大鼠肾冷缺血再灌注损伤模型的建立

目的 建立大鼠肾冷缺血再灌注损伤(IRI)的模型.方法 封闭群SD大鼠24只,随机分为2组(n=12):A组(对照组),B组(实验组).A组切除右肾并游离左肾蒂,60 min后关闭腹腔切口.B组采用冷缺血再灌注模型,主要步骤:(1)冷灌注:右肾动脉插管对左肾原位灌注.通过右肾静脉插管将灌注液引流出体外,完成冷灌注后切除右肾,阻断左肾蒂.(2)冷缺血保存:将已充分游离的左肾牵至腹腔外,在自制保存袋中冷保存.(3)再灌注:60min后,去除保存袋,开放血流,再灌注左肾,左肾复位,缝合切口;2组大鼠均在术后24 h再次手术切除左.肾.肾组织进行光镜、电镜形态学检查,检测肾组织匀浆中超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量,术前与术后24 h取血标本进行测定血尿素氮(BUN)、肌酐(Cr)评估肾功能.结果 (1)形态学检查(光镜与电镜超微结构):A组肾脏组织形态结构正常,B组损伤表现明显;(2)A组手术前后比较血浆BUN、Cr测定值差异均无统计学意义(P＞0.05).IR后的B组均高于术前,差异有统计学意义(P＜0.05);(3)IRI后A组肾组织匀浆SOD活力高于B组(P＜0.05),A组肾组织匀浆MDA含量测定值低于B组,差异有统计学意义(P＜0.05).结论 建立的模型要求条件简单、易行,可用于肾移植冷缺血再灌注损伤相关的研究;

Abstract：

Objective In this study,for studying IRI in kidney transplantation. ,we established the models of cold ischemia and reperfusion injury in rats. Methods Twenty four SD rats were randomly assigned to two groups:control (A) ,and experimental (B) group. Group A was only removed the right kidney. Cold ischemia reperfusion was performed as the follow-listed model in Group B. The main process of the model: ( 1) Perfusing left kidney: after resected the right kidney of the rat, one pipe was put in the remainder right renal artery to perfuse the left kidney. The perfusion flowed out through another pipe in the right renal vein. The blood vessels of left kidney were clipped after cold perfusion. (2) Cold ischemic conservancy : the operation table was leant to left side, and the left kidney was taken out of abdominal cavity then stored in a cold bag which was full of ice and water,but the vessels of that were intact. (3) Reperfusing left kidney: after 60 minutes, the clip was removed. Left kidneys of all rats in two groups were removed to be detected. Structure of the kidney was evaluated by light microscopy and electronic microscopy. Superoxide dismutase ( SOD) activity and malondialdehyde ( MDA) content in the renal tissues was examined,and the renal function was also assessed by determining the levels of blood urea nitrogen ( BUN) and serum creatinine (CR) before and 24 hours after operation. Results (1) Morphologic change (hematoxylin-eosin staining) :A normal morphology was observed by light microscopy and electon microscopy in group A.Significant injury was detected in group B. (2 ) In group A, there was not significant difference about BUN and CR between before and after operation (P ＞0. 05) ,but in Group B,those increased significantly at 24 hour after operation (P ＜0. 05). (3) Activity of SOD in renal tissues in group A was higher than those in group B (P ＜ 0. 05 ) , meanwhile, Content of MDA in group A was lower than those in group B ( P ＜0. 05 ).Conclusion The rat renal cold ischemia reperfusion model we established is feasible regardless of experimental conditions, and can be studied as the events following IRI in kidney transplantation.     

