Prevention of early renal injury by mycophenolate mofetil and its mechanism in experimental diabetes

Previously it was shown that treatment with mycophenolate mofetil (MMF) attenuated renal inflammation and glomerular injury in a model of diabetes. However, the mechanism involved in the renoprotective effects of MMF in experimental diabetes has not been clearly delineated. Diabetes was induced by injection of streptozotocin (STZ) after uninephrectomy. Diabetic animals received no treatment or treatment with MMF (10 mg/kg once daily by gastric gavage) for 8 weeks, non-diabetic rats served as controls. Level of malondialdehyde (MDA) in renal tissue and urine as well as the activity of antioxidant enzymes (AOE) in renal tissue was determined. Renal injury was evaluated. Immunohistochemistry for ED-1 macrophages marker, intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) was performed. Expression of transforming growth factor (TGF)-beta1 protein was determined by Western blotting analysis. Treatment with MMF had no effect on blood glucose level, but did prevent increased urinary albumin excretion and glomerular damage in diabetic rats. Oxidative stress was reduced by MMF treatment, as indicated by a reduction in MDA level in renal tissue and urine. Activity of AOE such as glutathione peroxidase (GSH-PX) was markedly elevated while superoxide dismutase (SOD) and catalase (CAT) were not changed by MMF treatment. In diabetic animals receiving no treatment, there were increases in ED-1-positive cells, ICAM-1 expression and MCP-1 expression in glomeruli and tubulointerstitium, which were effectively suppressed by MMF treatment. Western blotting analysis showed that the expression of TGF-beta1 protein was increased by 1.92-fold in renal tissue in diabetic rats, and MMF treatment significantly reduced the increased expression of TGF-beta1 protein by 45%. Our data suggest that MMF treatment ameliorates early renal injury via the inhibition of oxidative stress and overexpression of ICAM-1, MCP-1 and TGF-beta1 in renal tissue in diabetic rats.     

石榴皮鞣质对糖尿病模型大鼠肾脏氧化应激的影响

目的:研究石榴皮鞣质对糖尿病模型大鼠肾脏氧化应激反应的影响。方法:将50只SD大鼠单次腹腔注射链脲佐菌素(75mg.kg-1)诱发实验性糖尿病,模型复制成功后随机分为模型(等容生理盐水)、维生素E(20mg.kg-1)与石榴皮鞣质高、中、低剂量(200、100、50mg.kg-1)组,另将10只SD大鼠作为正常对照组。灌胃给药,每天1次,连续21d。末次给药后观察大鼠日饮水量、日进食量,测定血糖(GLU)、血肌酐(Scr)、尿素(Urea),取一侧肾脏匀浆后测肾皮质超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH)活性、丙二醛(MDA)含量,另一侧肾脏做病理形态学检查。结果:与模型组比较,石榴皮鞣质高、中、低剂量组日饮水量、日进食量显著减少(P<0.01或P<0.05),GLU、Scr、Urea水平显著下降(P<0.01),SOD、GSH-PX活性显著减弱(P<0.01),MDA含量显著下降(P<0.01),肾组织病理学损害明显改善。结论:石榴皮鞣质能减轻糖尿病大鼠肾皮质氧化应激反应,有保护肾脏和延缓糖尿病肾病发生的作用。     

无创性肢体缺血预适应增强糖尿病大鼠缺血/再灌注损伤后心肌抗氧化能力

目的研究无创性肢体缺血预适应对糖尿病大鼠心肌缺血/再灌注损伤的保护作用,并从氧化-抗氧化角度初步探讨其作用机制。方法大鼠经尾静脉一次性注射链脲佐菌素(STZ)造成急性糖尿病模型后,被随机分为缺血/再灌注(I/R)、心脏缺血预适应(CIP)和无创肢体缺血预适应(NLIP)3组。NLIP组连续3d经历左后肢缺血预适应。d4,各组动物均经历心肌缺血/再灌注损伤,CIP组于缺血前行心肌缺血预适应。连续监测血压和心电图变化,检测心肌梗死范围,测定心肌组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、黄嘌呤氧化酶(XOD)活性以及丙二醛(MDA)含量。结果成模动物表现出血糖明显升高,体重下降。与I/R组比较,NLIP及CIP组ST-段抬高幅度降低,室早和室速出现时间推迟,持续时间缩短,室性心律失常发生率降低,心肌梗死范围缩小,SOD、GSH-PX活性升高,XOD活性降低,MDA含量减少。结论NLIP对糖尿病大鼠具有与CIP程度相当的心脏保护作用,其机制与增强心肌抗氧化能力有关。     

