骨髓间充质干细胞对失血性休克大鼠早期炎性反应的影响

目的探讨骨髓间充质干细胞对失血性休克大鼠血清炎性因子及重要脏器的影响。方法体外分离培养大鼠骨髓间充质干细胞。雄性SD大鼠随机分为假手术组、模型组、治疗组(n=20)。改良Wiggers法制备大鼠出血性休克模型,休克持续90 min。治疗组在复苏前给予106个第3代骨髓间充质干细胞磷酸盐缓冲液(PBS)悬液1 ml,假手术组和模型组给予相同体积PBS溶液。分别于复苏后6、12、24、48、72 h取血清,酶联免疫试验(ELISA)检测肿瘤坏死因子(TNF)-α,白介素(IL)-1β、IL-6和IL-10水平,苏木素-伊红(HE)染色观察心、肝、肺、肾病理损伤。结果治疗组血清TNF-α和IL-6在复苏后12~72 h内较模型组显著下降(P0.05);治疗组血清IL-1β在复苏后6~12 h内较模型组下降显著(P0.05);治疗组IL-10水平在复苏后6~48 h内均较模型组有显著升高(P0.05)。骨髓间充质干细胞减轻肺、肝、肾、心等器官的炎性细胞浸润。结论骨髓间充质干细胞能调节失血性休克早期重要炎性因子水平,促进机体促炎-抗炎系统平衡。     

高渗盐水对失血性休克时急性肺损伤的作用研究

目的:研究高渗盐水(HS)对创伤失血性休克所致急性肺损伤(ALI)的作用及其机制.方法:新西兰白兔30只随机分为3组,假手术组(Sham组)、生理盐水处理组(NS组)、高渗盐水治疗组(HS组).NS组和HS组复制创伤失血性休克动物模型,分别以NS、HS(75 g/L氯化钠,4 ml/kg)复苏.观察肺组织的病理改变;双抗体夹心ELISA法测定休克前、休克末、复苏后2、4 h血清TNFα、IL-6、IL-10和sICAM-1的浓度;逆转录-聚合酶链反应(RT-PCR)检测肺组织各细胞因子及ICAM-1的mRNA表达水平.结果:与NS组比较,HS组复苏后4 h肺组织的病理学损伤显著减轻,TNFα、IL-6、ICAM-1血清浓度及肺组织mRNA表达水平均有不同程度下降(P＜0.05),而IL-10的浓度及mRNA水平明显增高(P＜0.01).结论:HS治疗可抑制创伤失血性休克时促炎细胞因子及黏附分子的表达,同时增加抗炎细胞因子的释放与表达,减轻肺部的炎症反应,从而发挥对ALI的保护作用.     

RL联合PTX对重度失血性休克大鼠肺缺血再灌注损伤的影响

目的探讨乳酸钠林格液（RL）联合己酮可可碱（PTX）复苏对重度失血性休克大鼠肺缺血再灌注损伤的保护作用及机制。方法将48只健康雄性SD大鼠随机分为对照组、模型组、RL组及RL＋PTX组各12只,后三组均采用改良Wigger′s法制备重度失血性休克模型,模型制备成功后RL组予3倍失血量的RL复苏;RL＋FTX组复苏方案同RL组,但复苏液中加入PTX;对照组仅行麻醉。分别于休克前、复苏前及复苏后1、2,4h检测四组呼吸指数（RI）;复苏后4h检测肺通透指数、肺湿干质量比（W／D）,观察肺组织病理学变化并进行肺损伤评分,测定肺组织中基质金属蛋白酶-2（MMP-2）和IL-8水平。结果与对照组比较,其余三组啼损伤评分、肺W／D、肺通透指数均显著升高,尤以RL组和RL＋FIX组为著（P均〈0．05）;与RL组比较,RL／PTX组RI、肺通透指数、肺W／D显著降低,肺组织病理学变化显著减轻,肺损伤评分显著减少,肺组织MMP-2、IL-8水平显著降低（P均〈O．05）。结论 RL联合FTX复苏可显著减轻重度失血性休克大鼠肺缺血再灌注损伤,可能机制为抑制肺组织内IL-8和MMP-2生成而减轻炎性反应。     