褪黑素对大鼠肝缺血再灌注损伤的保护作用

目的 观察褪黑素(Mel)对大鼠肝组织caspase-3表达的影响及对肝缺血再灌注损伤的保护作用.方法 将72只Wistar大鼠,随机分为褪黑素处理3、6、12、24 h组(Mel组),同样乙醇溶媒对照组(Alc组)和生理盐水对照组(NS组)也分别按3、6、12、24 h各自分为4组,总共为12组.建立肝缺血再灌注损伤模型,于不同时点测定血清肝组织生化酶:ALT、AKP、对肝组织进行Caspase-3免疫组织化学染色.结果 ALT在再灌注后各时点Mel组均显著低于Alc及NS对照组(P＜0.05),AKP在再灌注后6、12、24 h,Mel组显著低于Alc及NS对照组(P＜0.05),Mel组再灌注后各时点的Caspase-3染色阳性细胞率均显著低于对照组(Alc组和Ns组,P＜0.05),以上各项指标在各时点Alc组与NS组比较差异无统计学意义(P＞0.05).结论 Mel能够减轻大鼠肝缺血再灌注损伤时的肝功能损害,抑制肝细胞Caspase-3的表达,减少肝细胞凋亡,对大鼠肝脏缺血再灌注损伤具有保护作用.     

新型铁螯合剂CHGN2957对大鼠肾缺血再灌注损伤的保护作用

目的 观察新型铁螯合剂CHGN2957对大鼠肾缺血再灌注损伤(I/R)急性期的保护作用.方法 选用雄性SD大鼠90只,随机分成5组(n=18):假手术组、CHGN2957高剂量组、低剂量组、溶剂组和阳性对照组.建成大鼠急性肾I/R模型.药物干预均从手术前2 d开始,直至术后12 d结束.观察大鼠死亡率、体质量变化,测定肾功能和肾组织中超氧化物歧化酶(SOD)活力、谷胱甘肽(GSH)还原酶活力和丙二醛(MDA)含量并进行肾组织病理切片观察.结果 术后第3天CHGN2957溶剂组的体质量(242.1±16.2)g、SOD活力(1.23±0.13)U/mg、GSH还原酶活力(336±15)U/L明显低于其他各组(P＜0.05),而血清尿素氮(62.3±3.1)mmol/L、血清肌酐(310.00±21.02)μmol/L、MDA含量(186.5±16.7)nmol/mg明显高于其他各组(P＜0.05).肾组织病理评分显示CHGN2957溶剂组的肾小管损伤明显重于其他各组(P＜0.05).结论 CHGN2957作为一种新型铁螯合剂,在大鼠急性肾I/R过程中能有效减轻大鼠肾I/R,并对肾起保护作用.

Abstract：

Objective To observe the protecgive effects of CHGN2957 on acute renal ischemia/reperfusion injury (I/R) model in rats. Methods Ninety Sprague-Dawley male rats were randomly divided into five groups ( n = 18 each): sham-operative group, high-dose CHGN2957 group, low-dose CHGN2957 group, CHGN2957 vehicle group and positive group. The administration lasted from two days before operation to twelve days after operation. After seccessful establishment of the model, mortality,weight changes, the renal function, superoxide dismutase ( SOD ) activity, glutathione ( GSH ) reductases activity and malondialdehyde (MDA) content in renal tissue were recorded, and the pathological changes were observed. Results Weight (242. 1 ± 16. 2) g, SOD activity (1. 23 ±0. 13) U/mg and GSH reductases activity (336 ± 15 U/L) in CHGN2957 vehicle group were reduced significantly as compared with other groups three days after I/R (P ＜0. 05), but SUN (62. 3 ± 3. 1) mmol/L, SCr (310. 00 ± 21. 02)μmol/L, MDA content ( 186. 5 ± 16. 7 ) nmol/mg were higher than others obviously ( P ＜ 0. 05 ). Pathological observation showed renal tubular injury was more serious in CHGN2957 vehicle group (P＜0.05).Conclusion CHGN2957 as a new iron chelator was effective to ameliorate renal I/R in rats.     

