) reduced in a concentration-dependent manner the production of 6-keto-PGF(1 alpha), NO2-, tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6 by lipopolysaccharide-stimulated J774 macrophages. In J774 cells, the inhibition of 6-keto-PGF(1 alpha) and NO2- production by roxithromycin and erythromycin was not dependent on direct inhibition of cyclooxygenase-2 and inducible nitric oxide synthase activity because it appears to be related to the inhibition of cyclooxygenase-2 and inducible nitric oxide synthase protein expression. In conclusion, the present study shows that macrolide antibiotics have anti-inflammatory activity, which likely depends on their ability to prevent the production of proinflammatory mediators and cytokines, and suggest that these agents, particularly roxithromycin, can exert therapeutic effects independently of their antibacterial activity.

关键词： 6-酮前列腺素F1α/生物合成肾上腺切除术麻醉抗菌药/药理学消炎药/药理学叠氮红霉素/药理学角叉菜胶细胞系克拉霉素/药理学环氧化酶2 细胞因子类/生物合成地诺前列酮/代谢剂量效应关系药物红霉素/药理学炎症介导素类/代谢同工酶类/代谢白三烯B4/代谢巨噬细胞/代谢硝酸盐类/代谢一氧化氮/生物合成一氧化氮合酶/代谢一氧化氮合酶Ⅱ型亚硝酸盐类/代谢胸膜炎/化学诱导胸膜炎/预防和控制前列腺素内过氧化物合酶类/代谢罗红霉素/药理学时间因素肿瘤坏死因子α/代谢动物小鼠大鼠

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Prostaglandin E₂ inhibits lesion formation in dextran sodium sulphate-induced colitis in rats and reduces the levels of mucosal inflammatory cytokines

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SCANDINAVIAN JOURNAL OF IMMUNOLOGY 2000年第1期51卷 23-28页

作者： Sasaki, S Hirata, I Maemura, K Hamamoto, N Murano, M Toshina, K Katsu, K Osaka Med Coll Dept Internal Med 2 Takatsuki Osaka Japan

Effects of rectally injected prostaglandin E-2 (PGE(2)) in rats with dextran sodium sulphate (DSS)-induced colitis were investigated in terms of histopathology, local myeloperoxidase (MPO) activity, local mRNA expression of interleukin-1 beta (IL-1 beta), tumour necrosis factor-alpha (TNF-alpha) and growth-regulated gene produced/cytokine-induced neutrophil chemoattractant (GRO/CINC)-1, and secretion of TNF-alpha and GRO/CINC-1. In animals with no PGE(2) treatment, DSS-induced erosion and ulceration were particularly severe in the rectum and extended to the proximal colon. Neutrophil infiltration was characteristically present in the lesions and surrounding mucosa. MPO activity at lesion sites was increased. IL-1 beta and GRO/CINC-1 mRNA expression was increased, while TNF-alpha mRNA expression was significantly decreased. GRO/CINC-1 secretion was increased but a similar elevation of TNF-alpha was not detected. In the PGE(2)-treated group, lesion formation was inhibited grossly and microscopically. Neutrophil infiltration and MPO activity in and around lesions were lessened. The reduction in TNF-alpha mRNA expression and secretion was not affected by PGE(2). The expression of mRNA for IL-1 beta and GRO/CINC-1 was reduced, as was the secretion of GRO/CINC-1. As mRNA expression and secretion of cytokines in lesions of non-PGE(2)-treated animals was similar to that reported in human ulcerative colitis, rectal injection of PGE(2) may prove to be an effective therapy.

关键词：碱基序列趋化因子CXCL1 趋化因子 CXC 趋化因子类/遗传学趋化因子类/代谢结肠炎溃疡性/化学诱导结肠炎溃疡性/免疫学结肠炎溃疡性/预防和控制细胞因子类/遗传学细胞因子类/代谢 DNA引物/遗传学硫酸葡聚糖/毒性地诺前列酮/投药和剂量地诺前列酮/药理学基因表达/药物作用生长物质/遗传学生长物质/代谢炎症介导素类/代谢胞间信号肽类和蛋白质类白细胞介素1/遗传学肠黏膜/药物作用肠黏膜/免疫学肠黏膜/病理学过氧化物酶/代谢 RNA 信使/遗传学 RNA 信使/代谢大鼠 Sprague-Dawley 肿瘤坏死因子α/遗传学肿瘤坏死因子α/代谢动物人类男(雄)性大鼠

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Inhibitory mechanism of aloe single component (alprogen) on mediator release in guinea pig lung mast cells activated with specific antigen-antibody reactions

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期292卷 114-121页

作者： Ro, JY Lee, BC Kim, JY Chung, YJ Chung, MH Lee, SK Jo, TH Kim, KH Park, YI Yonsei Univ Coll Med Dept Pharmacol Seoul 120752 South Korea Korea Univ Grad Sch Biotechnol Seoul 136701 South Korea Seoul Natl Univ Coll Med Dept Pharmacol Seoul South Korea Seoul Natl Univ Coll Pharm Dept Biochem Seoul South Korea Nam Yang Aloe Co Inst Life Sci Seoul South Korea

We previously reported that the glycoprotein extracted from aloe strongly inhibited the mediator releases caused by the activation of guinea pig lung mast cells. Therefore, this study aimed to purify a single component that has an antiallergic effect from crude aloe extract and then to assess the effects of aloe single component (alprogen) on the mechanism of mediator releases caused by the mast cell activation. We purified aloe extracts by using various columns. We also purified mast cells from guinea pig lung tissues by using enzyme digestion, rough and discontinuous density Percoll gradient. Mast cells were sensitized with IgG(1) (anti-ovalbumin) and challenged with ovalbumin. Histamine was assayed by using a fluorometric analyzer and leukotrienes by radioimmunoassay. [Ca2+](i) level was analyzed by using a confocal laser scanning microscope. Protein kinase activity was determined by the protein phosphorylated with [gamma-P-32] ATP. The phospholipase D activity was assessed by the labeled phosphatidylalcohol. The amount of mass 1,2-diacylglycerol (DAG) was measured by the [H-3] DAG produced when prelabeled with [H-3] myristic acid. Phospholipase A(2) activity was determined by measuring the lyso-phosphatidylcholine released from the labeled phospholipids. Alprogen significantly decreased histamine and leukotriene releases and blocked completely Ca2+ influx during mast cell activation. The protein kinase C and phospholipase D activities were decreased by alprogen in dose-dependent manner. Alprogen inhibited mass DAG formation and the phospholipase A(2) activity during mast cell activation. The data suggest that alprogen purified from aloe inhibits multiple signals as well as blocking Ca2+ influx caused by mast cells activated with specific antigen-antibody reactions and that then the inhibition of histamine and leukotriene release follows.

关键词：芦荟/化学抗原抗体反应/生理学钙/代谢细胞培养的仓鼠亚科甘油二酯类/代谢剂量效应关系药物电泳聚丙烯酰氨凝胶荧光组胺释放/药物作用免疫球蛋白G/药理学炎症介导素类/代谢白三烯类/分泌肺/药物作用肥大细胞/药物作用肥大细胞/代谢显微镜检查共焦卵白蛋白/药理学磷脂酶D/代谢磷脂酶A/代谢植物提取物/分离和提纯植物提取物/药理学植物药用蛋白激酶类/代谢放射免疫测定时间因素动物女(雌)性

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