黄芪对大鼠肝缺血再灌注损伤的影响

目的 探讨黄芪对大鼠肝缺血再灌注损伤的影响,以及与缺血预处理(IP)作用效果的比较.方法 清洁级健康雄性SD大鼠96只,随机分为假手术组、缺血再灌注组(IR组)、缺血预处理组(IP组)、黄芪组,每组又按再灌注时间(1、3、6、24 h)分为4个时相,每组各时相为6只.制作70%肝缺血再灌注模型,测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)水平;测肝组织髓过氧化物酶(MPO)含量;用免疫组化法检测IL-10、TNF-α表达;以及光镜及电镜观察大鼠肝形态学变化.结果 IR、IP、黄芪组ALT、AST、LDH和MPO含量均明显高于假手术组(P<0.01).与IR组相比,IP、黄芪组各个时相点的值均下降(P<0.05).与IP组比较,黄芪组各个时相点的值均降低(P<0.05).IR、IP、黄芪组肝组织TNF-α、IL-10的阳性细胞表达率均比假手术组高(P<0.05);与IR组比较,IP、黄芪组TNF-α的表达减少,而IL-10的表达增强(P<0.05);与IP组比较,黄芪组TNF-α的表达减少,IL-10表达增强(P<0.05).在光镜及电镜下观察肝形态学变化,可见IR组损伤甚为明显,IP及黄芪组损伤程度较IR组轻,黄芪组更轻,而假手术组肝形态正常.结论 IP和黄芪都可减轻缺血再灌注对肝脏的损伤,且后者较前者效果好.     

吸入高浓度氢气对大鼠肺缺血再灌注损伤的影响

目的 探究高浓度氢气对大鼠肺缺血再灌注损伤的影响。方法 雄性SD大鼠30只,体重220～260 g,随机分为3组(n=10):假手术组(Sham组)、缺血再灌注组(I/R组)和氢气组(H2组)。采用阻断左侧肺门30min,再灌注1h的方法制备大鼠肺缺血再灌注模型。Sham组,只开胸,不建立缺血再灌注模型,I/R组和H2组建立缺血再灌注模型,H2组在再灌注期间吸入67%H2。再灌注1h后,采用ELISA法检测肺组织中白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)的水平,采用黄嘌呤氧化酶法和硫代巴比妥酸法检测肺组织中超氧化物歧化酶(SOD)的活性和丙二醛(MDA)的水平,并且用Western blot方法测定凋亡相关蛋白caspase-3和caspase-9的含量。结果 与Sham组比较,I/R组IL-6、TNF-α和MDA水平显著升高,SOD的活性降低,caspase-3和caspase-9的含量明显升高(P<0.05)。与I/R组比较,H2组IL-6、TNF-α和MDA水平显著降低,SOD的活性升高,caspase-3和caspase-9的含量明显降低(P<0.0...     

黄芪甲苷降低缺血再灌注诱导的大鼠心肌损伤

目的本研究旨在观察黄芪甲苷对缺血再灌注模型损伤的大鼠心肌组织的保护作用。方法结扎大鼠左冠状动脉前降支建立心肌缺血再灌注损伤模型,观察心肌组织在缺血再灌注损伤模型及黄芪甲苷处理后的心肌组织损伤的变化。结果缺血再灌注损伤可使心肌左室舒张末期内径(LVEDD)显著增大、左室前壁舒张末期厚度(LVAW)显著变薄、左室射血分数(LVEF)显著降低(P<0.05),而黄芪甲苷的低、高剂量组均可在一定程度上恢复受损的心功能指标(P<0.05)。缺血再灌注损伤中,模型组大鼠心肌组织中乳酸脱氢酶(LDH)、心肌磷酸肌酸激酶(CK)、谷草转氨酶(AST)水平均明显升高(P<0.05),黄芪甲苷的低、可降低各心肌酶水平(P<0.05)。结论黄芪甲苷可在一定程度上恢复缺血再灌注损伤降低的大鼠心功能指标,降低升高的心肌酶。     