丙泊酚对大鼠急性肾缺血再灌注损伤的影响

目的 探讨丙泊酚预处理对急性肾缺血再灌注损伤(acute renal ischemia reperfusion injury ,ARIRI)的保护作用及其机制.方法 采用完全随机研究设计(randomized controlled trial,RCT),健康近交系清洁级的雄性SD大鼠63只,随机分为3组:假手术组(A组)、缺血再灌注组(B组)、丙泊酚预处理组(C组),每组21只SD大鼠.采用切除右侧肾,用无损伤微动脉夹夹闭左侧肾蒂60分钟后解除阻断,建立大鼠急性肾缺血再灌注损伤模型.用24号套管针股静脉穿刺置管,实验过程中各组使用微量注射泵注入不同注射液.分别于手术前15分钟、再灌注后2小时、24小时留取血和肾组织标本同时处死大鼠,检测血清尿素氮(BUN)、肌酐(Cr)、超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)及观察这三个时点肾组织的病理学改变.结果 丙泊酚预处理组各个时点的肾组织病理学变化均轻于缺血再灌注组.缺血再灌注组中血清BUN、Cr、MDA和TNF-α水平增加均高于丙泊酚预处理组(p＜0.05),丙泊酚预处理组血清SOD、IL-6水平均高于缺血再灌注组(p＜0.05).结论 丙泊酚预处理组血清BUN、Cr、MDA、TNF-α、SOD、IL-6水平与缺血再灌注组均有统计学差异.结果 表明丙泊酚能减少氧自由基释放,抑制和减少炎症反应,在急性肾缺血再灌注损伤能起到保护肾脏的作用.     

血红素氧合酶-1对大鼠肾缺血再灌注损伤的保护作用

目的　探讨钴卟啉 (CoPP)诱导的血红素氧合酶 (HO) 1高表达对大鼠肾缺血再灌注损伤 (IRI)的保护作用。方法　建立大鼠肾缺血再灌注损伤模型 ,随机将动物分为假手术组 ,对照组和实验组。动态检测血尿素氮 (BUN)、肌酐 (Cr)、超氧化物岐化酶 (SOD)、丙二醛 (MDA)的含量以及进行肾组织光镜形态学观察和酶联免疫吸附试验 (ELISA)和Westernblot分析HO 1。结果　对照组BUN、Cr升高 ,SOD下降 ,MDA升高 ,HO 1中度提高 (14 4.5± 13 .6) ,肾组织结构紊乱。实验组除HO 1含量大幅提高外 (62 9.4± 78.9) ,尚能显著逆转上述改变 ,两组间差异具有统计学意义 (P <0 .0 5 )。结论　CoPP预处理诱导HO 1在肾缺血之前高表达可通过清除氧自由基 (OFRs)而减轻大鼠肾IRI。     

含饱和氢气肾保存液对大鼠肾脏冷缺血再灌注损伤的影响

目的 评价含饱和氢气肾保存液对大鼠肾脏冷缺血再灌注损伤的影响.方法 健康雄性Wistar大鼠24只,周龄8～10周,体重200～ 250 g,采用随机数字表法,将其随机分为3组(n=8):对照组(H1组)大鼠仅切除右肾;普通肾保存液组(H2组)大鼠采用冷缺血再灌注模型,用4℃普通HC-A肾保存液对左肾行冷灌注和冷保存;含饱和氢气肾保存液组(H3组)大鼠操作同H2组,灌注液及保存液换用自制的4℃含饱和氢气HC-A肾保存液.于再灌注24 h时抽取下腔静脉血样,测定血清BUN、Cr、TNF-α和IL-6浓度;切取左肾,测定肾组织MDA和8-羟基脱氧鸟苷(8-OHdG)含量,光镜下观察肾组织病理学结果.结果 与H1组相比,H2组和H3组大鼠血清BUN、Cr、TNF-α和IL-6浓度及肾组织MDA和8-OHdG含量均升高(P＜ 0.05);与H2组相比,H3组血清BUN、Cr、TNF-α和IL-6浓度及肾组织MDA和8-OHdG的含量均降低(P＜0.05).H1组肾组织形态结构未见明显异常,H2组肾小管损伤明显,H3组肾小管损伤较H2组减轻.结论 含饱和氢气肾保存液可明显减轻大鼠肾脏冷缺血再灌注损伤.     

