性别对L-精氨酸诱发的昆明小鼠慢性胰腺炎的影响

目的:通过比较雌雄小鼠L-精氨酸诱发的慢性胰腺炎(CP)程度的差异,探讨性别对CP模型形成的影响。方法:健康昆明小鼠雌雄各42只,分为雌性对照组、雌性CP组、雄性对照组和雄性CP组(对照组n=18,每时点6只;CP组n=24,每时点8只)。CP模型组小鼠腹腔注射20%L-精氨酸(3 g/kg,每周1次,每次2轮,间隔1 h)诱发CP。分别于造模后第2、4、6周处死动物,取小鼠胰腺组织,HE及Masson染色检测各组小鼠胰腺形态学改变及纤维化程度;免疫组织化学观察胰腺组织F4/80的阳性染色率;real-time PCR检测胰腺组织白细胞介素6(interleukin-6,IL-6)、α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)及纤维连接蛋白(fibronectin,FN)的mRNA表达;Western blot检测胰腺组织α-SMA及FN蛋白的表达。结果:20%L-精氨酸腹腔注射后的第2、4和6周,HE及Masson染色显示雌雄CP组胰腺组织均可见病理损伤,但是同一时点雌雄小鼠胰腺损伤程度存在明显差异,雄性小鼠胰腺病变程度明显较重;胰腺F4/80染色显示雄性小鼠胰腺F4/80的表达水平在造模后各时点均明显高于同一时点的雌性小鼠;造模后第2和4周胰腺IL-6的mRNA表达在雌雄CP组均有所升高,但是雄性组表达水平明显高于雌性组(P0.05)。造模后α-SMA和FN在mRNA水平和蛋白质水平均可见高表达,但雄性小鼠表达时点更早,水平更高(P0.05)。结论:采用腹腔注射20%L-精氨酸可成功复制小鼠CP模型,但复制的模型在雌雄小鼠存在病变程度差异。L-精氨酸诱导的CP模型在雄性小鼠成模更早、纤维化程度更明显,其原因可能与雄性小鼠对L-精氨酸更敏感,引发的炎症反应程度更明显有关。雄性小鼠更适合于复制CP动物模型。     

木犀草素对重症急性胰腺炎小鼠胰腺的保护作用及可能的分子机制#br#

目的 探讨木犀草素对重症急性胰腺炎（SAP）小鼠胰腺的保护作用及其可能的分子机制。方法 将60只SPF级健康雄性C57BL/6小鼠随机分为3组,对照组、SAP模型组和治疗组,每组各20只。采用雨蛙素法构建模型,成功构建SAP模型后,应用ELASA法检测脂肪酶、淀粉酶、血红素加氧酶（HO)-1、肿瘤坏死因子（TNF）-α、丙二醛（MDA）及超氧化物歧化酶（SOD）水平。使用Western blotting和Real-time PCR测定各组小鼠核因子（NF）-κB、P38及p-P38 蛋白和mRNA水平。结果 与对照组比较,模型组和治疗组小鼠胰腺干湿重比、脂肪酶及淀粉酶、TNF-α水平、氧化应激指标HO-1及MDA水平均明显升高,SOD水平明显降低（P<0.05）;与模型组小鼠比较,治疗组小鼠胰腺干湿重比、脂肪酶及淀粉酶,TNF-α、MDA水平均明显降低,HO-1、SOD水平均明显升高（P<0.05）。与对照组比较,模型组和治疗组小鼠NF-κB、p-P38蛋白和mRNA水平明显升高（P<0.05）,P38蛋白和mRNA表达水平无显著变化（P>0.05）;与模型组小鼠比较,治疗组小鼠NF-κB、p-P38蛋白和mRNA水平均明显降低（P<0.05）。结论 木犀草素对SAP小鼠胰腺具有一定的保护作用,其可能的分子机制为缓解炎症应激和氧化应激,下调NF-κB及p-P38 蛋白的表达。     