Egb761对大鼠肺缺血再灌注损伤的保护作用

目的观察银杏叶提取物Egb761对大鼠缺血/再灌注损伤的保护作用,以及损伤后超氧化物歧化酶(SOD)的水平与Egb761的关系。方法 30只Wistar大鼠随机等分为假手术对照(S)组、缺血/再灌注(I/R)组及银杏叶提取物+缺血/再灌注(EGB+I/R)组。测定Egb761处理组和对照组之间的SOD、电镜下超微结构以及肺的干/湿重比。结果银杏叶提取物可使肺组织中超氧化物歧化酶含量升高,与S组、I/R组比较,差异有统计学意义(P<0.05)。肺组织湿干重比降低,减轻肺组织病理变化。结论银杏叶提取物Egb761对大鼠缺血/再灌注损伤的肺具有保护作用。     

黄芪甲苷对缺血再灌注诱导的大鼠心肌损伤及细胞自噬的调节作用

目的观察黄芪甲苷对缺血再灌注模型损伤大鼠心肌组织的保护作用及与心肌组织细胞自噬的关系。方法结扎大鼠左冠状动脉前降支建立心肌缺血再灌注损伤模型,采用细胞生物学及免疫组织化学法,观察心肌组织在缺血再灌注损伤模型及黄芪甲苷处理后的心肌组织损伤、细胞自噬的变化。结果缺血再灌注损伤使大鼠心肌组织中心肌灶性病变严重,兼有波浪改变及大片炎症细胞浸润,与假手术组相比损伤面积明显增多(P<0.05),而黄芪甲苷低、高剂量组均可使心肌灶性病变和炎症细胞浸润的面积明显减少(P<0.05)。Western blot结果显示,缺血再灌注损伤可激活心肌组织细胞中Beclin1的表达(P<0.05),而黄芪甲苷低、高剂量组均可降低缺血再灌注损伤诱导的心肌组织细胞Beclin1表达(P<0.05)。结论黄芪甲苷可在一定程度上减少缺血再灌注损伤的心肌面积,其机制可能是通过调节与自噬相关的Beclin1细胞信号转导通路而发挥作用。     

缺血缺氧预处理与肺缺血／再灌注损伤

人及多种哺乳类动物实验证实，短时夹闭1开放肺根或单独夹闭，开放主支气管造成的肺短暂缺血后再灌注及短时缺氧后再复氧，可启动肺预处理保护效应，对肺缺血／再灌注损伤有明显防治作用，本文对该领域的研究现状作一综述。     

氧化应激与总肺缺血再灌注细胞凋亡的相关性及川芎嗪干扰的影响

目的探讨氧化应激在兔肺组织细胞凋亡中的作用及川芎嗪的影响。方法制备兔在体原位肺缺血再灌注(IR)损伤模型(PIRI),于IR 1、3、5 h分别测各组血浆MDA及SOD活力。应用末端脱氧核苷酸转移酶(TdT)介导的dUTP缺口末端标记技术(TUNEL),检测IR损伤引起的肺细胞凋亡的变化;进行氧化应激指标与细胞凋亡的相关性分析。结果 IR组1、3、5 h各组血浆SOD活力较假手术组比较显著降低(均P<0.05),TMP组在缺血1 h再灌注1、3、5 h SOD与IR组比较SOD活力明显升高(P<0.05,P<0.01)。在缺血1 h再灌注1、3、5 h IR组与假手术组比较MDA含量显著增高(P<0.01),TMP组在再灌注1、3、5 h的MDA含量显著高于假手术组(P<0.05,P<0.01),但低于IR组(P<0.05,P<0.01)。肺IR后IR组1、3、5 h发生明显的肺细胞凋亡(均P<0.01),而TMP组细胞凋亡指数与同一时相IR组比较显著降低(P<0.05,P<0.01);SOD与细胞凋亡指数呈负相关(r=-0.665,P<0.05),MDA与细胞凋亡指数呈正相关(r=0.764,P<0.05)。结论氧化应激导致的细胞凋亡在肺IR损伤机制中可能发挥着重要作用,川芎嗪可抑制氧化应激反应从而减轻细胞凋亡的发生,此机制可能是川芎嗪减轻肺IR损伤的机制之一。     