饱和氢盐水对大鼠下肢缺血再灌注及远隔肺组织损伤的保护作用

目的 观察饱和氢盐水对大鼠下肢组织缺血再灌注及远隔肺组织损伤的保护作用.方法 将30只健康SD雄性大鼠随机分为3组:假手术组(S组)、生理盐水组(C组)、氢水治疗组(H组).建立大鼠下肢缺血再灌注损伤模型(阻断腹主动脉4 h,再灌注4 h),在再灌注前10min分别注入饱和氢盐水1 ml/100 g(H组),生理盐水1 ml/100 g(C组).再灌注4 h后比较肺及腓肠肌湿/干重(W/D)比值、观察病理切片的改变,测定血清、肺及腓肠肌组织中丙二醛(MDA)、肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6含量变化.结果 H组肌(4.04±0.22)、肺(4.47±0.23)组织湿/干重比低于C组肌(4.67±0.27),肺(4.67±0.27)、组织(P＜0.05),MDA、TNF-α及IL-6血浆[分别为(2.08±1.27)μmol/L、(528.22±221.17)、(41.14±13.01)ng/L]及组织[肺组织分别为(3.58±1.62)μmol/L、(1.17±0.15)、(0.79±0.29)ng/L;肌组织分别为(8.91±3.13)μmol/L、(3.13±0.41)、(3.07±1.69)ng/L)含量均低于C组(P＜0.05),腓肠肌及肺病理学损害明显减轻,与S组比较差异无统计学意义(P＞0.05).结论 缺血再灌注前输注饱和氢盐水可有效保护大鼠下肢缺血再灌注及远隔肺组织的损伤.

Abstract：

Objective To explore the protective effects of hydrogen-rich saline against hind limb ischemia reperfusion injury and associated remote lung injury in rats. Methods Thirty Sprague-Dawley rats were randomly divided into three groups: sham group ( group S) ; saline control group (group C) , undergoing intravenous infusion of saline (1 ml/100 g) at 10 min before reperfusion; hydrogen-treated group ( group H) , undergoing intravenous infusion of hydrogen-rich saline (1 ml/100 g) at 10 min before reperfusion. Hind limb ischemia reperfusion model was established by 4 h of the abdominal aorta ligation followed by a 4 h of reperfusion. Rats were killed at the end of reperfusion, and blood samples were collected for determination of serum levels of tumor necrosis factor-α ( TNF-α) , interleukin-6 (IL-6) and malonyldialdehyde ( MDA). Specimens of lung and gastrocnemius muscle were collected for measurement of wet-todry weight (W/D) ratio, light microscopic examination and detection of plasma TNF-α, IL-6 and MDA.Results The pathological changes were milder in group H than in group C. The lung (4. 47 ±0. 23) and gastrocnemius muscle (4. 04 ±0. 22) W/D ratio in group H was significantly lower than in group C (4. 67 ±0.27 vs4. 67 ±0.27, P＜0.05). The serum [(2.08 ± 1. 27) μmol/L, (528. 22 ±221. 17) , (41.14± 13. 01) ng/L, respectively] and homogenate levels [(3. 58 ± 1. 62) μmol/L, ( 1. 17 ±0. 15) , (0. 79±0.29) ng/L in the lung; (8.91 ±3. 13) μmol/L, (3. 13 ±0. 41) ,(3. 07 ± 1. 69) ng/L in the gastrocnemius muscle, respectively] of MDA, IL-6 and TNF-a were also significantly lower in group H than in group C (P ＜0. 05) , but there was no significant difference from group S. Conclusion Infusion of hydrogen-rich saline before reperfsion significantly alleviates the hind limb ischemia reperfusion injury and associated remote lung injury.     

缺血再灌注损伤对肝脏免疫原性的影响

目的 观察缺血再灌注损伤对肝脏免疫原性的影响.方法 30只大鼠均分为3组,利用免疫荧光及Western blol检测缺血30min再灌注组及缺血60min再灌注组及对照组的肝脏中共刺激分子B7蛋白的表达水平.结果 正常肝脏B7-1、B7-2表达处于极低水平(0.035±0.005、0.025±0.004),缺血再灌注后肝脏B7-1、B7-2的蛋白表达明显升高(P<0.01),缺血再灌注60min组的B7-1、B7-2的表达水平明显高于缺血30min再灌注组(B7-1:0.070±0.017比0.051±0.008,B7-2:0.042±0.004.比0.037±0.004,P<0.01).结论 缺血再灌注损伤使共刺激分子B7蛋白表达升高,提示缺血再灌注损伤可使移植肝免疫原性升高,这些均能促进急性排斥反应的发生.     