灯盏花素对大鼠糖尿病模型肾组织TGF-β1与CTGF表达影响的实验研究

目的　探讨灯盏花素对大鼠糖尿病模型肾组织转化生长因子 β1(TGF β1)与结缔组织生长因子 (CTGF)表达的影响。方法　建立STZ诱导的单侧肾切除糖尿病模型 ,随机分 :对照组、模型组、灯盏花素给药组 (2 0mg·kg-1·d-1,灌胃 )。观察 8wk后大鼠体重、肾重、肾重 /体重、2 4h尿白蛋白排泄率 (AER)、肾小球面积 (AG)和容量 (VG)及系膜区面积 (AM)的变化 ,并检测肾组织与尿MDA含量及肾组织SOD、CAT、GSH PX活性 ,通过免疫组化检测肾小球TGF β1与CTGF蛋白表达。结果　灯盏花素给药对大鼠糖尿病模型血糖、体重无明显影响 ,可明显抑制肾重、肾重 /体重、AER、AG、VG 及AM 的增加 (P <0 0 5 ) ;对肾组织及尿MDA含量的增加有明显抑制作用 (P <0 0 5 ) ,并明显提高肾组织SOD、CAT及GSH PX活性 (P <0 0 5 ,P <0 0 1)。免疫组化半定量分析显示 ,与对照组相比糖尿病大鼠肾小球TGF β1及CTGF表达明显增加 (P <0 0 1) ,灯盏花素给药对其有明显抑制作用 (P <0 0 5 )。结论　灯盏花素对大鼠糖尿病模型肾脏有明显保护作用 ,其机制部分与抑制肾组织TGF β1与CTGF过高表达有关     

地黄寡糖对二型糖尿病大鼠糖脂代谢及肝脏超微结构的影响

目的 观察地黄寡糖对2型糖尿病大鼠糖脂代谢的影响及肝脏的保护作用。方法 取♂SD大鼠用高脂高糖饲料喂养8周后,腹腔注射链脲佐菌素25 mg·kg^-1制备糖尿病大鼠模型,造模成功后随机分组为：糖尿病模型组、地黄寡糖高剂量组、地黄寡糖中剂量组、地黄寡糖低剂量组、二甲双胍组,每组10只;另取8只用普通大鼠饲料喂养8周后,腹腔注射等体积柠檬酸-柠檬酸钠缓冲液,作正常对照组。在第0,2,4,8周末各测定一次空腹血糖(FBG);第8周末测定血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)、和空腹血清胰岛素(FINS);实验结束处死大鼠,取肝组织检测谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)水平;HE染色后光镜观察肝脏病理变化;透射电镜观察肝脏超微结构的改变。结果 与糖尿病模型组比较,地黄寡糖中、高剂量组FBG、TG、TC、LDL-C、FINS水平均明显降低,HDL-C升高(P<0.05);糖尿病大鼠肝组织氧化应激水平增高,地黄寡糖中、高剂量组糖尿病大鼠SOD、GSH-Px活性均显著增加,MDA水平显著下降;HE染色显示,各地黄寡糖治疗组大鼠肝细胞脂肪变性明显减少,肝细胞排列基本规则。透射电镜结果显示,地黄寡糖高剂量组大部分线粒体结构清晰内质网完整。结论 地黄寡糖可降低糖尿病大鼠血糖、血脂,减轻肝细胞脂肪变性,从而达到保护肝脏的作用,其作用机制可能与其增强肝组织抗氧化作用,减缓糖尿病对肝组织的损伤有关。     