丙泊酚对大鼠肺缺血再灌注损伤细胞凋亡及相关蛋白的影响

目的 探讨丙泊酚对大鼠肺缺血再灌注损伤(LIRI)细胞凋亡及相关蛋白的影响.方法 雄性SD大鼠42只,随机分为3组:假手术组(S组)、缺血再灌注组(IR组)、丙泊酚组(P组).IR组、P组均建立大鼠原位肺缺血再灌注模型(缺血1 h,再灌3 h),P组于缺血前30 min静脉输注丙泊酚5 mg·kg-1·h-1.实验结束后立即取左肺标本,用免疫组化法检测Bcl-2与Bax蛋白表达情况,原位细胞凋亡检测(TUNEL)法检测肺上皮细胞凋亡指数(AI),同时光镜下观察肺组织的病理学变化.结果 与S组相比,IR组凋亡指数增加,肺组织中Bcl-2、Bax表达均增强,Bcl-2/Bax比值明显降低 (P＜0.05);与IR组相比,P组Bcl-2蛋白表达增加、Bax蛋白表达减少和细胞凋亡指数降低(P＜0.05),光镜下肺组织病理学变化明显轻于IR组.结论 丙泊酚对大鼠LIRI具有保护作用,其机制可能与调控Bcl-2/Bax蛋白表达从而减轻肺细胞凋亡有关.     

免疫因素在大鼠肺缺血再灌注损伤中的作用

目的探讨免疫因素在大鼠肺缺血再灌注(I/R)损伤中的作用。方法选取90只健康雄性Wistar大鼠,随机分为3组,即为I/R组(左肺I/R组),Sham组(假手术组),C组(对照组),均于缺血30 min、再灌注60、120 min时采集标本,检测肺组织的湿/干重比(W/D),支气管肺泡灌洗液的蛋白总量(TP),白细胞数目(WBC),中性粒细胞(PMN)的百分比及肺组织匀浆肿瘤坏死因子(TNF)-α、IL-1、IL-6及IL-8含量。结果在各组的对应时间点,I/R组中再灌注60、120 min时,W/D比值、WBC、PMN比例及TP含量明显高于C组及Sham组(P<0.05);I/R组中再灌注120 min,W/D比值、WBC、PMN比例及TP含量明显高于I/R组中再灌注60 min(P<0.05);I/R组中缺血30 min,肺组织匀浆TNF-α含量明显高于C组及Sham组(P<0.05);I/R组中再灌注60 min及再灌注120 min时,肺组织匀浆TNF-α、IL-1、IL-6及IL-8含量明显高于C组及Sham组(P<0.05);I/R组中再灌注120 min时,肺组织匀浆TNF-α、IL-1、IL-6及IL-8含量明显高于I/R组再灌注60 min时(P<0.05)。结论免疫因素在大鼠肺I/R损伤发挥重要作用。     

黄芪注射液对大鼠离体心脏缺血再灌注损伤的保护作用

目的探讨黄芪对大鼠缺血再灌注心肌的保护作用及机制。方法SD大鼠30只随机分为3组,非缺血灌注组(C组):正常灌注80min;缺血再灌注组(I/R组):灌流20min后,停灌30min,再灌30min;黄芪-缺血再灌注(H I/R组):K-H液中加入黄芪注射液(10mg/L),灌流20min后,开始停灌30min,再灌含有黄芪的K-H液30min。观察黄芪对大鼠全心缺血-再灌注心功能、肌酸激酶(CK)、心肌丙二醛(MDA)的影响。结果①心功能:H I/R组较I/R组显著改善缺血再灌注心肌的心功能;②心肌酶谱:C组在整个灌流过程中CK含量很低,I/R组在30min复灌后有大量的CK漏出,CK值高于C组(P<0.01),H I/R组冠状动脉流出液中CK为(1.20±0.02)IU/(gwt·min),I/R组为(2.32±0.06)IU/(gwt·min);③MDA:黄芪灌注后心肌组织中MDA明显下降。结论黄芪通过抑制氧自由基的产生、改善心肌舒张功能而发挥拮抗心肌再灌注损伤作用。     

Protective effect of resveratrol against endotoxemia-induced lung injury involves the reduction of oxidative/nitrative stress