Changes in regional renal perfusion following ischemia/reperfusion injury to the rat kidney

Summary Post-ischemic renal failure is associated with a zone of vascular hyperaemia in the outer medulla of the kidney. The effect of this lesion on regional renal perfusion is, however, unclear. Acute unilateral renal ischemia was applied to four groups of ten adult male Wistar rats for a period of 60 min, followed by revascularisation for 0, 15, 30 or 60 min. The aorta was then clamped and Microfil was injected at a standard pressure to fill the renal vasculature. Gross and histological examinations of the renal parenchyma and vasculature were then performed. Regional renal Microfil perfusion was quantified by examination of unstained histological sections, giving rise to a vascular perfusion index (VPI) for each vascular region of the kidney. The VPIs were similar in control and ischemic kidneys that were not subjected to reflow (group 1). In contrast, the VPI was markedly decreased in the inner stripe and inner medulla in animals in which revascularisation had occurred (groups 2–4), and the vasculature in these regions was histologically shown to be packed with red blood cells. Post-ischemic renal failure is associated with hyperperfusion of the medulla resulting from blockage of the vasculature that occurs during revascularisation.     

肝硬变大鼠肝脏缺血再灌注损伤

为比较硬化肝与正常肝在缺血再灌注损伤时的差异和意义。作者采用四氯化碳复制大鼠肝硬变模型,通过大鼠肝脏缺血再灌注损伤模型,检查不同时限大鼠门静脉血内毒素、肝静脉血一氧化氮。结果显示：肝硬变大鼠再灌注时门静脉内毒素水平更高;肝脏ＮＯ合成释放显著增加。作者认为肝硬变时对缺血再灌注损伤反应与正常大鼠不同,可能是肝硬变时对缺血再灌注损伤更敏感,更易发生肝功能衰竭的重要原因。     

乌司他丁对大鼠肾缺血/再灌注损伤的保护作用

目的探讨乌司他丁对大鼠肾缺血/再灌注(I/R)损伤的作用及其机制.方法雄性SD大鼠75只,随机分为三组假手术对照组(C组)、肾I/R组(I组)、乌司他丁组(U组),每组25只.I组和U组大鼠夹闭双侧肾蒂45min后重新开放肾脏血供,制作肾脏I/R模型,C组不夹闭双侧肾蒂.U组缺血前30min及再灌注开始时静脉注射乌司他丁1.25万单位,I组分别静脉注射生理盐水1ml.各组在再灌注后0、2、6、12、24h时取标本,测定血尿素氮(BUN)和血肌酐(Cr)浓度,并制备肾脏病理切片,采用免疫组化方法测定热休克蛋白70(HSP70)和bcl-2蛋白的表达.结果与I组比较,C组在再灌注后各时点血清BUN和Cr浓度均降低(P＜0.05),U组在再灌注后12、24h时血清BUN和Cr浓度也降低(P＜0.05).C组肾脏未发现明显的形态学改变;I组近曲小管上皮细胞空泡变性和坏死,肾小管腔扩张,内可见管型和坏死脱落细胞,可见管周血管明显扩张淤血;U组近曲小管上皮细胞肿胀、颗粒变性,罕见管型,管周稍有淤血.与I组比较,C组在再灌注后0、6、12、24h时Paller评分降低(P＜0.05),U组在再灌注后0、6、24h时Paller评分也降低(P＜0.05),C组再灌注后12、24h时HSP70表达降低(P＜0.05),U组在再灌注后6、24h时bcl-2蛋白表达增强(P＜0.05).结论乌司他丁对肾脏I/R损伤有保护作用,其机理可能与上调肾脏bcl-2蛋白表达有关.     