IL-10降低大鼠急性坏死性胰腺炎IL-1β释放

目的探讨重组人白介素10（IL-10）对大鼠急性坏死性胰腺炎（ANP）血清IL-1β的影响。方法健康雄性SD大鼠92只,随机分成对照组（C组）、ANP组（A组）和IL-10干预组（I组）。A组大鼠腹腔内注射6%的左旋精氨酸（L-Arginine）1.0mg/g体重,共3次,每次间隔1h,诱导ANP;I组于L-Arginine注射诱导胰腺炎后2、5和8h分别腹腔内注射重组人IL-101万U,共3万U;C组大鼠给予0.9%生理盐水。在诱导胰腺炎后第4、12、24和36h共4个时点检查胰腺组织,用酶联免疫吸附法（ELISA）检测血清淀粉酶水平、血清IL-1β水平。结果A组各时点IL-1β、血清淀粉酶水平以及胰腺组织病理学评分较C组明显增高（P〈0.05或P〈0.01）;其中,胰腺组织病理学评分及血清淀粉酶升高以24、36h最为显著;IL-1β则以4、12h升高明显;而I组组织病理学评分（除4h外）、血清淀粉酶、IL-1β各时点值均显著低于A组（P〈0.05或P〈0.01）。结论早期应用重组人IL-10可以抑制炎症细胞因子IL-1β释放,降低炎症反应的严重程度,减轻实验性胰腺炎的病理损害。有可能是治疗ANP的新途径。     

黄芩苷通过调控TGF-β1/TAK-NF-κB通路对胰腺纤维化的防治作用

目的:观察黄芩苷对慢性胰腺炎(CP)小鼠胰腺组织转化生长因子β1(TGF-β1)/TGF-β活化激酶(TAK)-核因子κB(NF-κB)信号通路的影响,探讨黄芩苷防治胰腺纤维化的作用机制。方法:健康雄性昆明小鼠58只,随机分为空白对照组、CP模型组和黄芩苷治疗组。除空白对照组外,其余小鼠均给予腹腔注射20%L-精氨酸诱发CP,治疗组于造模后2周开始腹腔注射黄芩苷(100 mg/kg,每天1次)。造模后2周、4周和6周分别处死动物,下腔静脉采血,摘取小鼠胰腺组织,HE及Masson染色检测各组小鼠胰腺组织形态学改变及纤维化程度;ELISA检测血清TGF-β1的表达;免疫组织化学法观察胰腺组织纤维连接蛋白(FN)和NF-κB的表达;Western blot检测胰腺组织FN、转化生长因子βⅠ型受体(TGF-βRⅠ)、磷酸化TAK1(p-TAK1)及NF-κB蛋白的表达;real-time PCR检测胰腺组织基质金属蛋白酶1(MMP-1)及金属蛋白酶组织抑制物1(TIMP-1)的mRNA表达。结果:腹腔注射20%L-精氨酸2周、4周和6周后,HE及Masson染色显示胰腺组织有纤维沉积,FN表...     

马齿苋对非酒精性脂肪肝小鼠的肝脏保护作用及对脂代谢的影响

目的:分析马齿苋对非酒精性脂肪肝(Non-alcoholic fatty liver disease,NAFLD)小鼠的肝脏保护作用及对脂代谢的影响.方法:选取健康雄性小鼠50只,按照体重随机分为对照组、模型组、马齿苋药物低、中、高剂量组五组,各10只,模型组及各剂量组以高脂饲料喂养16周造模;建模成功后,低、中、高剂量组分别给予马齿苋提取液0.18 g·kg-1、0.35 g·kg-1、0.70 g·kg-1灌胃,对照组及模型组给予等体积0.9％生理盐水灌胃,连续灌胃4周.采用全自动血液分析仪检测小鼠血清肝功能及脂代谢指标;取全肝,称肝湿重,制备病理切片,计算NAFLD活动度积分;利用荧光定量聚合链式反应检测肝组织Keap1-核因子E2相关因子2(Keap1-nuclear factor E2 related factor 2,Nrf2)表达,采用酶联免疫分析法测定肝组织匀浆超氧化物歧化酶(Superoxide dismutase,SOD)、丙二醛(Malondialdehyde,MDA)水平.结果:造模成功.较模型组,各剂量组小鼠肝湿重、NAFLD活动度及血清ALT、AST、TC、TG、LDL-C、肝组织匀浆MDA水平均降低,其中高剂量组更为明显(P<0.05);较模型组,各剂量组小鼠肝组织Nrf2 mRNA相对表达量及肝组织匀浆SOD水平均升高,其中高剂量组更为明显(P<0.05).结论:马齿苋可能通过发挥抗氧化、降脂作用,使NAFLD小鼠肝损伤减轻,延缓NAFLD进展.     

