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| 1 | Protective effects of Ligustrazine,Kakonein and Panax Notoginsenoside on the small intestine and immune organs of rats with severe acute pancreatitis显示文摘BACKGROUND:Severe acute pancreatitis (SAP) is characterized by fatal pathogenic conditions and a high mortality.It is important to study SAP complicated with multiple organ injury.In this study we compared the protective effects of three traditional Chinese medicines (Ligustrazine,Kakonein and Panax Notoginsenoside) on the small intestine and immune organs (thymus,spleen and lymph nodes) of rats with SAP and explored their mechanism of action.METHODS:One hundred forty-four rats with SAP were randomly divided into model control,Ligustrazine-treated,Kakonein-treated,and Panax Notoginsenoside-treated groups (n=36 per group).Another 36 normal rats comprised the sham-operated group.According to the different time points after operation,the experimental rats in each group were subdivided into 3-,6-and 12-hour subgroups (n=12).At various time points after operation,the mortality rate of rats and pathological changes in the small intestine and immune organs were recorded and the serum amylase levels were measured.RESULTS:Compared to the model control groups,the mortality rates in all treated groups declined and the pathological changes in the small intestine and immune tissues were relieved to different degrees.The serum amylase levels in the three treated groups were significantly lower than those in the model control group at 12 hours.The pathological severity scores for the small intestinal mucosa,thymus and spleen (at 3 and 12 hours) in the Ligustrazine-treated group,for the thymus (at 3 and 12 hours) and spleen (at 3 and 6 hours) in the Kakonein-treated group,and for the thymus (at 3 hours)and spleen (at 3 hours) in the Panax Notoginsenoside-treated group were significantly lower than those in the model control group.The pathological severity scores of the small intestinal mucosa (at 6 and 12 hours) and thymus (at 6 hours) in the Ligustrazine-treated group were significantly lower than those in the Kakonein-and Panax Notoginsenoside-treated groups.CONCLUSIONS:All the three traditional Chinese drugs significantly alleviated the pathological changes in the small intestine and immune organs of SAP rats.Ligustrazine was the most effective one among them. | Xi-Ping Zhang,Jun Jiang,Qi-Hui Cheng,Qian Ye,Wei-Juan Li,Hua Zhu and Jun-Ya Shen Department of General Surgery,Department of Gynecology and Obstetrics and Central Laboratory Department,Hangzhou First People’s Hospital,Hangzhou 310006,China Zhejiang Chinese Medical University,Hangzhou 310053,China | 2011 | Hepatobiliary & Pancreatic Diseases International2011，10，6： | 11 |