BackgroundResveratrol, a natural plant polyphenol, has received increasing attention because its varied bioactivities, including the inhibition of tumorigenesis, lipid modification and calorie-restriction. We aimed to investigate the effect of resveratrol on oxidative/nitrative stress in endotoxemia-associated acute lung injury.MethodsMice were injected with lipopolysaccharide (LPS, 5 mg/kg, ip). Resveratrol at a dose of 0.3 mg/kg was administered alone or immediately before injection of LPS. Twenty four hours later, lung tissues were collected for histopathologic examination, and determination of malondialdehyde (MDA), H₂O₂, reduced/oxidized glutathione (GSH/GSSG) ratio, total antioxidant capacity (T-AOC), superoxide dismutase (SOD) activity, catalase (CAT) activity, inducible nitric oxide synthase (iNOS) expression, nitric oxide (NO) and peroxynitrite production.ResultsResveratrol treatment improves histopathological changes in the lung during endotoxemia. Increased oxidative stress in endotoxemic lung was reversed by resveratrol treatment, as evidenced by the decreases of pro-oxidant biomarker (MDA and H₂O₂), and the increases of anti-oxidant biomarkers (GSH/GSSG ratio, T-AOC, CAT and SOD activity). Treatment with resveratrol inhibited endotoxemia-induced iNOS expression and NO production. Moreover, peroxynitrite formation in endotoxemic lung was significantly attenuated after resveratrol treatment.ConclusionsResveratrol exerts protective effects against acute endotoxemia-associated lung injury. These beneficial effects may be due to both the anti-oxidant and anti-nitrative properties of resveratrol. These findings support the potential for resveratrol as a possible pharmacological agent to reduce acute lung injury resulting from oxidative/nitrative damage.     

Role of sirtuins in ischemia-reperfusion injury

Ischemia-reperfusion injury(IRI)remains an unresolved and complicated situation in clinical practice,especially in the case of organ transplantation.Several factors contribute to its complexity;the depletion of energy during ischemia and the induction of oxidative stress during reperfusion initiate a cascade of pathways that lead to cell death and finally to severe organ injury.Recently,the sirtuin family of nicotinamide adenine dinucleotide-dependent deacetylases has gained increasing attention from researchers,due to their involvement in the modulation of a wide variety of cellular functions.There are seven mammalian sirtuins and,among them,the nuclear/cytoplasmic sirtuin 1(SIRT1)and the mitochondrial sirtuin 3(SIRT3)are ubiquitously expressed in many tissue types.Sirtuins are known to play major roles in protecting against cellular stress and in controlling metabolic pathways,which are key processes during IRI.In this review,we mainly focus on SIRT1 and SIRT3 and examine their role in modulating pathways against energy depletion during ischemia and their involvement in oxidative stress,apoptosis,microcirculatory stress and inflammation during reperfusion.We present evidence of the beneficial effects of sirtuins against IRI and emphasize the importance of developing new strategies by enhancing their action.     

应激大鼠胃黏膜氧化应激指标受褪黑素影响的研究

目的探讨褪黑素干预应激大鼠胃黏膜氧化应激指标影响的研究.方法采用浸水-束缚(WIR)应激实验复制大鼠应激性溃疡模型.应激前30 min,MT(melatonin)5、20mg·kg-1和应激组大鼠分别腹腔注射MT 5、20mg·kg-1和等体积生理盐水.应激6h后,观察各组大鼠胃黏膜病变情况,对溃疡指数(UI)进行评分,同时检测各组大鼠胃黏膜内丙二醛(MDA)含量、胃黏膜超氧化物歧化酶(SOD)活性和还原型谷胱甘肽(GSH)水平.结果WIR应激6h后,应激组大鼠胃黏膜MDA水平显著高于对照组(P＜0.01).MT 5、20mg·kg-1组较应激组MDA水平显著下降(P＜0.01),且MT 20mg·kg-1组显著低于MT 5mg·kg-1组(P＜0.01).应激组大鼠SOD、GSH活性较对照组明显降低(P＜0.01),MT 5、20mg·kg-1组较应激组SOD、GSH活性有升高趋势.比较各组UI发现,MT 5、20mg·kg-1组UI显著低于应激组(P＜0.01),其中MT 20mg·kg-1组UI显著低于MT 5mg·kg-1组(P＜0.05).结论褪黑素通过其抗氧化的作用对应激大鼠胃黏膜损伤起保护作用.     