Nrf-2基因过表达对急性胰腺炎大鼠胰腺的保护作用

目的探讨Nrf-2基因过表达对急性胰腺炎大鼠胰腺的保护作用。方法 32只雄性SD大鼠随机分为4组:正常对照组(NC)、Nrf-2过表达组(Nrf-2^+/+)、胰腺炎组(AP)、Nrf-2过表达胰腺炎组(Nrf-2^+/++AP)。各组均采用尾静脉注射慢病毒感染后,AP组和Nrf-2^+/++AP组通过腹腔内注射蛙皮素和脂多糖造模;造模后24 h处死大鼠取材,ELISA法检测大鼠血清C-反应蛋白(CRP)含量;检测胰腺组织超氧化物歧化酶(SOD)、丙二醛(MAD)和髓过氧化物酶(MPO)水平;RT-PCR检测胰腺Nrf-2mRNA相对表达量;Western blot检测Nrf-2蛋白相对表达量;H&E染色观察大鼠胰腺组织细胞形态。结果 AP组与NC组相比,大鼠血清C反应蛋白含量显著升高,SOD活性明显降低,MDA含量和MPO活性明显高于AP组,且AP组胰腺组织损伤较NC组明显增加;与AP组相比,Nrf-2过表达后,Nrf-2^+/++AP组大鼠血清C反应蛋白含量显著降低,SOD活性明显升高,MDA含...     

肠系膜淋巴管结扎对休克大鼠肾功能不全的干预机制

目的： 观察结扎肠系膜淋巴管对不同时期重症失血性休克大鼠肾组织自由基、炎症介质的影响，探讨肠淋巴途径对休克大鼠肾功能不全的干预机制。方法: 雄性Wistar大鼠78只，分为假手术组、休克组、结扎组。休克组与结扎组复制重症失血性休克模型，结扎组于休克复苏后行肠系膜淋巴管结扎术。于休克后90 min、输液复苏后0 h、1 h、3 h、6 h、12 h、24 h等时点处死大鼠，制备肾组织匀浆，检测MDA、SOD、NO、NOS、TNF-α、IL-6以及MPO水平，RT-PCR法测定各组大鼠肾组织iNOS mRNA表达。结果: 休克组大鼠输液复苏后不同时点肾组织匀浆MDA、NO、NOS、TNF-α、IL-6水平和MPO活性以及iNOS mRNA表达均有不同程度的升高，6 h-12 h持续在较高水平，均显著高于假手术组，肾组织匀浆SOD活性显著低于假手术组（P<0.01，P<0.05）；结扎组输液复苏后6 h、12 h、24 h肾组织匀浆MDA、NO、NOS、TNF-α、IL-6水平和MPO活性以及iNOS mRNA均显著低于休克组相应时点，SOD活性高于休克组相应时点（P<0.01，P<0.05）。结论: 肠系膜淋巴管结扎干预重症失血性休克大鼠肾功能不全的机制与减少肾PMN扣押、降低TNF-α、IL-6的释放、抑制NO生成及iNOS mRNA表达、减少自由基释放与SOD消耗等因素有关。     