| 2 | HMGB1在重症急性胰腺炎大鼠肺损伤中的表达及乌司他丁的干预效应显示文摘目的研究高迁移率族蛋白-1(HMGB1)在重症急性胰腺炎(SAP)大鼠肺损害的机理以及乌司他丁的干预效应。方法将54只SD大鼠随机分为对照组、SAP组和乌司他丁治疗组三组,每组各18只,每组再分为6h、12h和24h亚组(n=6)。以5%的牛磺胆酸造模SAP,对照组开腹并拨动胰腺组织,而治疗组在SAP基础上予乌司他丁干预。检测胰腺及肺组织的病理学及血氧分压改变;免疫法检测胰腺的HMGB1的水平;ELISA法检测胰腺、肺及血中的TNF-α、HMGB1、IL-1β蛋白浓度。结果 SAP组在血、胰腺、肺中的HMGB1蛋白浓度在6~24h持续上升,SAP组、治疗组明显高于对照组,差异均有统计学意义(P<0.05);SAP组血清中的IL-1β、TNF-α蛋白浓度在6~12h持续上升,于24h开始降低,SAP组、治疗组明显高于对照组且差异均有统计学意义(P<0.05);SAP组胰腺可见HMGB1强表达:SAP组>治疗组>对照组,从6~24h保持上升趋势,差异均有统计学意义(P<0.05)。结论 SAP大鼠的炎症机制可能是由于HMGB1部分结合TNF-α、IL-1β并通过JNK信号通路而导致的,而乌司他丁能降低SAP大鼠肺组织中HMGB1、TNF-α、IL-1β表达及中断JNK信号通路,能有效治疗SAP大鼠的胰腺及肺损伤。 | 王静 黄忠 魏尉 候聪 王霆宇 罗红发 | 2018 | 西部医学2018，30，2： | 10 |
| 3 | 氯膦酸二钠脂质体对大鼠重症急性胰腺炎肺损伤的影响及与Akt、MAPK(ERK1/2)通路的关系显示文摘目的:探讨氯膦酸二钠脂质体(LC)对大鼠重症急性胰腺炎(SAP)肺损伤的影响及与Akt、MAPK(ERK1/2)通路的关系。方法:将48只SD大鼠随机均分为假手术组、SAP模型组(模型组)、SAP模型+LC处理组(LC组),后两组采用膜下注射5%牛磺胆酸钠制作SAP模型,并分别于造模后尾静脉注射空白脂质体与LC。各组分别于术后2、6h后检测血清淀粉酶(AMS)、IL-6、TNF-α的含量,观察肺组织病理学变化,及肺组织中Akt和MAPK(ERK1/2)的表达。结果:与假手术组比较,模型组与LC组血清AMS、IL-6及TNF-α含量、肺组织病理学评分,肺组织Akt和MAPK(ERK1/2)表达水平均明显升高,且均随时间延长而更加明显(均P<0.05),但LC组的上述指标在各时间点上均明显低于模型组(均P<0.05)。结论:LC有减轻大鼠SAP肺损伤的作用,机制可能与肺泡巨噬细胞吞噬LC后,Akt和MAPK(ERK1/2)信号通路抑制,从而减少炎症细胞因子的释放有关。 | 李涛 刘源 李冉 刘路路 蒋国雄 党胜春 张建新 顾敏 | 2016 | 中国普通外科杂志2016，25，3： | 10 |
| 4 | Protective effect of clodronate-containing liposomes on intestinal mucosal injury in rats with severe acute pancreatitis显示文摘BACKGROUND: Severe acute pancreatitis (SAP) can result in intestinal mucosal injury. This study aimed to demonstrate the protective effect of clodronate-containing liposomes on intestinal mucosal injury in rats with SAP. METHODS: Liposomes containing clodronate or phosphate buffered saline (PBS) were prepared by the thin-film method SAP models were prepared by a uniform injection of sodium taurocholate (2 mL/kg body weight) into the subcapsular space of the pancreas. Sprague-Dawley rats were randomly divided into a control group (C group), a SAP plus PBS-containing liposomes group (P group) and a SAP plus clodronate-containing liposomes group (T group). At 2 and 6 hours after the establishment of SAP models, 2 mL blood samples were taken from the superior mesenteric vein to measure the contents of serum TNF-α and IL-12. Pathological changes in the intestine and pancreas were observed using hematoxylin and