前列腺素E2通过G蛋白偶联EP1受体对腰椎软骨终板细胞生长的影响

[目的]检测前列腺素E2( prostaglandin E2,PGE2)通过G蛋白偶联前列腺素E受体1(prostaglandin E receptorl,EP1)对腰椎软骨终板细胞生长的影响.[方法]常规方法培养腰椎软骨终板细胞；应用RT - PCR和蛋白免疫印迹技术检测细胞EP基因及蛋白质表达水平.应用MTT实验评估EP1受体选择性激动剂17 -P -T - PGE2和EP1受体选择性抑制剂SC 51322对细胞生长增殖的影响.[结果]RT - PCR和Western blotting实验检测结果表明,软骨终板细胞均表达EP1、EP2、EP3和EP4.MTT实验检测显示EP1受体激动剂17 -P -T - PGE2可促进软骨终板细胞生长,EP1受体选择性抑制剂SC 51322可抑制PGE2促起的软骨终板细胞生长.[结论]PGE2引起的软骨终板细胞增殖可能与EP,信号转导通路激活相关.     

前列腺素E2受体在前列腺素E2诱导H9c2心肌细胞肥大中的作用

目的 评价前列腺素E2受体(EP受体)在前列腺素E2(PCE2)诱导H9c2心肌细胞肥大中的作用.方法 培养H9c2心肌细胞,以4×104个/ml的密度接种于培养瓶(每瓶3ml)、24孔(每孔1 ml)或6孔(每孔2 ml)培养板.采用随机数字表法,将细胞随机分为4组(n=24):空白对照组(C组)不予任何处理,继续培养48 h;PGE2组在细胞培养液中加入PGE2(终浓度1μmol/L);AH6809组(A组)在细胞培养液中加入PGE2(终浓度1μmol/L)和AH6809(EP1及EP2受体拮抗剂,终浓度10μmol/L);GW627368X组(G组)在细胞培养液中加入PGE2(终浓度1μmol/L)和GW627368X(EP4受体拮抗剂,终浓度10 μmol/L).孵育48 h后采用免疫荧光观察心肌细胞形态,Image J医学图像分析系统测量心肌细胞直径,BCA法检测心肌细胞总蛋白含量,RT-PCR法测定胞浆ANP mRNA及BNP mRNA的表达水平.结果 与C组比较,PGE2组、A组和G组心肌细胞总蛋白含量和心肌细胞直径增加,胞浆ANPmRNA及BNPmRNA表达上调(P＜0.05).与PGE2组比较,G组心肌细胞总蛋白含量和心肌细胞直径降低,胞浆ANP mRNA及BNP mRNA表达下调(P＜0.05),A组上述各指标差异无统计学意义(P＞0.05).结论 EP4受体介导了PGE2诱导的心肌细胞肥大效应,而该效应与EP1和EP2受体无关.     

子宫内膜癌中前列腺素受体的表达及其生物学意义

目的:研究前列腺素PGE2受体EP2在子宫内膜癌中的表达,探讨EP2在子宫内膜癌中的表达变化及其在子宫内膜癌的发生、发展过程是否存在非雌激素依赖的作用.方法:选取50例子宫内膜癌组织,应用逆转录-聚合酶链反应(RT-PCR)技术,半定量研究各组中EP2的mRNA表达;采用免疫组织化学技术,测定组织中雌、孕激素受体的表达.结果:子宫内膜癌G1组、G2组、G3组均高于正常组(P<0.05),而且随细胞分化越差,受体表达水平呈上升趋势 (P<0.001);子宫内膜癌I期组、II期-IV期组均高于正常组(P=0.001);在子宫内膜癌中,雌激素受体表达阴性组比阳性组的EP2表达水平显著升高(P<0.001);而孕激素受体表达阴性组比阳性组的EP2表达水平高,但是差异无统计学意义(P>0.05);绝经前(20例)与绝经后(30例)患者的子宫内膜癌中EP2的表达分别为0.905±0.251 和0.941±0.336,二者差异无统计学意义(P=0.684).结论:在子宫内膜癌中EP2表达水平高于正常子宫内膜,并且随分期和分级升高有上升趋势,在雌激素表达阴性的子宫内膜癌比阳性者明显升高,提示PGE2及其受体EP2可能参与了子宫内膜癌的形成.在子宫内膜癌的形成过程中,,前列腺素及其受体EP2与非雌激素作用的子宫内膜癌形成过程存在某种联系,可能是PGE2通过EP2受体介导的信号通路的传导起作用.     