不同液体复苏对休克产兔急性肺损伤的影响

目的比较不同液体复苏失血性休克产兔致急性肺损伤的差异。方法 24只新西兰产兔制作失血性休克复苏模型,随机分为假休克组、生理盐水复苏组、羟乙基淀粉复苏组和高渗盐水复苏组（每组6只）;分别于放血前、休克期末、复苏期间以及复苏期末4个时间点采血测定TNF-α、IL-10;复苏期持续3 h后处死动物,取肺组织检测丙二醛（MDA）、超氧化物歧化酶（SOD）、髓过氧化物酶（MPO）、核因子-κB（NF-κB）活性、干湿质量比（DW/WW）和细胞间黏附因子1（ICAM-1）mRNA表达。结果除假休克组,休克复苏期各组血清TNF-α、IL-10均升高,其中高渗盐水复苏组TNF-α、IL-10水平低于生理盐水复苏组和羟乙基淀粉复苏组;休克复苏后高渗盐水复苏组产兔肺组织MDA、MPO、DW/WW、ICAM-1 mRNA表达和NF-κB活性均明显低于另两组,SOD水平较高。结论高渗盐水对失血性休克产兔所致的急性肺损伤具有一定的保护作用,其调节机制可能与抑制NF-kB的活化,减少中性粒细胞黏附分子ICAM-1的表达有关。     

连续性肾脏替代治疗多脏器功能障碍综合征患者血清细胞因子的变化及意义

目的探讨多脏器功能障碍综合征（MODS）患者应用连续性肾脏替代治疗（CRRT）血清细胞因子的变化及预后价值。方法选择MODS患者34例,常规治疗后行CRRT。根据随访患者28 d结局分为存活组19例、死亡组15例。分别在CRRT治疗前,治疗后6、12、18、24、48、72 h检测两组IL-1β、IL-1Rα、IL-6、TNF-α、IL-10、可溶性肿瘤坏死因子受体1（sTNFR1）,同时各时点进行动态急性生理和慢性健康评分（APACHEⅡ评分）。结果①与治疗前比较,存活组CRRT治疗后不同时间血清IL-1β、IL-6、TNF-α、sTNFR1、IL-10水平显著下降（P〈0.05或〈0.01）,血清sTNFR1/TNF-α明显升高（P〈0.01）;死亡组IL-1Rα在12 h明显升高（P〈0.01）,TNF-α在6 h明显下降（P〈0.05）。存活组与死亡组比较,TNF-α水平在72 h差异有统计学意义（P〈0.05）。②存活组中APACHEⅡ评分在48、72 h与治疗前相比明显下降（P〈0.05或〈0.01）。存活组与死亡组比较,能明显降低APACHEⅡ评分,在48、72 h有统计学意义（P均〈0.01）。③血清IL-6、TNF-α、IL-10水平以及sTNFR1/TNF-α与APACHEⅡ评分呈正相关（r分别为0.893、0.747、0.864、0.752,P〈0.05或〈0.01）。结论 MODS患者应用CRRT后血清IL-1β、IL-6、TNF-α、sTNFR1、IL-10水平降低,血清sTNFR1/TNF-α升高,这些细胞因子可预测MODS患者的预后。     

腔镜甲状腺术后患者血清和创腔引流液中IL-6及TNF-α的表达变化

目的探讨腔镜甲状腺手术对机体的创伤。方法20例腔镜甲状腺手术患者为观察组（LT）,20例开放甲状腺手术患者为对照组（OT）,术前及术后6、24、72 h检测并比较两组患者血清和创腔引流液中的IL-6及TNF-α。结果术后6 h观察组血清及创腔引流液中IL-6、TNF-α明显低于对照组（P均〈0.05）;对照组术后72 h血清IL-6、TNF-α浓度仍高于术前（P均〈0.05）;两组创腔引流液中IL-6、TNF-α均高于血清（P均〈0.05）。结论腔镜甲状腺手术对机体的创伤明显小于开放甲状腺手术,细胞因子形成的部位应为创腔。     

慢性阻塞性肺疾病并发贫血的机制探讨

目的从系统炎症的角度探讨阻塞性肺疾病并发贫血的机制。方法选择慢性阻塞性肺疾病急性加重期患者80例,根据血红蛋白水平分成血红蛋白正常组35例,高血红蛋白组30例,贫血组15例,运用ELISA法测血清中IL-6、TNF-α、促红细胞生成素（EPO）、C反应蛋白。比较各组之间的差异。结果高血红蛋白组和贫血组中促红细胞生成素明显高于血红蛋白正常组（P〈0.05）,IL-6、TNF-α、CRP在三组之间无统计学差异（P〉0.05）,高血红蛋白组中促红细胞生成素与血红蛋白水平呈正相关（r=0.843,P〈0.05）,贫血组中IL-6与EPO血红蛋白与EPO呈负相关（r=-0.912,P〈0.05）。IL-6、CRP、TNF-α与EPO之间在各组中均无明显的相关性（P〉0.05）。结论 COPD并发贫血与促红细胞生成素抵抗有关,但全身炎症反应并不能解释其发生的机制。     