eosin staining, while apoptosis was detected using TUNEL staining. In addition, the macrophage markers cluster of differentiation 68 (CD68) in the intestinal tissue was assessed with immunohistochemistry. RESULTS: At the two time points, the levels of TNF-α and IL-12 in the P group were higher than those in the C group (P<0.05) Compared with the P group, the levels of TNF-α and IL-12 decreased in the T group (P<0.05). The pathological scores of the intestinal mucosa and pancreas in the T group were lower than those of the P group. In the T group, large numbers of TUNEL-positive cells were observed, but none or few in the C and P groups. The number of CD68-positive macrophages decreased in the T group.CONCLUSIONS: Clodronate-containing liposomes have prote- ctive effects against intestinal mucosal injury in rats with SAP. The blockade of macrophages may provide a novel therapeutic strategy in SAP. | Jian-Xin Zhang, Sheng-Chun Dang, Kai Yin and De-Li Jiang Department of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China School of Chemistry and Chemical Engineering of Jiangsu University, Zhenjiang 212013, China | 2011 | Hepatobiliary & Pancreatic Diseases International2011，10，5： | 10 |
| 5 | 复合益生菌制剂对急性坏死性胰腺炎大鼠的保护作用显示文摘背景:肠道细菌易位是重症急性胰腺炎(SAP)时胰腺坏死感染的主要来源,因此保护肠黏膜屏障对SAP的治疗具有重要意义。目的:探讨复合益生菌制剂对急性坏死性胰腺炎(ANP)大鼠肠黏膜屏障和胰腺损伤的保护作用。方法:50只SPF级大鼠随机分为假手术组(n=10)、ANP模型组(n=20)和益生菌干预组(n=20)。采用胰腺被膜下均匀注射牛磺胆酸钠制备ANP模型,干预组术前30 min以双歧杆菌四联活菌片溶液灌胃。术后6 h采集标本,检测血淀粉酶、二胺氧化酶(DAO)、TNF-α水平,观察胰腺组织病理学表现和末端回肠组织超微结构。结果:ANP模型组血淀粉酶、DAO、TNF-α水平和胰腺组织学评分均显著高于假手术组(P<0.05),益生菌干预组各项指标均较ANP模型组有所改善(P<0.05)。假手术组末端回肠黏膜结构完整;ANP模型组回肠黏膜上皮细胞微绒毛萎缩、排列稀疏,细胞间连接松弛;益生菌干预组微绒毛稍稀疏,细胞间连接紧密度较ANP模型组增高。结论:复合益生菌制剂对ANP大鼠具有保护作用,不仅能减轻肠黏膜损伤,保护肠黏膜屏障功能,还能减轻胰腺局部损伤和全身性炎症反应。 | 孙丽群 王品发 雷森林 孙津明 | 2013 | 胃肠病学2013，18，6： | 9 |
| 6 | 重症急性胰腺炎实验动物模型的研究进展显示文摘为探讨重症急性胰腺炎(severe acute pancreatitis,SAP)的病因、发病机制、病理生理变化及其治疗方法,已用多种方式建立了活体动物SAP模型.鉴于各种活体SAP模型能在不同侧面模拟人类SAP病变过程,但操作及控制各异、部分便于动态观察各项指标变化及治疗效果,可根据不同的实验目的选择合适、操作简单、重复性好的建模方案进行研究.本文简述目前SAP研究现状,启迪未来探索方向. | 杨元生 崔淑兰 陈垦 王晖 | 2009 | 世界华人消化杂志2009，17，25： | 9 |
| 7 | HMGB1、TLR4在重症急性胰腺炎大鼠胰腺组织中的表达及乌司他丁的干预效应显示文摘目的探讨HMGB1、TLR4在重症急性胰腺炎大鼠胰腺组织中的作用机制以及乌司他丁的干预效应。方法将54只SD大鼠分为对照组、SAP组和乌司他丁治疗组,3组又分为6、12h和24h3个小组(每小组n=6)。对照组开腹后仅翻动胰腺组织,SAP组用5%的牛磺胆酸钠制备SAP模型,治疗组在SAP造模成功后经尾静脉注射乌司他丁。观察3组大鼠胰腺组织的病理学改变;EPS-G7法检测血清中的淀粉酶;ELISA法检测血清及胰腺组织中的HMGB1;Envision两步免疫法检测胰腺组织中的HMGB1、TLR4的表达水平。结果 SAP组、治疗组各时间点的淀粉酶与对照组比较明显升高,病理学改变明显,差异均有统计学意义(P<0.05),示SAP造模成功;SAP组在胰腺组织及血清中的HMGB1表达在6h开始升高,于12h快速上升,至24h保持上升趋势,与对照组大鼠相同时间点比较明显升高,差异有统计学意义(P<0.05),治疗组与SAP组相同时间点的HMGB1比较明显降低,差异有统计学意义(P<0.05);SAP组胰腺组织中的TLR4表达在6h开始升高,12h达高峰,24h开始下降,与对照组大鼠相同时间点比较明显升高,差异有统计学意义(P<0.05)。治疗组与SAP组相同时间点的TLR4比较明显降低,差异有统计学意义(P<0.05)。结论 HMGB1在SAP大鼠胰腺中的致炎作用可能是部分结合其受体TLR4并通过MyD88依赖性途径而实现的,而乌司他丁可能是通过中断SAP大鼠胰腺组织中的HMGB1、TLR4信号通路发挥保护作用。 | 王静 王烜 邓明明 孟娅 | 2015 | 重庆医学2015，44，4： | 8 |