PGE2通过促进EP4受体表达调控脂多糖诱导的膀胱上皮细胞炎症反应

目的探讨PGE2对脂多糖诱导的膀胱上皮细胞炎症反应的影响及相关机制。 方法利用脂多糖诱导人正常膀胱上皮细胞（SV-HUC-1）建立膀胱炎细胞模型，采用实时荧光定量PCR检测PGE2作用后膀胱上皮细胞中EP4受体的表达水平变化。利用EP4受体激动剂和拮抗剂作用于膀胱上皮细胞，MTT方法检测其对细胞增殖的影响。最后分别利用PGE2及EP4受体激动剂、拮抗剂作用于膀胱上皮细胞，ELISA方法检测细胞培养液中IL-10、IL-6、IL-1β和TNF-α的变化。 结果PGE2促进膀胱上皮细胞中EP4受体的表达，并呈时间依赖。EP4受体激动剂（CAY10598）促进膀胱上皮细胞的细胞增殖，而EP4受体拮抗剂（AH23848）抑制细胞增殖（P<0.05）。ELISA法检测发现，PGE2和CAY10598能促进膀胱上皮细胞培养液中IL-10、IL-6、IL-1β和TNF-α等炎症因子的表达，而AH23848则起到抑制作用（P<0.05）。 结论PGE2通过上调EP4受体表达促进脂多糖诱导的膀胱上皮细胞炎症反应，PGE2/EP4受体有望是膀胱炎治疗的潜在靶点。     

黄芩素对糖尿病肾病患者外周血NF-κB、VEGF、TGF-β_1的影响

目的:探讨黄芩素对糖尿病肾病患者外周血核因子-κB(NF-κB)、血管内皮生长因子(VEGF)、转化生长因子β_1(TGF-β_1)水平的影响及其临床疗效观察。方法:随机筛查我院就诊的糖尿病肾病患者100例,进行3个月基础治疗,分为糖尿病肾病微量蛋白尿组50例(尿白蛋白/尿肌酐30～300 mg/g),糖尿病肾病大量蛋白尿组50例(尿白蛋白/尿肌酐大于300 mg/g),予以黄芩素铝胶囊1. 2 g每日三次治疗3个月。比较糖尿病肾病患者治疗前后血清肌酐、血糖、糖化血红蛋白、尿白蛋白/尿肌酐和外周血单个核细胞NF-κBP65、血清TGF-β_1及VEGF变化。结果:与正常组比较,不同蛋白尿水平的糖尿病肾病患者及糖尿病患者外周血NF-κBp65均有明显激活(P 0. 05),与ACR成正相关;糖尿病肾病组治疗后与治疗前比较,黄芩素可抑制NF-κBP65、TGF-β_1、VEGF表达,减少尿白蛋白排泄(P 0. 05)。通过糖尿病肾病微量蛋白尿组及大量蛋白尿组治疗前后比较,黄芩素明显减少糖尿病肾病微量蛋白尿组尿白蛋白排泄。结论:黄芩素可抑制糖尿病肾病患者外周血NF-κB活化及降低VEGF、TGF-β_1水平,减少尿白蛋白排泄延缓糖尿病肾病进展,对早期糖尿病肾病进展延缓明显。     

黄芪联合前列腺素E1治疗糖尿病肾病疗效观察

糖尿病肾病(DN)是糖尿病常见的并发症,是糖尿病(DM)患者死亡的主要原因之一.在发达国家,透析治疗的终末期慢性肾衰竭患者中,DN已占据首位,在我国发病率也逐年上升.我们用黄芪联合前列腺素E1(PGE1)治疗DN,并与单用PGE1组进行对比有明显差别.兹报道如下.     