灯盏花素对糖尿病大鼠肝脏保护作用的实验研究

目的　探讨灯盏花素对糖尿病大鼠肝脏保护作用。方法　建立STZ诱导的糖尿病模型 ,随机分 4组 :对照组、模型组、灯盏花素给药组、维生素E给药组 ,每组 10只 ,观察8wk。应用分光光度法检测肝组织MDA含量及SOD、CAT与GSH PX活性 ;HE染色对肝组织作病理检查 ;油红O染色观察肝组织脂肪浸润 ;肝组织ED1(单核 巨噬细胞表面标志 )免疫组织化学采用SABC技术。结果　灯盏花素给药组对糖尿病大鼠血糖、体重无明显影响 ,维生素E给药组可降低血糖 ,延缓体重下降。HE染色模型组部分肝细胞脂肪变性 ;各给药组对肝细胞保护效果较好。模型组肝细胞油红O染色评分为 2 11± 0 82 ,对照组为 0 35± 0 15 ,相比差异有显著性 (P <0 0 1) ;灯盏花素给药组评分为 0 75± 0 6 6 ,维生素E给药组评分为 1 13± 0 78,与模型组相比差异均有显著性 (P均 <0 0 1)。模型组肝组织MDA含量明显升高 ,SOD、CAT、GSH PX活性明显降低 ,各给药组均可降低肝组织MDA含量 ,提高SOD、CAT与GSH PX活性。免疫组织化学显示各给药组均能抑制糖尿病肝组织单核 巨噬细胞浸润的增加。结论　灯盏花素对糖尿病大鼠肝脏保护作用机制部分与抑制肝内脂肪浸润、氧化应激及巨噬细胞浸润有关。     

糖尿病大鼠肾脏抗氧化防御系统机能的改变

目的：探讨糖尿病对肾脏抗氧化防御机能的影响。方法：观察12周糖尿病大鼠肾皮质丙二醛(MDA)及谷胱甘肽(GSH)水平,以及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、谷胱甘肽S转移酶(GSH-ST)和过氧化氢酶(CAT)活性的变化。结果：糖尿病大鼠肾组织中SOD、CAT活性下降;GSH含量显著降低;MDA没有变化;GSH-PX活性却明显增强。结论：糖尿病大鼠肾组织抗氧化防御机能明显下降。     

大蒜胶囊对糖尿病大鼠肾脏TGF-β_1表达影响及保护性研究

目的观察糖尿病大鼠肾脏TGF-β1表达及大蒜胶囊的治疗作用。方法采用STZ注射法制作糖尿病（DM）大鼠模型30只,随机分为正常对照组、DM组、大蒜胶囊组,各10只。灌胃给药8周后,采用免疫组化等技术测定24h尿白蛋白排泄（UAER）,肾小球滤过率（GFR）,肾皮质TGF-β1、Col-Ⅳ、FN的表达。结果（1）功能学变化：大蒜胶囊组大鼠的24hUAER和GFR显著低于DM组,差异均有统计学意义（P〈0.05）;（2）免疫组化：大蒜胶囊组大鼠肾皮质TGF-β1、FN、Col-Ⅳ的表达显著低于DM组,差异均有统计学意义（P〈0.05）。结论与DM组相比,大蒜胶囊组24hUAER、GFR及肾体质量指数明显降低,肾皮质TGF-β、FN、Col-Ⅳ的表达程度明显减轻。     

Renoprotective effects of fenofibrate in diabetic rats are achieved by suppressing kidney plasminogen activator inhibitor-1

To investigate mechanisms of protective effects of fenofibrate on the diabetic kidney, male Wistar rats were divided into control, untreated diabetes, and fenofibrate-treated (32 mg kg(-1) d(-1), 8 weeks) diabetes groups. Diabetes induced by streptozotocin (25 mg/kg) and a high-fat diet was characterized by the disorders of plasma glucose and lipids. In untreated diabetic rats, there were increases in glomerular volume, matrix content, expressions of laminin and urinary albumin excretion. These nephropathies were associated with the upregulations of plasminogen activator inhibitor 1 (PAI-1) mRNA expression and its protein activity in the renal cortex, and a significant increase in transforming growth factor beta1 (TGF-beta1) expression. Treatment with fenofibrate suppressed the expression of PAI-I mRNA and its protein activity, and inhibited TGF-beta1 overexpression. It also partially reversed metabolic disorders and pathophysiologic changes associated with diabetic nephropathy. Our results indicate that fenofibrate delays the progression of diabetic nephropathy in rats to some extent. These renoprotective effects are likely to be achieved through suppression of PAI-1 and TGF-beta1 in the renal cortex, and consequently less extracellular matrix deposition.     