| 8 | 血清IL-2、IL-10及肠黏膜Fas在重症急性胰腺炎大鼠中的动态变化显示文摘目的:探讨重症急性胰腺炎大鼠血清IL-2、IL-10、sFas及IL-2/IL-10动态变化以及Fas在肠黏膜的表达及意义.方法:将SD大鼠64只,随机分为对照组和胰腺炎组.经大鼠胰腺被膜下均匀注射50 g/L牛磺胆酸钠制作重症急性胰腺炎模型,对照组仅胰腺被膜下注射等量生理盐水.通过肠系膜上静脉取血测定血清IL-2、IL-10和sFas水平,并计算IL-2/IL-10比值.分别对胰腺损伤、肠损伤程度进行病理评分.免疫组化方法检测大鼠肠组织内Fas蛋白的表达水平.结果:0.5 h后血清IL-2水平胰腺组较对照组明显升高(3.53±0.62 ng/L vs 2.79±0.51 ng/L,4_35±1.11 ng/L vs 2.93±0.89 ng/L,6.94±1.55 ng/L vs 4.81±1.23 ng/L,4.80±1.10 ng/L vs 3.41±0.72 ng/L,P<0.01),并于6 h达到最高点.胰腺炎组6 h后血清IL-10水平较对照组明显升高(494.98±11.23 ng/L vs 89.18±32.52 ng/L,93.28±25.81 ng/L vs 77.15±22.60 ng/L,P<0.01)。12 h血清IL-10水平较6 h降低.胰腺炎组的IL-2/IL-10先降低后升高,0.5 h后即开始下降,6 h时达到最低点然后开始升高,显著低于对照组(P<0.01),12 h接近对照组.与对照组比较,胰腺炎组各时相胰腺及肠黏膜病理改变明显加重.免疫组化结果显示,在正常的肠黏膜未见明显表达.造模0.5 h后,大鼠肠组织内Fas表达增加,至12 h达最高水平.结论:Fas参与胰腺炎肠损伤的病理过程,其机制可能与其介导的Th细胞凋亡有关. | 党胜春 张建新 毛正发 瞿建国 王旭青 朱蓓 | 2007 | 世界华人消化杂志2007，15，35： | 5 |
| 9 | Clodronate-containing liposomes attenuate lung injury in rats with severe acute pancreatitis显示文摘Objectives:Severe acute pancreatitis(SAP) can lead to acute lung injury(ALI) .The purpose of this paper is to investigate the protective effect of clodronate-containing liposomes on ALI in rats with SAP.Methods:The thin film method was used to prepare liposomes.Sprague-Dawley rats were randomly divided into three groups.After the SAP model was established by injecting 5%(w/v) sodium taurocholate(2 ml/kg body weight) into the subcapsular space of the pancreata,normal saline was administered to the control(C) group,phosphate buffer solution(PBS) -containing liposome to the Pgroup,and clodronate-containing liposome to the Tgroup through tail veins.Blood samples were obtained from the superior mesenteric vein at 2 and 6 h to measure the levels of amylase,interleukin-6(IL-6) ,and tumor necrosis factor-α(TNF-α) .Morphological changes in the pancreata and lung were observed using hematoxylin and eosin(H&E) staining,while cell apoptosis was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling(TUNEL) .In addition,the macrophage marker cluster of differentiation 68(CD68) in lung tissue was detected with immunohistochemistry.Results:Blood levels of amylase,IL-6,and TNF-αwere significantly increased in the Pgroup compared to those in the Tgroup(P<0.05) .In the Tgroup,large