寻常型银屑病患者外周血单个核细胞Toll样受体9基因和血清IL-20表达水平的研究

目的:探讨寻常型银屑病患者外周血单个核细胞Tol l样受体9基因表达和血清I L-20表达水平及两者之间的相关性。方法:采集32例寻常型银屑病患者及30例健康正常人外周血,分别采用荧光实时定量PCR法检测外周血单个核细胞TLR9 mRNA表达,双抗体夹心ELISA法检测血清IL-20的表达水平。结果:银屑病组TLR9 mRNA的表达为(1.361±0.041)较正常人对照组(0.857±0.027)明显增高,在统计学上差异有显著性(P<0.01)。银屑病组IL-20表达水平为(30.73±21.84)×10-3g/L,较正常人对照组(13.56±7.17)×10-3g/L明显增高,在统计学上差异有显著性(P<0.01)。且银屑病患者外周血单个核细胞TLR9 mRNA表达与血清IL-20水平呈正相关,r=0.7239。结论:TLR 9及IL-20可能在银屑病发病过程中起重要作用。     

IgA肾病患者腭扁桃体单个核细胞IgA类别转换基因表达变化

目的 研究脂多糖(LPS)或溶血性链球菌(HS)刺激IgA肾病和非肾脏疾病慢性扁桃体炎患者腭扁桃体单个核细胞Iα-Cα胚系转录本、激活诱导的胞嘧啶脱氨酶(AID)mRNA和蛋白的表达,以探讨IgA肾病腭扁桃体单个核细胞IgA及IgA1产生异常的分子机制.方法 入组2009年1月到2010年2月在我院住院的IgA肾病患者27例,非肾脏疾病慢性扁桃体炎患者27例作为对照.通过单个核细胞分离液和密度梯度离心法分离出腭扁桃体单个核细胞.IgA肾病组及非肾脏疾病慢性扁桃体炎组腭扁桃体单个核细胞分别分为3组:LPS刺激组,HS刺激组和未刺激组.ELISA法检测培养上清中IgA和IgA1的浓度.实时PCR检测Iα-Cα胚系转录本和AID mRNA的表达;Western印迹检测AID蛋白的表达.结果 IgA肾病组腭扁桃体单个核细胞IgA和IgA1的分泌,特别是IgA1/IgA较慢性扁桃体炎组显著增加(P＜0.05),Iα-Cα和AID mRNA和AID蛋白的表达较慢性扁桃体炎组显著增加(均P＜0.05).IgA肾病组腭扁桃体单个核细胞IgA和IgA1的水平在刺激后明显增加(P＜0.05);Iα-Cα和AID mRNA的表达明显上调(均P＜0.05);AID蛋白表达明显增加(LPS刺激组P＜0.05,HS刺激组P＜0.01).结论 LPS和HS均能够诱导IgA肾病患者腭扁桃体单个核细胞IgA和IgA1的分泌、AID和Iα-Cα的表达增加,提示IgA肾病患者腭扁桃体IgA和IgA1的分泌增加可能与IgA类别转换相关基因AID和Iα-Cα高表达有关.     

前列腺素E1对高糖诱导足细胞肾素受体表达的影响

目的:观察前列腺素E1(prostaglandin E1,PGE1)对高糖培养小鼠肾脏足细胞肾素受体(renin receptor,RR)表达的影响。方法:体外培养和分化小鼠足细胞,随机分为4组分别以0 ng/ml、1 ng/ml、10 ng/ml、20 ng/ml浓度的PGE1进行干预24 h,以Western印迹法、实时定量PCR(quantitative PCR,q-PCR)法检测RR表达的情况。结果:各组分别加不同浓度的PGE1后对照组、高渗组和高糖1组RR mRNA表达总的趋势先上升后下降,高糖2组RR mRNA表达随PGE1浓度升高逐渐下降,10 ng/ml、20 ng/ml组下降有显著意义(P=0.002,P=0.003)。结论:在不同葡萄糖浓度环境中足细胞RR表达不同,对PGE1的干预反应不同,总的趋势为在PGE1低浓度时表达上调,在PGE1高浓度时表达下调,且有显著意义。     

过氧化物酶体增殖物激活受体-γmRNA表达水平与肺动脉压力的关系

目的探讨慢性阻塞性肺疾病（COPD）所致的肺动脉高压（PAH）患者外周血单个核细胞过氧化物酶体增殖物激活受体（PPAR）-γ的表达水平与肺动脉压力的关系。方法63例COPD患者中30例肺动脉收缩压≥40mmHg（1mmHg=0．133kPa）患者为PAH组,33例肺动脉收缩压〈40mmHg患者为COPD组。20例健康体检者为对照组。采用实时荧光定量RT-PCR法测定外周血单个核细胞PPAR-γ mRNA表达水平。结果COPD组及PAH组PPAR-γ mRNA表达水平分别相当于对照组的0．213、0．003,P〈0．05;PAH组与对照组比较肺动脉压力明显增高,PPAR-γ mRNA表达水平下降更加明显。PPAR-γ表达水平与肺动脉压力呈负相关（r=-0．683,P〈0．05）。结论COPD患者PPAR-γ表达下调,PAH时PPAR-γ表达下调更为显著,PPAR-γ表达水平与肺动脉压力呈负相关,PPAR-γ表达下调可能与PAH形成有关。     