Mangiferin protects the streptozotocin-induced oxidative damage to cardiac and renal tissues in rats

The role of oxidative stress in streptozotocin (STZ)-induced toxicity and its prevention by a xanthone glucoside, mangiferin was investigated. To induce diabetes mellitus, adult male Wistar rats were injected STZ intravenously at 55 mg/kg body weight. The effect of mangiferin (10 and 20 mg/kg, i.p., 28 days) was investigated in STZ-induced diabetic male rats. Insulin-treated rats (6 U/kg, i.p., 28 days) served as positive control. Diabetic rats given normal saline served as negative control. Normal rats that neither received STZ nor drugs served as normal control. On day 28, the diabetic rats showed significant increase in serum creatine phosphokinase (CPK) and total glycosylated haemoglobin. Kidney revealed tubular degeneration and decreased levels of superoxide dismutase (SOD) and catalase (CAT) with an elevation of malonaldehyde (MDA). Cardiac SOD, CAT and lipid peroxidation were significantly increased. Histopathological findings revealed cardiac hypertrophy with haemorrhages. Analysis of erythrocyte revealed significantly elevated levels of MDA with insignificant decrease in CAT and SOD. Repeated intraperitoneal injections of mangiferin (10 and 20 mg/kg) and insulin (6 U/kg) controlled STZ-induced lipid peroxidation and significantly protected the animals against cardiac as well as renal damage. From the study, it may be concluded that oxidative stress appears to play a major role in STZ-induced cardiac and renal toxicity as is evident from significant inhibition of antioxidant defence mechanism in renal tissue or a compensatory increase in antioxidant defence mechanism in cardiac tissue. Intraperitoneal administration of mangiferin exhibited significant decrease in glycosylated haemoglobin and CPK levels along with the amelioration of oxidative stress that was comparable to insulin treatment.     

Mechanisms underlying the chronic pravastatin treatment-induced improvement in the impaired endothelium-dependent aortic relaxation seen in streptozotocin-induced diabetic rats

1. We investigated the effects of chronic pravastatin treatment on the impaired endothelium-dependent relaxation seen in aortae from established streptozotocin (STZ)-induced diabetic rats. Starting at 6 weeks of diabetes, pravastatin (10 mg kg(-1)) was administered to STZ-induced diabetic rats for 4 weeks. 2. The increased total cholesterol and low-density lipoprotein (LDL) cholesterol levels seen in STZ-induced diabetic rats were not restored to normal by pravastatin. Aortae from pravastatin-treated diabetic rats did not show an impaired endothelium-dependent relaxation to acetylcholine. The expression of the mRNA for endothelial nitric oxide synthase was unaffected by diabetes or pravastatin. 3. The enhanced level of malondialdehyde (MDA)-modified LDL seen in STZ-induced diabetic rats was normalized by pravastatin treatment. The resistance of LDL to oxidation was assessed by measuring the amount of MDA or conjugated dienes generated by incubation with copper ions. LDL isolated from diabetic rats, but not those from pravastatin-treated diabetics, showed enhanced the susceptibility to oxidation, but incubation in vitro with pravastatin had no effect on LDL oxidation. 4. Following incubation of control aortae for 6 h with LDL (0.1 mg protein ml(-1)) isolated from diabetic rats, the endothelium-dependent relaxation to acetylcholine or A23187 was impaired, but LDL isolated from control or pravastatin-treated rats had no such effect. This inhibitory effect of diabetic LDL was prevented by superoxide dismutase (SOD), a superoxide scavenger. 5. These results suggest that pravastatin preserves endothelial function in aortae from STZ-induced diabetic rats without lowering plasma cholesterol, and its effect may be due to decreased LDL oxidation.     

糖尿病并发症相关性氧化应激的实验研究

目的链脲佐菌素(STZ)诱导大鼠1型糖尿病模型的基础上,探讨糖尿病氧化应激指标的变化。方法采用一次性腹腔注射STZ的方法,监测不同时点大鼠的空腹血糖、体质量及血浆中的丙二醛(MDA)和超氧化物歧化酶(SOD)等指标,并对结果进行统计学处理。结果大鼠注射STZ 72h后血糖值达到成模标准,并逐渐出现糖尿病表现,观察7周,始终满足成模标准,未见转复。DM组大鼠肾脏及肝脏肥大指数较CON组显著增加。氧化应激相关指标测定表明,较对照组相比,实验组大鼠血浆中脂质过氧化产物MDA水平显著升高,而SOD水平显著下降。结论本实验Ⅰ型糖尿病模型大鼠造模成功且模型稳定,氧化应激指标改变。     

Effect of treatment with vitamin D plus calcium on oxidative stress in streptozotocin-induced diabetic rats

Background

In diabetes mellitus, uncontrolled hyperglycemia has been reported to induce oxidative stress, which may lead to health complications. Vitamin D, however, acts as a non-enzymatic antioxidant to protect cells against oxidative stress and damage.