柴胡疏肝散对NAFLD大鼠肝脏脂质代谢及AMPK/SIRT1通路的影响

 目的: 观察柴胡疏肝散对高脂饮食建立的非酒精性脂肪性肝病(NAFLD)大鼠肝组织脂质代谢和腺苷酸活化蛋白激酶(AMPK)/sirtuin 1(SIRT1)通路相关蛋白的影响。方法: 选用SPF级SD大鼠24只,随机分为正常(NC)组、高脂(HFD)组和柴胡疏肝散(CSP)组,每组8只。采用高脂饲料喂养大鼠16周建立NAFLD大鼠模型,用药组大鼠同时灌服柴胡疏肝散浸膏剂(9.6 g·kg^-1·d^-1)进行干预,16周后取血和肝组织样本,全自动生化仪检测血清和肝匀浆总胆固醇(TC)、甘油三酯(TG)以及血清丙氨酸转氨酶(ALT)和天门冬氨酸转氨酶(AST)含量;HE染色观察肝组织病理损伤变化;油红O染色观察肝组织脂质蓄积程度,透射电镜观察肝细胞内超微结构变化;Western blot法检测肝组织AMPK、磷酸化AMPK(pAMPK)、SIRT1和解偶联蛋白2(UCP2)的蛋白水平。结果: 大鼠肝组织HE染色、油红O染色和电镜结果证实肝细胞脂质蓄积严重,提示NAFLD大鼠模型建立成功。与NC组比较,HFD组血清和肝组织匀浆TC、TG含量显著升高(P < 0.01),血清AST含量显著升高(P < 0.01),肝组织pAMPK和SIRT1蛋白水平显著降低(P < 0.01),UCP2蛋白水平显著升高(P < 0.01);与HFD组比较,CSP组大鼠肝组织脂质蓄积程度明显改善,血清和肝匀浆TC和TG含量呈下降趋势,其中肝匀浆TC和TG含量下降显著(P < 0.05),血清AST含量显著降低(P < 0.05),肝组织pAMPK和SIRT1蛋白水平显著升高(P<0.05),UCP2蛋白水平显著下调(P < 0.01),但各组大鼠总AMPK蛋白水平差异无统计学显著性。结论: 柴胡疏肝散能够改善16周高脂饮食诱导的NAFLD大鼠肝脏脂肪代谢紊乱、减轻肝脏脂质蓄积,其作用机制可能与其激活AMPK/SIRT1通路有关。     

抗B7-H3单克隆抗体抑制雨蛙肽诱导的小鼠急性胰腺炎炎症反应和组织损伤

目的探究抗B7-H3单克隆抗体(m Ab)在雨蛙肽诱导的急性胰腺炎(AP)中的作用。方法将小鼠随机分为对照组、AP组、抗B7-H3 m Ab治疗组。采用腹腔注射雨蛙肽的方法制备小鼠AP模型,治疗组于造模前1 h皮下注射抗B7-H3 m Ab,于造模后6、12、24 h,收集各组小鼠血液、胰腺及肺组织。采用Western blot法和免疫组织化学染色检测对照组及AP组小鼠胰腺组织B7-H3蛋白表达。应用全自动生化免疫分析仪检测各组小鼠血清淀粉酶及脂肪酶活性;胰腺组织湿干比评估各组小鼠胰腺组织水肿变化;HE染色评估各组小鼠胰腺及肺组织病理变化,利用ELISA检测各组小鼠血清中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、IL-1β水平。结果 B7-H3蛋白在AP模型小鼠胰腺组织高表达,且在12 h左右达到高峰;AP组血清淀粉酶及脂肪酶明显高于对照组,抗B7-H3 m Ab处理后明显降低;AP组胰腺及肺组织出现明显炎症反应,治疗组炎症反应明显减弱,胰腺组织湿干比大幅降低;AP组TNF-α、IL-6、IL-1β水平随时间延长而升高,12 h达到高峰后开始下降,而治疗组促炎因子水平相对降低。结论 B7-H3在雨蛙肽诱导的AP模型中存在高表达,抗B7-H3 m Ab可以减弱炎症反应,缓解胰腺及肺组织的损伤。     