Studies on antinephritic effect of lipo PGE1 (1). Effect of lipo PGE1 on crescentic-type anti-GBM nephritis in rats

The present study was designed to examine the anti-nephritis effect of Lipo PGE1 on crescentic-type anti-glomerular basement membrane (anti-GBM) nephritis in rats. Lipo PGE1, given i.v. twice a day at 20-80 g/kg from the day after the anti-GBM serum injection (the 1st day), remarkably inhibited the urinary protein excretion as wall as glomerular histopathological changes such as crescent formation, adhesion of capillary walls to Bowman's capsule, and fibrinoid necrosis. Lipo PGE1 at doses, which the anti-nephritic action was recognized, significantly inhibited the elevation of platelet aggregation in renal vein and the decrease of renal blood flow. In addition, Lipo PGE1 significantly inhibited the elevation of plasma antibody titer against rabbit gamma-globulin the apparently reduced the deposition of rat IgG in glomeruli. These results suggest that intravenous Lipo PGE1 may be useful for the treatment of rapidly progressive glomerulonephritis and this agent may mainly exert the anti-nephritic action by reducing the deposition of immune complex in glomeruli via the suppression of host antibody formation. Furthermore, the inhibition of platelet aggregation and the increase in renal blood flow by Lipo PGE1 may be also in part related to the anti-nephritic action of this agent.     

PGE(1) therapy for Martorell's ulcer

Martorell's ulcer is a type of ischaemic ulcer of the lower leg, defined by severe pain and female-to-male predominance. The aim of this article is to assess the therapeutic effectiveness of PGE(1), both in pain control and in the healing times of Martorell's ulcers for patients already undergoing antihypertensive treatment. Between January 2004 and December 2008, we recruited 10 patients with Martorell's ulcers. These patients were organized into two groups (A and B). Group A included six patients who underwent only antihypertensive treatment with calcium channel blockers or angiotensin converting enzyme inhibitors. Group B consisted of four patients who underwent continuous administration of PGE(1) through a single-day elastomer (120 μg/24 hours) for 7 days. In both groups, we observed a progressive reduction in the surface area of Martorell's ulcers until complete recovery, but there was a significant difference with regards to healing time. We also observed a significant improvement in symptomatic pain after only 2 days of PGE(1) therapy. It has now been proved that antihypertensive treatment leads to ulcers healing but, according to our experience, intravenous infusion of prostaglandins improves peripheral perfusion and symptomatic pain and decreases healing time.     

Afterload reduction therapy with prostaglandin E1 (PGE1)

Increases in afterload cause marked decreases in cardiac output and left ventricular stroke volume in patients with congestive heart failure. We studied the effects of afterload reduction therapy with prostaglandin E1 in three patients with intraoperative heart failure and two patients with low output syndrome after coronary artery bypass grafting. After 120 minutes, mean pulmonary arterial pressure decreased from 25.6 to 17.4 mmHg, pulmonary wedge pressure from 20.0 to 10.2 mmHg and right atrial pressure from 10.2 to 6.8 mmHg. Cardiac index increased from 1.73 to 2.80 l.min-1.m-2. The improvement of peripheral circulatory failure was remarkable and all patients recovered from heart failure. This study suggests that PGE1 is effective for afterload reduction therapy.     

Interaction of halothane and PGE1 on ICG excretion

We performed ICG-test during surgery to study the effect of halothane on ICG excretion in humans. We also evaluated the effect of PGE1 on ICG excretion concomitantly used during halothane anesthesia. A significant decrease in ICG clearance occurred in the patients who received only halothane to reduce the systolic arterial pressure (SAP) to 70% of the preoperative value. The reduction in SAP induced by PGE1 together with halothane, however, did not decrease the ICG clearance rate. We conclude that halothane may decrease the hepatic blood flow, but PGE1 may neutralize the effect of halothane, and maintain the hepatic blood flow in man.     