吡格列酮对STZ糖尿病大鼠肾组织氧化应激的影响

目的观察不同剂量盐酸吡格列酮对STZ诱导的糖尿病大鼠肾组织氧化应激的影响。方法 STZ腹腔注射建立糖尿病大鼠模型。成模糖尿病大鼠随机分为模型组和不同剂量吡格列酮组,并设正常对照组,干预8周后检测肾皮质MDA含量,SOD活性,肾组织NADPH氧化酶亚单位p22phoxmRNA和p47phox mRNA表达。结果各吡格列酮组较模型组MDA含量,p22phox mRNA和p47phox mRNA表达明显降低,SOD活性明显升高(P<0.05)。结论吡格列酮可抑制STZ糖尿病大鼠肾脏NADPH氧化酶表达,降低肾脏氧化应激水平,并具有一定的剂量依赖性,该作用可能与其肾脏保护部分有关。     

姜黄素对糖尿病大鼠肾脏TGF-β1影响及保护性研究

目的观察糖尿病大鼠肾脏TGF—β1表达及姜黄素胶囊的治疗作用。方法采用STZ注射法制作糖尿病（DM）大鼠模型,随机分为正常组,DM组,姜黄素组。灌胃给药8周后,采用免疫组化等方法测定24h尿白蛋白排泄率（UAER）、肾小球滤过率（GFR）、肾皮质TGF-β1、FN、Col—Ⅳ的表达。结果（1）功能学变化：姜黄素组大鼠的24hUAER和GFR显著低于DM、对照组,差异有统计学意义（P〈0．05）。（2）免疫组化：姜黄素组大鼠肾皮质TGF—β1、FN、Col—Ⅳ的表达显著低于DM组,差异有统计学意义（P〈0．05）。结论姜黄素胶囊有降低早期糖尿病肾病大鼠尿白蛋白排泄率及减少过高的GFR、抑制‘肾组织增生、抑制。肾皮质TGF-β1、FN、Col—Ⅳ表达等保护作用。     

羟苯磺酸钙对2型糖尿病模型大鼠肾脏氧化应激的影响

目的 :观察羟苯磺酸钙对2型糖尿病模型大鼠肾脏氧化应激的影响。方法 :将大鼠分为正常对照组、糖尿病组、羟苯磺酸钙组 ,比较各组大鼠肾组织中丙二醛 (MDA )含量、超氧化物歧化酶 (SOD)和谷胱甘肽过氧化物酶 (GSH -PX)活性 ,同时观察血糖、肾功能和肾脏形态的变化。结果 :与糖尿病组比较 ,羟苯磺酸钙组肾脏MDA含量明显下降 ,SOD、GSH -PX活性显著上升 ,肾功能和肾脏形态均明显改善。结论 :羟苯磺酸钙通过抑制氧化应激反应对2型糖尿病模型大鼠肾脏产生保护作用。     

两种不同提取方法所得鹰嘴豆总皂苷对2型糖尿病大鼠肾脏功能的影响

糖尿病肾病(diabetic nephropathy,DN)的发病机制迄今尚未完全明了,目前认为与糖脂代谢紊乱、血流动力学的改变、遗传因素、氧化应激、血管活性物质等多种因素有关。鹰嘴豆(Cicer arietinum L.)在维吾尔医药中已有两千多年应用历史,为一年生栽培植物,维吾尔语称其为诺胡提(音译)。鹰嘴豆属于高营养豆类植物,具有较高的药用价值。据《维吾尔常用药材》记载,鹰嘴豆具有主消渴、解百毒、润肺     

伊贝沙坦预防链脲佐菌素诱导糖尿病大鼠肾损伤的作用机制(英文)