清胰汤对L-精氨酸诱发的重症急性胰腺炎小鼠胰腺p-STAT3表达的影响

目的: 观察L-精氨酸(L-Arg)诱发的重症急性胰腺炎小鼠胰腺组织p-STAT3表达的变化,以及清胰汤对p-STAT3表达的影响,从而探讨STAT3在急性胰腺炎中的作用和清胰汤治疗急性胰腺炎的机制。方法: 健康雄性成年昆明种小鼠30只,随机分为3组(n=10):对照组、模型组和清胰汤组。除对照组外,其余各组给予腹腔注射20 % L-精氨酸(3 g/kg,间隔1 h再注射1次);清胰汤组在第2 次腹腔注射20 %L-Arg 30 min 后给予清胰汤浓缩液灌胃(10 mL/kg),之后每天灌胃2次。在造模后72 h麻醉处死动物检测血清淀粉酶活性;取胰腺组织计算胰腺湿重比,HE染色观察胰腺病理学改变;取肺组织匀浆检测髓过氧化物酶(MPO)的活性,HE染色观察肺病理学改变; Western blotting及real-time PCR分别检测胰腺组织p-STAT3蛋白及单核细胞趋化蛋白-1(MCP－1)mRNA的表达变化。结果: L-Arg诱发急性胰腺炎72 h后,血清淀粉酶活性明显升高、胰腺湿重比增加、肺组织MPO显著增加,与对照组比较差异显著(P<0.05);而清胰汤组血清淀粉酶的活性、胰腺湿重比、MPO水平明显降低,与模型组相比差异显著(P<0.01);模型组72 h胰腺及肺可见明显病理损伤,胰腺组织p-STAT3蛋白及MCP-1 mRNA的表达明显增强;清胰汤治疗组胰腺及肺病理损伤减轻,胰腺组织p-STAT3蛋白及MCP-1 mRNA的表达减少。结论: L-Arg诱发的重症急性胰腺炎小鼠胰腺组织STAT3蛋白表达明显增加,STAT3活化可能参与了L-Arg诱发的急性胰腺炎进展;抑制胰腺STAT3活化是清胰汤治疗急性胰腺炎的作用机制之一。     

Ascorbic acid alleviates pancreatic damage induced by dibutyltin dichloride (DBTC) in rats

PURPOSE: Because previous studies have reported depleted antioxidant capacity in patients with chronic pancreatitis (CP), prevention of free radical production has gained importance in antifibrotic treatment strategies for CP. The aim of this study was to investigate the effects of ascorbic acid on oxidative capacity and pancreatic damage in experimental CP. MATERIALS AND METHODS: CP was induced in male Sprague-Dawley rats by infusion of dibutyltin dichloride (DBTC) into the tail vein. Ascorbic acid was given intraperitoneally at a daily dose of 10 mg/kg body weight. The treatment groups were as follows: group 1, DBTC plus intraperitoneal physiologic saline; group 2, DBTC plus intraperitoneal ascorbic acid; group 3, solvent plus intraperitoneal physiologic saline; group 4, no operation plus intraperitoneal physiologic saline. Each group contained 15 animals. Treatment was started after CP was established. After 4 weeks of treatment, serum hyaluronic acid and laminin levels were determined by radioimmunoassay, pancreatic tissue oxidative stress was analyzed, and the degree of pancreatic damage was determined. RESULTS: Ascorbic acid treatment markedly increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) concentrations in pancreatic tissue (p < 0.01 for both). Significant serum hyaluronic acid and laminin reductions were observed in group 2 as compared with group 1 (p < 0.05). However, the serum hyaluronic acid and laminin levels remained elevated when compared with those of groups 3 and 4 (p < 0.05). Histopathologic scores were also lower in animals with CP that underwent ascorbic acid-treatment (p < 0.05). CONCLUSION: Ascorbic acid treatment alleviated the degree of oxidative stress and pancreatic damage in rat CP. Antioxidant treatment might be considered a potential option to improve the pathologic process in CP.     