Initial experiences with prostaglandin E1 and PGE1 prepared injections]

Between April and August 1989 we treated 50 patients with an erectile dysfunction. 23 patients (46%) had an organic, 17 (34%) a psychogenic and 7 patients (14%) a mixed origin of their impotence. In 3 patients the diagnosis has yet to be made. To induce pharmacological erections we used 20 micrograms of prostaglandin-E1 in a ready to use syringe. 64% (32 patients) achieved a full erection. Of the 18 patients insufficiently responding, 12 (67%) had an organic (in 11 patients vascular), 4 a psychogenic and 1 patient a mixed erectile dysfunction. In one patient the diagnosis has not been established at present. 14% (7) of the patients complained to have painful erections disturbing intercourse. The mean erection time was 2.5 hours (range 0.5-5.5). In one patient the intracavernous injection of prostaglandin-E1 resulted in a prolonged erection of more than seven hours, which was successfully treated by aspiration of blood from the corpora cavernosa and intracavernous injection of phenylephrine-hydrochloride. Nevertheless prostaglandin-E1 appears to be more physiological and to have less side-effects than papaverin-chloride.     

Preventative effect of PGE1 for postoperative liver damage

The efficacy of a low dose of PGE₁-use on the postoperative liver damage was evaluated. PGE₁ was infused in with the mean rate of 0.026µg·kg^–1·min^–1 during surgical procedure to 93 patients under GO-enflurane anesthesia (the PG). Serum GOT, GPT and total bilirubin (TBIL) values measured before, at the end of (End) and 3 days (3d) after the operation were compared to those obtained from 43 patients without PGE₁ administration (the control).This dose of PGE₁ did not change blood pressure and heart rate, but slightly decreased Pa_{O 2}. In patients with preoperative normal values of GOT, GPT and TBIL, increases in GOT, GPT and TBIL observed at End in the PG were significantly lower than those in the control (31.9 vs 72.2IU, 25.9 vs 61.9IU, 0.68 vs 0.83mg·dl^–1, respectively). GOT, GPT and TBIL at 3d significantly increased in both groups, and these levels were identical between the two groups. In patients with preoperative abnormal values, only GOT at End increased in both groups, while no significant difference between the PG and the control group was noted. GOT at 3d and GPT at End and 3d did not significantly changed in either group. These results suggest that the low dose of PGE₁ administered during an operation prevents the development of postoperative liver damage, but does not treat the damaged hepatic cells.(Iwatsuki N, Yasuda A, Tokutomi S, et al.: Preventative effects of PGE₁ for postoperative liver damage. J Anesth 6: 131–137, 1992)     

前列腺素E1透皮乳膏局部用药扩血管效应的实验研究

目的　探讨前列腺素E1 (PGE1 )透皮乳膏剂局部应用的扩血管效果 ,为临床开发理想的局部扩血管药物提供实验依据。方法　新西兰成年兔 60只 ,分为 6组 (每组 10只 ) :实验 1组 (含透皮剂的 0 .1%PGE1 乳膏组 ) ,实验 2组 (含透皮剂的 0 .2 %PGE1 乳膏组 ) ,实验 3组 (含透皮剂的 0 .4%PGE1 乳膏组 ) ,实验 4组 (含透皮剂的 0 .8%PGE1 乳膏组 ) ,不含透皮剂的 0 .4%PGE1 乳膏的药物对照组及空白对照组。全麻后 ,用 0 .1%盐酸肾上腺素注射于兔耳部制成血管痉挛模型 ,出现典型血管痉挛后于每只兔耳皮肤表面抹药。测量注射肾上腺素前、痉挛后 10min时及用药后 10 ,15 ,3 0 ,60 ,90和12 0min各时间点血管管径及血液灌流量的变化。结果　同一组内各时间段血管管径与血液灌流量成正比关系。实验 3 ,4组在用药 10min起血管管径及血液流量均已恢复注射肾素前的水平 ,且在各时间段的结果与实验 1,2组、药物对照组及空白对照组相比均有显著性差异 (P <0 .0 1) ,而第 3 ,4组间各时间段结果无显著性差异 (P >0 .0 5 )。结论　PGE1 在透皮剂作用下可透过皮肤有效缓解肾上腺素所致的血管痉挛 ,其扩血管效果与药物浓度成依赖关系。该药作为局部扩血管药物具有适应证广 ,显效快 ,副作用小 ,作用持久等特点 ,可能会成为一种     

PGE1 reduces injury in hepatic allografts following preservation.