钴原卟啉诱导血红素氧合酶-1高表达减轻大鼠肾脏缺血再灌注损伤

目的 探讨钴原卟啉(CoPP)诱导血红素氧合酶-1(HO-1)高表达对大鼠肾脏缺血再灌注损伤(IRI)的影响及其机理.方法 以Wistar大鼠为实验对象,CoPP组分别于左肾血流阻断前48 h和24 h腹腔注射CoPP 2.5 mg/kg,然后阻断左肾血流47 min,恢复左肾血流的同时切取大鼠右肾,采用免疫组织化学染色和免疫印迹法检测其HO-1的表达.在再灌注24 h后,处死大鼠,取其下腔静脉血和左肾,测定血肌酐(Cr)和尿素氮(BUN)浓度,观察肾组织学变化,检测肾组织中HO-1的表达.IRI组除不用CoPP处理外,其余同CoPP组.CoPP组和IRI组另有部分大鼠的血流阻断时间延长至80 min,恢复血流后不处死,观察14 d,记录其存活情况.结果 IRI组血清Cr及BUN分别为(134.37±24.26)μmol/L和(30.10±3.09)mmol/L,明显高于CoPP组的(48.92±12.92)μmol/L和(13.99±5.00)mmol/L(P＜0.05).IRI组肾小管细胞大片坏死,管型形成,与之相比,CoPP组肾小管坏死范围稍小,但肾小管病变范围仍较广泛,肾小管上皮细胞多处于水变性阶段,"缺血样"肾小球减少,管型形成较少.缺血前及再灌注24 h后,CoPP组的肾组织中HO-1均为高表达,主要位于肾间质的毛细血管处,IRI组再灌注24 h后也见肾组织中HO-1为高表达.术后14 d内,IRI组的6只大鼠中有4只死亡,而CoPP组的5只大鼠全部存活,两组大鼠存活率的差异有统计学意义(P＜0.05).结论 缺血前使用CoPP可减轻大鼠肾脏缺血再灌注损伤,该保护作用可能是通过CoPP诱导肾脏高表达HO-1来实现的.     

缺血再灌流肾组织内皮素—1动态变化的实验研究

在大鼠肾缺血６０分钟再灌注的模型上观察不同时相肾静脉血、肾皮质、外髓和内髓的内皮素１（ＥＴ１）浓度变化，肾组织ＥＴ１光镜和电镜免疫组织化学变化。结果发现：缺血再灌流肾组织ＥＴ１基因表达及分泌明显增强，主要分布在血管内皮细胞及平滑肌细胞、系膜细胞、肾小管上皮细胞。其分布特点与细胞类型和活性有关。本实验结果提示了缺血再灌注肾内ＥＴ１的变化规律。     

环状RNA在缺血/再灌注损伤中的作用研究进展

缺血/再灌注损伤（ischemia/reperfusion injury, I/RI）涉及复杂的病理生理过程,但具体分子生物学机制尚不确切。近年研究表明环状RNA在I/RI中也发挥了重要作用。环状RNA是一类特殊编码的RNA,由于对核酸外切酶不敏感,相比线性RNA,其表达更为稳定,且不易降解,这使环状RNA在作为新型临...     

1,6二磷酸果糖对大鼠脑缺血-再灌注损伤后凋亡细胞及p38和Ref-1的研究

目的探讨1,6二磷酸果糖（FDP）对大鼠脑缺血-再灌注（I-R）损伤的作用及其机制。方法雄性SD大鼠90只,随机分为果糖治疗（F）组、脑缺血（I）组和假手术对照（c）组,每组30只。I组和F组大鼠在凝断双侧椎动脉24h后夹闭双侧颈总动脉,5min后重新开放,制作全脑缺血模型。F组再灌注开始时静脉注射FDP 1．5ml／kg,I组及C组分别静脉注射生理盐水1．5ml／kg。各组在再灌注后2、6、12、24、48、72h时取标本,制备脑组织病理切片,采用免疫组织化学染色方法测定p38蛋白和Ref-1蛋白的表达,TUNEL检测凋亡细胞数目。结果与C组比较,I组凋亡细胞显著增多（P〈0．05）;与C组比较,I组在再灌注后各时点p38蛋白、Ref-1蛋白表达均显著增强（P〈0．05）,F组较C组表达增强但较I组表达显著减弱（P〈0．05）。结论FDP对全脑I-R损伤有保护作用,其机理可能与其参与细胞信号转导减弱p38、Ref-1蛋白表达强度有关。     