numbers of TUNEL-positive cells were observed,but no or few in the C and Pgroups.Gross inspection and H&E staining of pancreata and lung showed dramatic tissue damage,including inflammation and necrosis in the Pgroup.Less remarkable changes were noted in the Tgroup,and the C group exhibited normal histology.The histological scores according to Kaiser's criteria were consistent with H&E findings.The number of CD68-positive macrophages decreased in the Tgroup.Conclusions:Clodronate-containing liposomes have a protective effect against ALI in rats with SAP.Blockade of macrophages may represent a novel therapeutic strategy in SAP. | Sheng-chun DANG De-li JIANG Min CHEN Di LI Jian-xin ZHANG | 2010 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2010，11，11： | 4 |
| 10 | 乌司他丁对急性坏死性胰腺炎大鼠肝损伤中高迁移率族蛋白1表达的拮抗作用显示文摘急性坏死性胰腺炎(acute necrotizing pancreatitis,ANP)常累及肝脏。高迁移率族蛋白1(high mobility groupbox 1 protein,HMGBl)可能作为晚期炎性反应介质参与ANP的病理生理过程。乌司他丁(ulinastatin)能抑制炎性反应介质和细胞因子的释放,但其对HMGBl有否拮抗作用尚不明确。本研究拟探讨HMGBl在ANP大鼠肝损伤中的表达以及乌司他丁对其表达的拮抗作用,为ANP肝损伤的防治提供实验依据。 | 王静 王烜 邓明明 孟娅 | 2014 | 中华消化杂志2014，34，3： | 3 |
| 11 | Clodronate—SPIO脂质体对重症急性胰腺炎大鼠肝损伤的保护作用及MRI评价显示文摘摘要:目的 探讨Clodronate-SPIO脂质体对重症急性胰腺炎(SAP)大鼠肝损伤的保护作用及磁共振成像(MRI)对肝损害程度的评价.方法 利用化学共沉淀法制备超顺磁性Fe3O4纳米微粒.利用薄膜法制备Clodronate-SPIO脂质体.采用胰腺被膜下均匀注射(2 ml/kg体重)牛磺胆酸钠制作SAP模型.将SD大鼠随机分为对照组、SAP-SPIO脂质体组、SAP+Clodronate-SPIO脂质体组.6 h后对各组大鼠肝脏的相同层面进行MRI扫描,测定T2WI.扫描结束后,取肠系膜上静脉血液检测各组大鼠血清中ALT、AST的含量,观察肝脏和胰腺组织的病理学变化.结果 透射电镜检查见脂质体大小均匀.对照组胰腺未见明显改变,SAP+Clodronate-SPIO脂质体组大鼠的胰腺及肝脏病理变化均较SAP-SPIO脂质体组明显减轻.SAP+SPIO脂质体组6 h ALT和AST含量较对照组明显升高(P<0.01);SAP+Clodronate-SPIO脂质体组血清ALT和AST水平均显著低于SAP+SPIO脂质体组(P<0.01).肝组织信号强度SAP+SPIO脂质体组及SAP+Clodronate-SPIO脂质体组较对照组明显减低,SAP+Clodronate-SPIO脂质体组信号强度较SAP+SPIO脂质体组降低(P<0.01).结论 Clodronate脂质体对SAP大鼠肝损害有保护作用,SPIO可作为MRI检查的示踪剂. | 党胜春 张勇 沙鑫 蔡华忠 姜德立 陈敏 张建新 | 2010 | 中华肝胆外科杂志2010，16，11： | 2 |
| 12 | 氯磷酸二钠脂质体对胰腺炎大鼠肺泡巨噬细胞凋亡的影响显示文摘目的研究氯磷酸二钠脂质体对急性坏死性胰腺炎肺泡巨噬细胞凋亡影响。方法将8只急性坏死性胰腺炎SD大鼠利用肺泡灌洗液,经差时贴壁法,分离、纯化肺泡巨噬细胞,并进行原代培养,分别取5孔分为ANP对照组、ANP+空白脂质体组(50μl,100μl)、ANP+氯磷酸二钠脂质体组(50μl,100μl),用MTT比色法检测大鼠肺泡巨噬细胞光密度值、吖啶橙荧光染色、苏木精染色对所分离的细胞进行凋亡鉴定。结果加入空白脂质体为50μl、100μl时对肺巨噬细胞无显著差异(P〉0.05)。当加入氯磷酸二钠脂质体为50μl/ml时有显著性差异(P〈0.05)、100μl时亦有显著性差异(P〈0.01)。细胞荧光染色和苏木精染色可以明确细胞凋亡情况。结论脂质体包裹氯磷酸二钠可以诱导大鼠肺泡巨噬细胞凋亡。 | 张建新 党胜春 崔磊 瞿建国 王旭青 尹江涛 | 2010 | 中华肝胆外科杂志2010，16，3： | 2 |