下肢缺血预适应对急性心肌梗死大鼠细胞因子及HO-1的影响

目的研究下肢缺血预适应后急性心肌梗死（AMI）大鼠细胞因子TNF-α、IL-6、IL-10及血红素氧合酶-1（HO-1）的动态变化,探讨其在AMI心肌作用中的机制。方法将72只健康雄性成年SD大鼠随机分为AMI组（A组）、下肢缺血预适应组（B组）和对照组。A、B组大鼠分别在AMI后2、4、6、12 h时间点处死取材。ELISA法测定血清IL-6、IL-10、TNF-α的含量;RT-PCR测定心肌组织中HO-1 mRNA表达情况。结果B组梗死区比重较A组低（P〈0.05）;A、B组4、6和12 h血清IL-6水平均较对照组高（P〈0.05）;A、B组2、6、12 h血清IL-10水平较对照组高（P〈0.05）,B组4 h血清IL-10水平较A组和对照组高（P〈0.01）;A、B组各时间点TNF-α均较对照组高（P〈0.01）,但两组间仅4 h时有差异（P〈0.05）。B组各时间点HO-1 mRNA表达较A组升高（P〈0.05或P〈0.01）。结论下肢缺血预适应对心脏的保护作用可能是通过下调IL-6、TNF-α等细胞因子的释放,上调IL-10及HO-1的水平,使心肌组织损伤减轻。     

重症超声联合中心静脉血氧饱和度可指导脓毒症休克患者液体复苏治疗

目的：探讨重症超声联合中心静脉血氧饱和度（ScvO2）对脓毒症休克患者容量复苏的效果评价。方法：选取脓毒症休克患者86例，随机分为观察组（43例）和对照组（43例）。对照组采用ScvO2指导容量复苏，观察组采用重症超声联合ScvO2指导容量复苏。观察2组患者复苏前、复苏6h心率（HR）、平均动脉压（MAP）、中心静脉压（CVP）、血乳酸（LAC）、急性生理和慢性健康状况评估（APACHEⅡ）评分及液体复苏量、机械通气时间、重症监护病房（ICU）住院时间、6h复苏达标率、28d死亡率。结果：复苏6h时，观察组患者血LAC水平显著低于对照组（P＜0.05）。与复苏前比较，复苏6h时对照组患者MAP、CVP水平显著升高，LAC水平显著降低（P均＜0.05）；观察组患者MAP、CVP水平显著升高，HR、LAC水平显著降低（P均＜0.05）。观察组患者复苏液体量、机械通气时间、ICU住院时间显著低于对照组，6h复苏达标率显著高于对照组（P均＜0.05）；2组患者28d死亡率比较，差异无统计学意义（P＞0.05）。结论：重症超声联合ScvO2指导脓毒症休克患者容量复苏可降低复苏6h血LAC水平及复苏液体量，缩短机械通气及ICU住院时间，提高复苏效果。     

输注同系鼠骨髓间充质干细胞对大鼠移植肝的抗排斥作用观察

目的观察输注与受体同系鼠骨髓间充质干细胞对大鼠移植肝脏的抗排斥作用。方法实验鼠随机分为A、B、C组。A组仅行DA-Lewis大鼠原位肝移植,B组行DA-Lewis大鼠原位肝移植术后予环孢素,C组行DA-Lewis大鼠原位肝移植同期输注Lewis大鼠骨髓间充质干细胞。结果术后C组血清ALT、AST、TBIL较A组显著降低（P均〈0.05）,与B组相近;B、C组IL-2、IL-4、IL-10和IFN-γ均升高（P均〈0.05）,但低于A组（P均〈0.05）;B、C组移植肝仅呈急性轻度排斥反应,A组呈急性重度排斥反应;B、C组生存时间长于A组（P均〈0.05）。结论大鼠肝移植后输注与受体同系鼠骨髓间充质干细胞能减轻移植肝的排斥反应。     

Small volume resuscitation with 7.5% hypertonic saline, hydroxyethyl starch 130/0.4 solution and hypertonic sodium chloride hydroxyethyl starch 40 injection reduced lung injury in endotoxin shock rats: comparison with saline