姜黄素对肝缺血再灌注损伤保护作用的研究

目的探讨姜黄素对自体肝移植大鼠肝脏缺血再灌注损伤(IRI)的保护作用及其可能机制。方法54只SD雄性大鼠随机分为假手术(SO)组、自体肝移植模型姜黄素预处理(CU)组以及自体肝移植模型溶剂对照(CM)组,术后或再灌注2,6,24 h每组分别处死6只大鼠进行谷丙转氨酶(ALT)、谷草转氨酶(AST)、髓过氧化物酶(Myeloperoxidase MPO)的含量检测。结果血清ALT及AST水平,CM组及CU组均较SO组明显升高,但CM组又明显高于CU组;MPO在SO组含量明显低于CM组和CU组,而CU组又显著低于CM组。结论姜黄素对自体肝移植大鼠肝缺血再灌注损伤有保护作用,其机制可能与减轻中性粒细胞浸润有关。     

大鼠肾脏缺血再灌注损伤中垂体中叶素及降钙素受体样受体的表达

目的 观察垂体中叶素（IMD）及其受体降钙素受体样受体（CRLR）在大鼠肾脏缺血再灌注损伤中的表达变化。 方法 将健康雄性Wistar大鼠随机分为假手术组和手术组,夹闭大鼠双侧肾动脉制作肾脏缺血再灌注损伤（IRI）模型,于缺血再灌注后0、6、12、24、48、72 h 6个时间点各取6只大鼠,留取血清及肾组织标本,对肾脏病理损伤评分并行半定量分析; Western印迹法半定量分析肾组织IMD及其受体CRLR的表达变化;放射免疫法检测血浆中IMD的表达变化。 结果 手术组大鼠发生了急性肾小管坏死（ATN）,以缺血再灌注48 h时病理损伤最重。与假手术组比较,IMD及CRLR在缺血再灌注12、24、48、72 h表达显著增高（均P < 0.01）;血浆中IMD在缺血再灌注12、48、72 h表达显著增高（均P < 0.05）。 结论 IMD及受体CRLR在大鼠肾脏缺血再灌注损伤中表达增加,血浆中IMD表达上调,提示其可能在肾脏缺血再灌注损伤病理生理过程中发挥作用。     

肾脏缺血再灌注损伤过程中天然免疫分子高迁移率族蛋白B1释放变化

目的 观察高迁移率族蛋白B1(HMGB1)在小鼠肾脏缺血再灌注损伤(IRI)中的表达变化.方法 建立小鼠IRI模型,再灌注0、3、6 h或24 h后取外周血及左肾,测定血肌酐(Cr)和尿素氮(BUN)水平,免疫组织化学及Western blot检测肾组织全蛋白和胞质蛋白HMGB1的表达,并观察病理学变化(HE)及细胞凋亡.结果与假手术组比较,再灌注0 h时小鼠血清Cr和BUN无明显升高,而再灌注3、6、24 h后呈阶梯性显著性升高.假手术组肾组织HMGB1几乎均表达于细胞核内,而肾脏缺血损伤后HMGB1即开始在(主要是肾小管上皮细胞)胞质或胞外表达,且HMGB1在细胞核外的表达量在再灌注3 h时最强,之后缓慢减弱,而24 h内细胞总蛋白HMGB1表达量未见明显变化.再灌注0、24 h病理损伤渐进性加重,而凋亡细胞显著性增加.结论 HMGB1在肾IRI早期表达总量恒定而表达部位发生改变,且表达部位的改变先于肾功能的变化,HMGB1可能作为重要早期炎症因子在IRI启动中发挥作用.