| 13 | 氯膦酸二钠脂质体对重症急性胰腺炎大鼠肠黏膜Akt、MAPK(ERK1/2)活性的影响显示文摘目的:研究氯膦酸二钠脂质体(liposomal clodronate,LC)对重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠肠黏膜蛋白激酶B(protein kinase B,Akt)和丝裂原活化蛋白激酶1/2[mitogen-activated protein kinase,MAPK(ERK1/2)]活性的影响,探讨LC治疗SAP肠黏膜损伤的保护作用.方法:利用薄膜法制备LC.SD大鼠48只,随机分为3组:对照组(C组)、SAP+空白脂质体治疗组(P组)、SAP+Clodronate脂质体治疗组(T组).P组和T组采用胰腺被膜下均匀注射5%牛磺胆酸钠制作SAP模型后,分别经尾静脉注射空白脂质体和Clodronate脂质体,C组仅注射等量生理盐水.制模后2、6 h分别取肠系膜上静脉血液,检测各组大鼠血清中淀粉酶(amylase,AMS)的含量,同时检测各组大鼠血清中白介素-6(interleukin-6,IL-6)和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的含量,观察各组肠黏膜的病理学变化及病理评分,采用免疫组织化学方法检测肠黏膜巨噬细胞Akt和MAPK(ERK1/2)的表达情况.结果:P组大鼠在制模后2、6 h的血清AMS水平较C组明显升高(P<0.01).与P组比较,T大鼠各时相的血清AMS水平均显著降低(P<0.01).P组较C组2、6 h血清IL-6和TNF-α明显升高(P<0.01).T组各时相较P组血清IL-6和TNF-α显著降低(P<0.01).T组大鼠的肠黏膜病理变化均较P组明显减轻,病理学评分明显降低(P<0.01).T组肠黏膜Akt和MAPK(ERK1/2)的表达较P组明显减少.结论:巨噬细胞在SAP大鼠肠黏膜损伤中起重要作用,LC可选择性清除巨噬细胞,减少肠黏膜Akt、MAPK(ERK1/2)的表达,对肠黏膜损伤有一定的保护作用. | 陈吉祥 刘彬 党胜春 陈敏 姜德立 王坤 王平江 张建新 | 2013 | 世界华人消化杂志2013，21，26： | 2 |
| 14 | 氯膦酸二钠脂质体对重症急性胰腺炎大鼠心肌损伤的保护作用显示文摘目的:探讨氯膦酸二钠脂质体(clodronate liposome,LC)对重症急性胰腺炎(SAP)大鼠心肌损伤的保护作用。方法:将48只SD大鼠随机分为假手术组、SAP组及SAP+LC组,各组再分为术后2 h和6 h组(n=8)。测定大鼠血清IL-6、淀粉酶及肿瘤坏死因子α(TNF-α)的含量,HE染色观察LC对SAP大鼠心肌组织病理损伤的影响,普鲁士蓝染色法观察LC对SAP大鼠心肌细胞间巨噬细胞的影响,免疫组化法观察LC作用后SAP大鼠丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)的表达。结果:假手术组术后2、6 h血清IL-6、淀粉酶、TNF-α含量均分别明显低于SAP组和SAP+LC治疗组(P<0.05),SAP+LC组明显低于SAP组(P<0.05)。假手术组术后2、6 h心肌组织病理学评分明显低于SAP组和SAP+LC组(P<0.05),SAP+LC组明显低于SAP组(P<0.05)。假手术组术后2、6 h心肌细胞间巨噬细胞数量明显低于SAP组和SAP+LC组,SAP+LC组明显低于SAP组。假手术组术后2、6 h心肌组织MAPK评分明显低于SAP组和SAP+LC组(P<0.05),SAP+LC组明显低于SAP组(P<0.05)。结论:LC可选择性清除单核/巨噬细胞,对SAP大鼠心肌损伤起到保护作用。 | 谭克 张建新 党胜春 | 2018 | 江苏大学学报(医学版)2018，28，3： | 1 |
| 15 | 氯膦酸二钠脂质体对重症急性胰腺炎大鼠胰腺损伤的影响显示文摘目的:探讨氯膦酸二钠脂质体(liposomal clodronate)对重症急性胰腺炎(SAP)大鼠胰腺损伤的保护作用。方法:利用薄膜法制备氯膦酸二钠脂质体。采用胰腺被膜下均匀注射5%牛磺胆酸钠制作SAP模型。SD大鼠48只,随机分为对照组(C组)、空白脂质体组(P组)、氯膦酸二钠脂质体组(T组)。P组和T组大鼠制作SAP模型。制模2h和6h后取肠系膜上静脉血液,检测各组大鼠血清中淀粉酶、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的含量,观察各组胰腺组织的病理学变化及胰腺病理评分,免疫组化检测胰腺Caspase-3的表达。结果:P组大鼠的血清淀粉酚水平较C组明显升高(P<0.01),T组大鼠的血清淀粉酶水平显著低于P组。P组较C组2、6h血清IL-6、TNF-α明显升高(P<0.01),T组较P组大鼠的2、6h血清IL-6、TNF-α水平显著降低(P<0.01)。T组大鼠的胰腺病理变化较P组明显减轻,胰腺组织病理学评分明显降低(P<0.01)。胰腺Caspase-3阳性表达增多。结论:氯膦酸二钠脂质体可选择性清除单核/巨噬细胞,对SAP大鼠胰腺损伤有保护作用。 | 张勇 党胜春 沙鑫 蔡华忠 陈敏 姜德立 张建新 | 2010 | 江苏大学学报(医学版)2010，20，2： | 1 |
| 16 | Effects of Chuanxiongqin hydrochloride on increasing the fluidity of brain cell membrane and scavenging free radicals in model rats with ischemia/reperfusion injury显示文摘BACKGROUND: The fluidity of cell membrane can be affected by various factors. Many experiments have confirmed that the ischemia/reperfusion of organic tissue can increase the contents of free radicals, which lead to high rigidity and low fluidity of cell membrane, and the conditions can be changed by