BackgroundThe aim of this study was to investigate the effects of small volume resuscitation with 7.5% hypertonic sodium chloride (HSS), hydroxyethyl starch 130/0.4 solution (HES), and hypertonic sodium chloride hydroxyethyl starch 40 injection (HSH) on endotoxin shock rat lung.MethodsThirty Sprague–Dawley (SD) rats were divided randomly into 5 groups ,Group C (negative control group), Group E (lipopolysaccharide, LPS +4 ml/kg saline), Group HSS (LPS +4 ml/kg HSS), Group HES (LPS +4 ml/kg HES) and Group HSH (LPS +4 ml/kg HSH). Endotoxin shock model of rat was produced by injection with LPS. Then small volume resuscitation with different fluids was implemented in each group, respectively.ResultsCompared to Group C(negative control group）, lung injury in the other four groups was increased. Compared to Group E(LPS +4 ml/kg normal saline), lung injury of Group HSS(LPS +4 ml/kg HSS), HES(LPS +4 ml/kg HES), and HSH (LPS +4 ml/kg HSH)was lessened. Compared to Group C, oxygenation index in Groups E, HSS, HES, and HSH were decreased (P < 0.01). Compared to Group E, oxygenation indexes in Groups HSS, HES, and HSH were significantly increased (P < 0.01). Data of tumor necrosis factor (TNF)-α of lung tissue had similar results. However, protein concentration of bronchoalveolar lavage fluid and hydrogen sulfide (H₂S) concentration indicated contrary results.ConclusionSmall volume resuscitation with 7.5% hypertonic sodium chloride, hydroxyethyl starch 130/0.4 solution, and hypertonic sodium chloride hydroxyethyl starch 40 injection could lessen lung injury caused by lipopolysaccharide. And this effect had relation to change of TNF-α and H₂S.     

Effects of desferrioxamine therapy on chronic disease anemia associated with rheumatoid arthritis

Objective. To investigate the effects of desferrioxamine (DFO) infusion on chronic disease anemia (CDA) of rheumatoid arthritis (RA) by evaluating interleukin-6 (IL-6) and erythropoietin (EPO) production.Patients and methods. Five patients with RA and CDA (group I) were treated with DFO, 500 mg daily, through a continuous 10-h subcutaneous infusion 5 days a week for 4 weeks. One month after withdrawal, DFO was resumed in all five group I patients (group II) with an increase to 1 g daily following the previous treatment schedule. Clinical and laboratory parameters were evaluated weekly during the two study periods. Serum EPO was measured by radioimmunoassay. IL-6 was detected by the enzyme-linked immunoabsorbent assay method.Results. No significant variations in hematological parameters, IL-6 or EPO levels were observed in group I patients. After 1 week of DFO 1 g daily, reticulocyte counts and EPO improved significantly. Hemoglobin and hematocrit rose significantly after 3 weeks of 1 g daily DFO therapy. Four weeks after DFO withdrawal, EPO, reticulocyte counts, hemoglobin and hematocrit returned to baseline levels. A significant improvement in the clinical parameters of disease activity was observed, particularly in group II patients.Conclusion. DFO improves CDA in RA patients. The beneficial effects on erythropoiesis seem to be related to improved EPO responsiveness to the anemia.     

Anaemia of chronic disease in rheumatoid arthritis: in vivo effects of tumour necrosis factor alpha blockade

Anaemia of chronic disease (ACD) is a common feature of active rheumatoid arthritis (RA). Inflammatory cytokines, particularly tumour necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1) and interleukin- 6 (IL-6), are thought to contribute to the pathogenesis of ACD, possibly by inhibiting erythropoietin (EPO) production. In this study, we examined the in vivo effects of TNF-alpha blockade with a chimeric monoclonal antibody, cA2, on erythropoiesis in RA patients with ACD. Administration of cA2 led to a dose-dependent increase in haemoglobin levels compared to placebo and these changes were accompanied by a reduction in both EPO and IL-6 levels. The data support the notion that TNF-alpha is important in the causation of ACD, but suggest a mechanism independent of EPO suppression. Instead, TNF-alpha may act directly on bone marrow red cell precursors.      

Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis

AIM： TO investigate the effect of exogenous erythro- poietin （EPO） administration on acute lung injury （ALI） in an experimental model of sodium taurodeoxycholate- induced acute necrotizing pancreatitis （ANP）. METHODS： Forty-seven male Wistar albino rats were randomly divided into 7 groups： sham group （n = 5）, 3 ANP groups （n = 7 each） and 3 EPO groups （n = 7 each）. ANP was induced by retrograde infusion of 5% sodium taurodeoxycholate into the common bile duct. Rats in EPO groups received 1000 U/kg intramuscular EPO immediately after induction of ANP. Rats in ANP groups were given 1 mL normal saline instead. All animals were sacrificed at postoperative 24 h, 48 h and 72 h. Serum arnilase, IL-2, IL-6 and lung tissue malondialdehyde （MDA） were measured. Pleural effusion volume and lung/body weight （LW/BW） ratios were calculated. Tissue levels of TNF-a, IL-2 and IL-6 were screened immunohistochemically. Additionally, ox-LDL accumulation was assessed with immune-fluorescent staining. Histopathological alterations in the lungs were also scored.RESULTS： The mean pleural effusion volume, calculated LW/BW ratio, serum IL-6 and lung tissue MDA levels were significantly lower in EPO groups than in ANP groups. No statistically significant difference was observed in either serum or tissue values of IL-2 among the groups. The level of tumor necrosis factor-（~ （TNF-（~） and IL-6 and accumulation of ox-LDL were evident in the lung tissues of ANP groups when compared to EPO groups, particularly at 72 h. Histopathological evaluation confirmed the improvement in lung injury parameters a~er exogenous EPO administration, particularly at 48 h and 72 h. CONCLUSION： EPO administration leads to a significant decrease in ALI parameters by inhibiting polymorphonuclear leukocyte （PMNL） accumulation, decreasing the levels of proinflammatory cytokines in circulation, preserving microvascular endothelial cell integrity and reducing oxidative stress-associated lipid peroxidation and therefore     

The effect of thrombopoietin on erythroid progenitors in Diamond-Blackfan anemia

Diamond-Blackfan anemia (DBA) is a rare congenital red blood cell aplasia. Usually, erythropoiesis in vitro is defective, and decreased numbers of erythroid progenitors are found in colony assays performed with bone marrow cells. Recently, some investigators showed that thrombopoietin (TPO) also works on common multipotent progenitor cells and stimulates erythropoiesis. We examined the effect of TPO together with erythropoietin (EPO), stem cell factor (SCF), and/or interleukin-3 (IL-3) on erythroid burst-forming units (BFU-E) of bone marrow nonadherent mononuclear cells from 2 patients with DBA using a serum-free culture system. Very few BFU-E appeared in cultures containing EPO alone. Adding IL-3, SCF, or both to cultures containing EPO induced an increase in the number of BFU-E. When TPO was added to cultures containing EPO and IL-3, SCF, or both, the number of BFU-E further increased. Especially in patient 2, BFU-E formation was grossly equal to that in normal controls. We conclude that TPO enhances bone marrow erythropoiesis in patients with DBA in the presence of EPO and SCF and/or IL-3. The data raise the possibility of the combination of TPO and SCF as a therapeutic agent in DBA.     

Interactive role of trauma cytokines and erythropoietin and their therapeutic potential for acute and chronic wounds

If controllable, stem cell activation following injury has the therapeutic potential for supporting regeneration in acute or chronic wounds. Human dermally-derived stem cells (FmSCs) were exposed to the cytokines interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α) in the presence of erythropoietin (EPO). Cells were cultured under ischemic conditions and phenotypically characterized using flow cytometry. Topical EPO application was performed in three independent clinical wound healing attempts. The FmSCs expressed the receptor for EPO. EPO had a strong inhibitory effect on FmSC growth in the absence of IL-6 and TNF-α. With IL-6, the EPO effects were reversed to that of growth stimulation. TNF-α had the strongest stimulatory effect. In contrast, IL-1β had an inhibitory effect. Topically applied EPO considerably enhanced wound healing and improved wound conditions of acute and chronic wounds. Site specificity of stem cell activation is mediated by IL-6 and TNF-α. In trauma, EPO ceases its inhibitory role and reverts to a clinically relevant boosting function. EPO may be an important therapeutic tool for the topical treatment of acute and chronic wounds.     