芥子气经腹腔和气管致大鼠ALI模型氧化应激反应的机制

目的 经腹腔和气管建立大鼠芥子气(sulfur mustard,SM) ALI动物模型,比较2种大鼠ALI模型氧化应激反应的差异.方法 选取Sprague Dawley大鼠136只,随机分为5组,正常对照组8只,其他4个组(腹腔SM组、腹腔丙二醇组、气管SM组、气管丙二醇组)每组32只.腹腔SM组腹腔内注入稀释的SM 0.1 ml(0.96 LD50＝8 mg/kg),气管SM组气管内注入稀释的SM0.1 ml(0.98 LD50=2 mg/kg),正常对照组不做任何处理.采用酶联免疫吸附试验和免疫组化,判断氧化应激情况.结果 腹腔SM组各时间段BALF中乳酸脱氢酶、谷胱甘肽过氧化物酶水平均高于气管SM组(P值均＜0.05).腹腔SM组各时间段血清γ-谷氨酰转肽酶、硫代巴比妥酸反应产物水平均高于气管SM组(P值均＜0.05).腹腔SM组大鼠肺组织各时间段肺泡间隔8-羟基脱氧鸟苷阳性细胞表达率、红系衍生的核因子2相关因子2和血红素氧合酶1蛋白阳性表达率均高于气管SM组(P值均＜0.05).结论 大鼠在经腹腔和气管SM浓度相似的情况下,经腹腔途径肺氧化应激指标与经气管相比显著升高,推测可能与腹腔对SM的快速吸收有关.     

Systemic oxidative stress in patients with pulmonary sarcoidosis

BackgroundA local redox imbalance has been reported in pulmonary sarcoidosis. However, so far no study has described a systemic redox imbalance in this context. The aim of the present study was to evaluate the systemic oxidative stress in patients with sarcoidosis and determine its relationship to treatment and indices of disease severity.Methods35 patients with histologically proven pulmonary sarcoidosis and 13 healthy volunteers were included in the study. All patients were studied during a stable phase of their disease. Systemic oxidative stress was quantified in serum with the use of a commercially available spectrophotometric method (D-ROM test) which determines overall oxidative stress, by measuring total hydroperoxides. Oxidative stress was expressed in conventional units, i.e. Carratelli Units (UCarr), where 1 UCarr corresponds to 0.8 mg/L H₂O₂.ResultsSerum oxidative stress levels were significantly higher in patients with sarcoidosis compared to those of normal subjects (390 ± 25 vs 300 ± 18 UCarr respectively, p = 0.04). Patients not receiving systemic corticosteroids had higher levels of oxidative stress compared to steroid-treated patients (461.5 ± 38 vs 315 ± 20, p < 0.01) and compared to controls (461.5 ± 38 vs 300 ± 18 UCarr, p < 0.01). Oxidative stress did not correlate with diffusion lung capacity (DLCO), partial arterial oxygen tension (PaO₂), MRC dyspnoea scale or chest X-ray stage.ConclusionsSystemic oxidative stress is increased in patients with stable pulmonary sarcoidosis who do not receive systemic corticosteroids. This finding suggests a sustained oxidative burden even when clinical, functional and radiological criteria indicate disease stability.     

普罗布考对糖尿病肾病大鼠氧化应激的影响

目的 观察普罗布考(PB)对糖尿病肾病(DN)大鼠氧化应激的影响.方法 60只Sprague-Dawley (SD)雄性大鼠随机分成4组:正常对照组(NC组)8只,右肾血管结扎组(RL组)8只,DN组22只,DN+ PB组22只.RL组、DN组和DN+ PB组首先进行右肾血管结扎,1周后DN组和DN+ PB组应用50 ...     

Effects of methylprednisolone on inflammatory activity and oxidative stress in the lungs of brain-dead rats

OBJECTIVE:

To evaluate the effects that early and late systemic administration of methylprednisolone have on lungs in a rat model of brain death.

METHODS:

Twenty-four male Wistar rats were anesthetized and randomly divided into four groups (n = 6 per group): sham-operated (sham); brain death only (BD); brain death plus methylprednisolone (30 mg/kg i.v.) after 5 min (MP5); and brain death plus methylprednisolone (30 mg/kg i.v.) after 60 min (MP60). In the BD, MP5, and MP60 group rats, we induced brain death by inflating a balloon catheter in the extradural space. All of the animals were observed and ventilated for 120 min. We determined hemodynamic and arterial blood gas variables; wet/dry weight ratio; histological score; levels of thiobarbituric acid reactive substances (TBARS); superoxide dismutase (SOD) activity; and catalase activity. In BAL fluid, we determined differential white cell counts, total protein, and lactate dehydrogenase levels. Myeloperoxidase activity, lipid peroxidation, and TNF-α levels were assessed in lung tissue.