目的:探讨血管紧张素Ⅱ受体拮抗剂伊贝沙坦(Irb)对链脲佐菌素(STZ)诱导的糖尿病大鼠的肾保护作用机制。方法:SD大鼠随机分为3组:正常对照组(N组,n=7),糖尿病肾病组(DN组,n=6)Irb治疗组(DNI组,n=7)。SD大鼠单侧肾切除后,腹腔注射STZ诱导糖尿病模型,观察治疗后第4, 8,12周的血糖(BG)、体重(BW)、尿白蛋白排泄、24小时尿总蛋白的改变,同时观察12周时肌酐清除率(Ccr)、肾重(KW)、肾脏肥大指数(KW/BW)、肾组织总蛋白含量(RTP)、肾小球面积(A_G)和体积(V_G)、肾小球毛细血管基底膜(GBM)厚度的改变。通过免疫组化观察肾组织结缔组织生长因子(CTGF)和转化生长因子-β_1(TGF-β_1)的表达。结果:DN组和DNI组间BG无差异(p>0.05)。Irb可显著抑制大鼠尿白蛋白、24小时尿总蛋白的排泄,抑制过度增高的Ccr(均为P<0.01)。而且Irb可显著抑制糖尿病大鼠KW、KW/BW、RTP、A_G和V_G的增加(P<0.05或P<0.01)。我们首次证实Irb能够显著抑制GBM的增厚和CTGF的表达(均为P<0.01)。另外,大鼠肾脏CTGF的表达与TGF-β_1的表达和肾小球体积呈显著正相关(均为P<0.01)。结论:早期应用Irb对糖尿病大鼠的肾保护作用可能与抑制肾脏肥大和肾脏CTGF表达有关。     

鸡矢藤提取物对STZ致糖尿病小鼠肾脏的氧化应激作用和晚期糖基化终产物的影响

目的：研究鸡矢藤提取物（EPS）对链脲佐菌素（STZ）所致糖尿病肾病小鼠的疗效观察。方法：雄性昆明小鼠适应性喂养后尾静脉注射150 mg·kg^-1 STZ,72 h后检测小鼠空腹血糖（FBG）以建立糖尿病模型。糖尿病小鼠随机分为5组：模型对照组,二甲双胍阳性对照组,EPS低、中、高剂量组（2.5,5,10 g·kg^-1）。另设空白对照组。各组小鼠连续灌胃给药4周,空白和模型对照组给予等量生理盐水。末次给药后测定小鼠FBG,收集尿液,检测24 h尿蛋白含量;测定血清中肌酐（Cr）、尿素氮（BUN）和总胆固醇（TC）的含量;检测肾脏组织中丙二醛（MDA）含量,超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性以及晚期糖基化终产物（AGE）水平;HE染色法观察肾脏病理学变化。结果：与模型对照组比较,EPS能显著降低糖尿病小鼠的FBG,并明显降低血清生化指标,降低肾脏组织中MDA、AGE含量和增强SOD、GSH-Px活性,改善肾小管空泡变性和肾小球萎缩。结论：鸡矢藤提取物能有效降低糖尿病肾病小鼠血糖,改善肾功能状态,对STZ所致糖尿病小鼠的肾脏保护作用可能与其能降低AGE的积聚、改善组织的氧化应激状态有关。     

茎叶人参皂甙和维生素E对百草枯所致大鼠急性肺损伤保护作用的比较研究

目的研究茎叶人参皂甙和维生素E（VE）对百草枯所致大鼠急性肺损伤（ALI）的保护作用。方法采用百草枯所致大鼠急性肺损伤模型,随机分为正常对照组（NS组）、肺损伤组（ALI组）、维生素E干预组（VE组）和皂甙干预组（GS组）。观察皂甙和VE对大鼠急性肺损伤时MDA等水平、病理改变及肺系数等影响。结果GS组和VE组可明显降低肺损伤所致血浆、组织中MDA等水平的升高,并能降低肺系数;同时又能显著升高肺组织中SOD、GSH-PX的水平,且GS组和VE组之间差异无统计学意义（P〉0.05）。结论茎叶人参皂甙和VE可通过抑制MDA的表达,改善SOD、GSH-PX等方式减少氧自由基的产生,减轻肺损伤程度,对百草枯所致急性肺损伤有明显的保护作用。