Chuanxiongqin. OBJECTIVE: To observe the effect and mechanism of Chuanxiongqin hydrochloride on the fluidity of brain cell membrane in rat models of ischemia/reperfusion. DESIGN: A completely randomized controlled animal trial. SETTINGS: Institute of Brain Sciences; Department of Physiology, Medical College, Datong University. MATERIALS: Twenty male grade Ⅰ Wistar rats of 170-220 g were randomly divided into model group (n =10) and control group (n =10). Chuanxiongqin hydrochloride (molecular mass was 172.2) was purchased from the National Institute for the Control of Pharmaceutical and Biological Products (batch number: 0817-9803); Spin labelers: 5-doxyl-stearlic acid methylester (5DS), 16-doxyl-stearlic acid methylester (16DS), xanthine, xanthine oxidase (XOD) and 5,5-dimeth-1-pyrroline- N-oxide (DMPO) from Sigma Company; Bruker ESP 300 electron paramagnetic resonance (EPR) spectrometer by Bruker Company (Germany). METHODS: The experiments were carried out in the State Key Laboratory of Natural and Biomimetic Drugs, Peking University from June 2001 to July 2002. In the model group, rats were made into models of cerebral ischemia by 30-minute ligation and 2-hour reperfusion of common carotid arteries; The rats in the control group were not made into models. The order parameter (S) and rotational correlation time (τc) were detected with the ESR spectrometer by means of spin labeling. The greater the S and τc, the smaller the fluidity. Meanwhile, the clearance rate of free radicals was detected with ESR spin trapping. The measurement data were compared using the t test. MAIN OUTCOME MEASURES: The S, τc and clearance rates of O2 · and OH· free radicals were compared between the model group and control group. RESULTS: The S and τc in the model group [0.738 4±0.003 5; (8.472±0.027)×10-10 s/circle] were obviously different from those in the control group [0.683 9±0.008 3; (7.945±0.082)×10-10 s/circle, t =5.731, 5.918, P < 0.05], which suggested that ischemia/reperfusion injury decreased the fluidity of brain cell membrane. After adding Chuanxiongqin hydrochloride, there were no obvious differences between the model group [0.688 5±0.030 5; (7.886±0.341)×10-10 s/circle] and control group (P > 0.05), indicating that Chuanxiongqin hydrochloride could recover the fluidity of brain cell membrane after ischemia/reperfusion injury close to the level in the normal control group. Chuanxiongqin hydrochloride could directly scavenge the O2 · and OH· free radicals, and the maximal clearance rates