RESULTS:

No significant differences were found among the groups in terms of hemodynamics, arterial blood gases, wet/dry weight ratio, BAL fluid analysis, or histological score-nor in terms of SOD, myeloperoxidase, and catalase activity. The levels of TBARS were significantly higher in the MP5 and MP60 groups than in the sham and BD groups (p < 0.001). The levels of TNF-α were significantly lower in the MP5 and MP60 groups than in the BD group (p < 0.001).

CONCLUSIONS:

In this model of brain death, the early and late administration of methylprednisolone had similar effects on inflammatory activity and lipid peroxidation in lung tissue.     

Effects of Wy14643 on hepatic ischemia reperfusion injury in rats

AIM： To investigate the effects and possible mechanisms of Wy14643 on hepatic ischemiareperfusion （I/R） injury in rats. METHODS： Thirty male Sprague-Dawley rats weighing 220-280 g were randomly divided into five experimental groups： sham group （G1, n = 6）： a sham operation was performed （except for liver I/R）, I/R-untreated group （G2, n = 6）： rats underwent liver ischemia for 90 min followed by reperfusion for 4h; and I/R ＋ Wy14643 groups （G3, G4, G5; n = 6）： after the same surgical procedure as in group 2, animals were pretreated with Wy14643 at the dose of 1, 5 and 10 mg/kg 1 h before ischemia, respectively. Hepatic ischemia-reperfusion （I/R） was induced by clamping blood supply to the left lateral and median lobes of the liver for 90 min, and atraumatic clamp was removed for 4 h reperfusion. Blood samples and liver tissues were obtained at the end of reperfusion to assess serum and hepatic tissue homogenate aminotransferase （ALT）, aspartate aminotransferase （AST）, myeloperoxidase （MPO）, serum interleukin- 1β（IL-1β） and tumor necrosis factor alpha （TNF-α）, as well as activity of superoxide dismutase （SOD） and content of malondialdehyde （MDA） in the hepatic tissue homogenate. RESULTS： Hepatic I/R induced a significant increase in the serum levels of ALT, AST, TNF-α, IL-1β and MPO, as well as the levels of ALT, AST and MDA in the liver tissue homogenate, which were reduced by pretreatment with Wy14643 at the dose of 1, 5 and 10 mg/kg, respectively. The activity of SOD in the liver tissue homogenate was decreased after hepatic I/R, which was enhanced by Wy14643 pretreatment. In addition, serum and liver tissue homogenate ALT and AST in the Wy14643 10 mg/kg group were lower than in the Wy14643 1 mg/kg and 5 mg/kg groups, respectively. CONCLUSION： Wy14643 pretreatment exerts significant protection against hepatic I/R injury in rats. The protective effects are possibly associated with enhancement of anti-oxidant and inhibition inflammation res     

三七总皂苷预处理对大鼠小肠缺血再灌注损伤的保护作用

目的:探讨三七总皂苷对大鼠小肠缺血再灌注(ischemia-reperfusion,IR)损伤的保护机制.方法:用肠系膜上动脉夹闭-松夹方式复制SD大鼠IR模型.检测血浆脂多糖和D-乳酸含量;取血液、肝、脾、肠系膜淋巴结,做细菌培养;免疫组织化学检测小肠组织中的NF-B及TNF-表达;用脱氧核糖核酸末端转移酶介导的缺口末端标记技术检测小肠组织细胞凋亡.结果:PNS组肝、脾、肠系膜淋巴结及血液细菌培养阳性数显著低于模型组(P<0.05);三七总皂苷200mg/kg和400mg/kgPNS组血浆脂多糖浓度分别是461EU/L,320EU/L,与模型组(570EU/L)比较差异显著(P<0.05);PNS组的血浆D-乳酸浓度分别是0.37mmol/L,0.31mmol/L,与模型组(0.44mmol/L)比较差异显著(P<0.05);三七总皂苷也可降低NF-B和TNF-的表达,且细胞凋亡数密度低于模型组.结论:三七总皂苷通过降低NF-B和TNF-表达,减轻细胞因子对小肠的损伤,减少小肠黏膜细胞凋亡,发挥对小肠IR损伤的保护作用.