大黄素对肝纤维化大鼠肺损伤的保护作用

 目的:探讨不同剂量大黄素对肝纤维化大鼠肺损伤的保护作用。方法:采用复合致病因素法（CCl 4、乙醇、高脂、高胆固醇和低胆碱）建立肝纤维化大鼠模型并以不同剂量（20 mg/kg和40 mg/kg）大黄素进行治疗。4周后,测定肝指数,检测血清内毒素、同型半胱氨酸、反映肝功能的指标白蛋白、天门冬氨酸氨基转移酶、丙氨酸氨基转移酶、总胆红素、总胆固醇、甘油三酯和肝纤维化指标透明质酸、层黏连蛋白、Ⅳ型胶原蛋白、Ⅲ型前胶原蛋白的含量,观察肝组织病理学改变; 测定肺指数,光镜下行肺组织病理学观察,检测肺组织匀浆肿瘤坏死因子α(TNF-α)、丙二醛(MDA)、一氧化氮(NO)和过氧亚硝基阴离子(ONOO-)含量。结果:大鼠肝纤维化模型复制成功,模型组大鼠肺指数明显增加,肺脏发生水肿、炎症反应,肺匀浆TNF-α、MDA、NO和ONOO-含量明显增加;大黄素治疗组肺指数较模型组下降,肺组织病理性损伤明显减轻,肺组织TNF-α、MDA、NO和ONOO-含量明显降低。结论:大黄素对肝纤维化大鼠的肺损伤具有一定的保护作用。     

A preliminary approach to pathological and biochemical changes of the lungs injured by domestic pingyangmycinum]

Two hundred male mice, weighing 18-24g, were randomized into four groups. A model of lung injury was established in mice by intratracheal administration of a single dose of domestic pingyangmycinum (Bleomycin A5). The dose-effect relationship for different doses of pingyangmycinum (0.05, 0.1, 0.2 mg) on the lung injury, and the change of hydroxyprolin (Hyp), ceruloplasmin (CP), angiotensin converting enzyme (ACE), superoxide dismutase (SOD) in mice were investigated. The results showed that the pathological changes of alveolitis and pulmonary interstitial fibrosis were more severe, and mortality of the mice was increased when pingyangmycinum dose was increased. During 2-6 weeks of this experiment, Hyp, CP, ACE and SOD in serum and Hyp in lung tissue were increased in different degrees. However, the activity of SOD in lung tissue was decreased. The possible mechanism of this lung injury is also discussed.     

苦瓜对实验性大鼠肝纤维化的干预作用及可能机制

目的: 探讨苦瓜(BM)对四氯化碳(CCl₄)诱导大鼠肝纤维化的干预作用及相关机制。方法: 随机将32只雄性健康Wistar大鼠分为4组:对照组(C组);模型组(CCl₄,M组);BM低剂量组(BM 100g/kg饲料+CCl₄,BM-L组)、BM高剂量组(BM 200g/kg饲料+CCl₄,BM-H组)。饲养中除C组外的各组大鼠均皮下注射50%CCl₄-橄榄油溶液2 mL/kg,2次/周,共8周,诱导肝纤维化动物模型。8周后处死大鼠,留取大鼠肝脏和血清。计算肝体指数;测定血清丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性;测定肝匀浆总蛋白(TP)和白蛋白(Alb)含量、谷胱甘肽过氧化物酶(GSH-Px)活性、羟脯氨酸(HYP)含量和单胺氧化酶(MAO)活性;胶原纤维染色观察大鼠肝组织变性与胶原沉积病理改变。结果: 与M组比较,摄入BM后的各剂量组大鼠肝体指数显著降低(P<0.01);血清MDA含量及肝匀浆HYP含量和MAO活性均明显降低(P<0.01),而血清SOD活性、肝组织TP和Alb含量、GSH-Px活性明显增强(P<0.01)。与正常大鼠相比,模型大鼠肝脏有明显胶原沉积与肝纤维化,伴有不同程度的肝细胞炎性损伤坏死;BM组明显减轻模型大鼠肝组织损伤坏死与胶原沉积等病理变化,以高剂量组更明显。结论: BM具有抗CCl₄诱导大鼠肝纤维化作用,其机制可能与其抗脂质过氧化、降低肝HYP含量及MAO活性的作用有关。     

Trillin Reduces Liver Chronic Inflammation and Fibrosis in Carbon Tetrachloride (CCl4) Induced Liver Injury in Mice