Prostaglandins of the E series have been shown to decrease renal and hepatic ischemic injury as well as improve hepatic function in patients with primary nonfunction following transplantation. We wished to determine the effect of prostaglandin E1 (PGE1) on hepatic allograft reperfusion injury in the isolated perfused rat liver (IPRL) model. Livers were harvested from adult male Sprague-Dawley rats and the bile duct, portal vein, and suprahepatic vena cava were cannulated. Control livers were placed immediately on the IPRL apparatus and perfused for 2 hr with a blood-Kreb's solution. Group A and B allografts were stored for 8 hr in heparinized lactated Ringer's solution at 4 degrees C. Group A livers were then perfused with a PGE1 infusion at 0.1 micrograms/kg/min while B livers received a placebo infusion of NS at the same rate. Temperature, pH, and inflow pressures were kept constant. Oxygen consumption, portal flow, and resistance were calculated for each group and found not to be statistically different. LDH, SGOT, superoxide anion (SOA), and bile flow were measured at 30-min intervals. At the end of the 2-hr perfusion, the placebo Group B (N = 5) had LDH, SGOT, and SOA higher than those of either Group A (N = 5) or control (N = 4) livers. The difference between Group A and Group B was significant for SGOT and SOA (P less than 0.05). Bile flow was highest in the control group (24.2 +/- 1.8 microliters/g/30 min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prostaglandin E1 (PGE1) attenuates vasoconstriction induced by PGE2, PGD2 and phorbol myristate acetate in the perfused rat liver

It has been shown that prostaglandins (PGs) produced by Kupffer and endothelial cells play an important role in mediating physiological responses to various immunological stimuli. We studied the effect of prostaglandin E₁ (PGE₁) on the hemodynamic and metabolic changes induced by prostaglandin E₂ (PGE₂), D₂ (PGD₂) and phorbol 12-myristate 13-acetate (PMA), a potent inducer of PGs in the isolated rat liver perfused with Krebs-Ringer-bicarbonate (KRB) solution at a constant pressure of 12cmH₂O. The liver was taken from overnight-fasted male Sprague-Dawley rats weighing 260 to 310g. Both PGE₂ and PGD₂ significantly decreased hepatic flow when their initial concentration was elevated to micromolar range. Although 1 × 10^–6M of PGE₁ did not have a major effect on hepatic flow, it significantly attenuated the declines of hepatic flow produced by 4 × 10^–6M of PGE₂ and PGD₂. However, none of PGs tested influenced glucose and lactate concentrations in the medium. Continuous infusion of PGE₁ into the medium at a rate of 5µg·min^–1 significantly diminished the decreases in hepatic flow and oxygen consumption induced by 2 × 10^–8M of PMA. These results suggest that administration of PGE₁ may preserve hepatic blood flow by modifying the intrahepatic regulatory mechanism involving the activation of Kupffer and endothelial cells.(Inaba H, Araki M, Numai T, et al.: Prostaglandin E₁ (PGE₁) attenuates vasoconstriction induced by PGE₂, PGD₂ and phorbol myristate acetate in the perfused rat liver. J Anesth 7: 56–65, 1993)     

脂质体携载前列腺素E1对扩张皮瓣缺血-再灌注损伤的影响

目的 观察脂质体携载前列腺素E1 (liposome prostaglandin E1,Lipo PGE1)对扩张皮瓣缺血-再灌注损伤的影响.方法 采用中国小型猪背部扩张随意皮瓣缺血再灌注损伤模型,实验分为两组:实验组(Lipo PGE1干预组)及对照组.在其背部形成8 cm×2 cm扩张皮瓣,通过不同时间远端扩张皮瓣组织匀浆中髓过氧化酶(MPO)及丙二醛(MDA)含量测定,以及皮瓣微血管密度(MVD)、皮瓣存活率和皮温测定,观察Lipo PGE1对皮瓣成活的影响.结果 实验组皮瓣存活率明显高于对照组(P＜0.05),术后两组MPO及MDA含量差异有统计学意义(P＜0.05),实验组明显低于对照组.两组MVD含量差异无统计学意义(P＞0.05).实验组用药后皮肤温度明显升高.结论 应用Lipo PGE1可以减轻缺血-再灌注损伤,提高扩张皮瓣存活率.