Effect of flt3 ligand on the ex vivo expansion of human CD34+ hematopoietic progenitor cells

A ligand for the tyrosine kinase receptor flt3/flk-2, referred to here as flt3 ligand (flt3L), was recently cloned. The effect of flt3L on purified human CD34+ progenitor cells was examined. flt3 receptor (flt3R) was detected on the surface of human bone marrow cells that were enriched for CD34 expression. The effects of flt3L and the c-kit ligand Steel factor (SLF) on hematopoietic progenitors were compared in clonal colony assays. Both factors synergized with Pixy321 (interleukin- 3 [IL-3]-granulocyte-macrophage colony-stimulating factor fusion protein) to induce granulocytic-monocytic (GM) and high proliferative potential (HPP) colonies and synergized with Pixy321 + erythropoietin (EPO) to induce multipotent granulocytic-erythroid-monocytic- megakaryocytic colonies. Although SLF had a potent effect on colony formation of erythroid restricted progenitor cells (burst-forming unit- erythroid), no effect by flt3L was observed. The addition of flt3L to irradiated long-term marrow cultures seeded with CD34+ cells augmented both total and progenitor cell production. Ex vivo expansion studies with isolated CD34+ bone marrow cells from normal donors showed that flt3L alone supported maintenance of both GM and HPP progenitors for 3 to 4 weeks in vitro. The addition of flt3L to a growth factor combination of IL-1 alpha + IL-3 + IL-6 + EPO resulted in a synergistic effect on progenitor cell expansion comparable to that observed with the addition of SLF to IL-1 alpha + IL-3 + IL-6 + EPO. These data show a function for flt3L in the regulation of both primitive multipotent and lineage-committed hematopoietic progenitor cells.     

Transformation of severe aplastic anemia into acute myeloblastic leukemia with monosomy 7

 A cytogenetically normal man with severe aplastic anemia was treated with granulocyte colony-stimulating factor (G-CSF), erythropoietin (EPO), cyclosporin A, anti-thymocyte globulin, and interleukin-6 (IL-6), which resulted in a gradual improvement in his neutrophil count and hemoglobin level. After 2 years of the therapy, monosomy 7 was detected during cytogenetic analysis of his bone marrow, which evolved during a period of 5 months into acute myeloblastic leukemia. An in vitro proliferation assay of cytokine responses showed that leukemic blasts were sensitive only to G-CSF, and not to EPO or IL-6. Although allogeneic bone marrow transplantation from an HLA-matched unrelated donor was carried out in the non-remission stage, the patient died of systemic fungal infection on day 25, without any evidence of hematological engraftment. As long-term use of cytokines and immunomosuppressants in patients with severe aplastic anemia may induce or hasten the onset of a malignant transformation, careful attention must be paid to clonal evolution. Due to the poor prognosis of secondary myelodysplasia and leukemia, allogeneic bone marrow transplantation for such patients must be carried out early in the course of the disease. Received: 27 September 1995 / Accepted: 19 December 1995     

花生四烯酸细胞色素p450表氧化酶基因对野百合碱诱导的肺动脉高压大鼠IL-6,IL-8的影响

目的观察花生四烯酸色素p450表氧化酶基因CYP2J2过表达对野百合碱（MCT）诱导的肺动脉高压大鼠炎症细胞因子IL-6、IL-8、CRP和TNF-α表达的影响,探讨CYP2J2作用于肺动脉高压的机制。方法 ：选取8周龄250-280gSD大鼠60只随机分为正常对照组（n=30）和模型组（MCT组）（n=30）,模型组注射野百合碱（60mg/kg）造模。三周后分为6组：NS组（n=10）,pCDNA3.1（n=10）,pCDNA3.1-CYP2J2（n=10）,MCT＋NS（n=10）,MCT＋pCDNA3.1（n=10）,MCT＋pCDNA3.1-CYP2J2（n=10）,注射质粒三周后,检测大鼠平均肺动脉压（mPAP）,计算右心肥大指数（RVHl=RV/LV＋S）。ELISA法检测大鼠血清中IL-6、IL-8、CRP和TNF-α水平。RT-PCR检测大鼠肺组织中IL-6和IL-8的mRNA表达。结果 ：模型对照组mPAP、RVHI值、血清IL-6、IL-8、CRP和TNF-α水平及肺组织中IL-6和IL-8的mRNA表达均显著增高,与正常对照组相比有显著性差异（P〈0.01）;pCDNA3.1-CYP2J2治疗组mPAP、RVHI值、血清IL-6、IL-8、CRP和TNF-α水平及肺组织中IL-6和IL-8的mRNA表达均明显下调（P〈0.05）,但仍高于正常对照组（P〈0.05）。结论花生四烯酸色素p450表氧化酶基因可通过抑制MCT诱导大鼠肺动脉高压模型中肺组织炎性细胞因子的表达、下调大鼠炎性细胞因子的分泌达到对肺动脉高压的治疗作用。