were 83.92% and 44.99% respectively. CONCLUSION: Chuanxiongqin hydrochloride increases the fluidity of membrane of ischemia-injured brain cell by scavenging both O2 ·and OH· free radicals. | Chenxu Li Institute of Brain Sciences Department of Physiology, Medical College, Datong University, Datong 037008, Shanxi Province, China | 2006 | Neural Regeneration Research2006，1，8： | 1 |
| 17 | Caspase-3激活在实验性重症急性胰腺炎肺损伤中的作用显示文摘目的探讨重症急性胰腺炎大鼠血清IL-2,IL-10及IL-2/IL-10动态变化以及半胱氨酸天冬氨酸蛋白酶3(Caspase-3)在肺组织的表达及意义。方法SD大鼠64只,随机分对照组、胰腺炎组。经大鼠胰腺被膜下均匀注射0.5%牛磺胆酸钠制作重症急性胰腺炎模型,对照组仅胰腺被膜下注射等量生理盐水。通过肠系膜上静脉取血用于血清IL-2,IL-10及Caspase-3水平的测定,并计算IL-2/IL-10比值。分别对胰腺损伤、肺损伤程度进行病理评分,免疫组化方法检测肺组织内Caspase-3蛋白的表达水平。结果0.5h后血清IL-2水平胰腺炎组较对照组明显升高(P<0.01),并于6h达到最高点。胰腺炎组6h后血清IL-10水平较对照组明显升高(P<0.01),12h血清IL-10水平较6h降低。胰腺炎组的IL-2/IL-10先降低后升高,0.5h后即开始下降,6h时达到最低点然后开始升高,显著低于对照组(P<0.01),12h接近对照组(P>0.01)。胰腺炎组的IL-2/IL-10先升高后降低,0.5h后即开始升高,6h时达到最低点然后开始升高,显著低于对照组(P<0.01),12h接近对照组(P>0.01)。与对照组比较,胰腺炎组各时相胰腺及肺组织病理改变明显加重。免疫组化结果显示在正常的肺组织未见明显表达。造模0.5h后,大鼠肺组织内Caspase-3表达增加,至12h达最高水平。结论Caspase-3参与了胰腺炎肺损伤的病理过程,其机制可能与其介导的Th细胞凋亡有关。 | 张建新 崔磊 尹江涛 党胜春 瞿建国 | 2009 | 广东医学2009，30，1： | 0 |
| 18 | 血管内皮祖细胞移植对大鼠重症急性胰腺炎肾损伤的保护作用显示文摘目的:探讨内皮祖细胞(endothelial progenitor cells,EPCs)对大鼠重症急性胰腺炎(severe acute pancreatitis,SAP)合并肾损伤的保护作用。方法:通过共沉淀法制备超顺磁性氧化铁(superparamagnetic iron oxide,SPIO);密度梯度离心法分离培养SD大鼠骨髓来源EPCs;使用SPIO标记EPCs;将72只SD大鼠随机分为对照组、SAP组和SPIOEPCs组,采用胰腺被膜下均匀注射5%牛磺胆酸钠制作SAP模型。对照组和SAP组经尾静脉注射生理盐水,SPIOEPCs组注射等量的SPIO-EPCs;分别于造模2,6,12 h检测各组大鼠血清中淀粉酶、尿素氮、肌酐和肿瘤坏死因子-α(TNF-α)的水平;苏木精染色观察肾组织各时相病理变化及进行病理评分,普鲁士蓝染色观察肾组织各时相铁颗粒含量。结果:SAP组2,6,12 h的血清淀粉酶、尿素氮、肌酐和TNF-α的水平较对照组明显升高(P<0.01);而SPIO-EPCs组均显著低于SAP组(P<0.01)。与对照组比较,SAP组2,6,12 h肾病理改变明显加重,肾病理评分明显提高(P<0.05);与SAP组比较,SPIO-EPCs组肾病理改变明显减轻,肾病理评分明显降低(P<0.05)。普鲁士蓝染色见SPIOEPCs组在2,6和12 h肾组织血管内皮铁颗粒含量逐渐增多。结论:移植EPCs可减少炎症介质释放,减轻SAP肾的血管内皮损伤,对大鼠SAP肾损伤具有保护作用。 | 党胜春 王平江 曾艳华 陈荣芳 王豪 冯舒 崔磊 张建新 | 2014 | 江苏大学学报(医学版)2014，24，1： | 0 |
| 19 | 急性坏死性胰腺炎大鼠血清IL-2/IL-10的动态变化及杏丁的干预效应显示文摘目的探讨IL-2/IL-10在急性坏死性胰腺炎时的动态变化及其杏丁的干预效应。方法SD大鼠96只,随机分对照组、胰腺炎组、杏丁治疗组,每组32只。各时相点动物处死后,通过肠系膜上静脉取血用于血清IL-2和IL-10水平的测定,并计算IL-2/IL-10比值,同时取胰腺组织用于胰腺的病理评分。结果与C组比较,P组各时相病理改变明显加重。P组血清IL-2水平在制模后0.5、2、6、12h明显升高(P<0.05或P<0.01),IL-10在6、12h时明显增高(P<0.01)。P组IL-2/IL-10先升高,后逐渐减低,在3h起开始升高,6h达峰值,在12h接近C组水平(P﹥0.05)。与P组比较T组各时相病理改变明显减轻,T组各时相血清IL-2在6、12、24h水平较P明显降低(P<0.01),IL-10在12、24h时明显降低(P<0.05)。T组与P组比较IL-2/IL-106h起明显降低(P<0.01或P<0.05)。结论ANP时IL-2/IL-10比例失调,呈现由升高到相对平衡,再转为降低的过程。杏丁可下调IL-2/IL-10比值,其机理考虑为通过双向调节IL-2、IL-10的水平。 | 顾敏 党胜春 | 2009 | 临床医学工程2009，16，10： | 0 |
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