Trillin is an active ingredient isolated from Dioscorea nipponica Makino. This study investigated the anti-inflammatory and anti-fibrosis effects of trillin on CCl₄-induced hepatotoxicity in C57BL/6 mice. Chronic inflammation and fibrosis were induced by intraperitoneal administration of CCl₄ 0.5 μL/g of body weight twice a week for 6 weeks. Trillin (50 mg/kg, 100 mg/kg) was administered by gavage for 12 days before finishing the CCl₄ induction. Aspartate amino-transferase (AST) and glutamic-pyruvic transaminase (ALT) in serum were determined by AST and ALT kits. Superoxidase dismutase (SOD) activity and malondialdehyde (MDA) levels in serum were assayed by SOD and MDA kits. Meanwhile, the levels of inflammatory mediators including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in serum were detected by enzyme-linked immunosorbent assay (ELISA) method. Pathological changes were observed by hematoxylin-eosin (HE) staining. The proteins of the NF-κB pathway and the TGF-β/Smad pathway were measured by western blot. The trillin-treated group exhibited reduced AST, ALT, MDA, IL-6, TNF-α, and IL-1β, and increased SOD. Histological analyses of the trillin-treated group exhibited reduced inflammatory process and prevented liver fibrosis. Western blot analyses of the trillin-treated group showed reduced NF-κB pathway and TGF-β/Smad pathway. Significance: Based on the results of the present study, trillin can be used as a potential anti-inflammatory drug for chronic hepatic inflammation.     

Protective Effects of BML-111 on Cerulein-Induced Acute Pancreatitis-Associated Lung Injury via Activation of Nrf2/ARE Signaling Pathway

The aim of this study was to investigate whether BML-111 can exert protective effects on cerulein-induced acute pancreatitis-associated lung injury (APALI) via activation of nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant responsive element (ARE) signaling pathway. Severe acute pancreatitis (SAP) was established by intraperitoneal injection of cerulein (50 μg/kg) seven times at hourly intervals and Escherichia coli lipopolysaccharide (10 mg/kg) once after the last dose of cerulein immediately. BML-111 (1 mg/kg) was administered 1 h before the first injection of cerulein. Samples were taken at 3, 6, 12, and 24 h after the last injection. Pathologic lesions of the pancreas and lung tissues as well as the levels of serum amylase were analyzed; Myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), Nrf2, heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) of lung tissue were determined. The findings revealed that the injuries of pancreas and lung were typically induced by cerulein. The administration of BML-111 reduced the levels of serum amylase, lung MPO, lung MDA, the wet-to-dry weight ratio, and the pathology injury scores of the lung and pancreas, which increased in the SAP group. The expressions of Nrf2, HO-1, NQO1, and activity of SOD in lung tissue increased in the BML-111 group compared with those in the SAP group. This study indicates that BML-111 may play a critical protective role in APALI induced by cerulein. The underlying mechanisms of protective role may be attributable to its antioxidant effects through the activation of Nrf2/ARE pathway.     

H3N2猪流感病毒诱导的小鼠急性肺损伤与SOD、NO、MDA和OH·变化的相关性

目的: 探讨超氧化物歧化酶(SOD)活性以及一氧化氮(NO)、丙二醛(MDA)和羟自由基(OH·)含量的变化与H3N2猪流感病毒诱导的小鼠肺损伤的关系。方法: 选用6-8周龄、SPF级BALB/c小鼠80只,随机分为H3N2病毒感染急性肺损伤组和模拟感染对照组,每组各40只。在感染后的第3、5、7、10和14 d,每组处死小鼠6只,做如下处理:其中2只小鼠取肺组织进行HE染色,观察肺组织的病理学变化;剩余4只小鼠处死,收集血液分离血清;然后进行支气管肺泡灌洗,收集支气管肺泡灌洗液(BALF)。测BALF 和血清内SOD活性以及NO、MDA和OH·含量。结果: 病毒感染小鼠肺脏 组织学变化表现为以严重的肺泡间质水肿、炎性细胞渗出、出血为特征的弥漫性肺泡损伤;与模拟感染对照组相比,感染组BALF与血清内的NO、MDA和OH·的含量均明显增加,差异显著;感染组SOD活性与对照组相比显著下降。BALF内SOD、NO、MDA和OH·的变化幅度明显大于血清的变化。结论: 感染小鼠血清和BALF内NO、MDA和OH·显著升高,表明在H3N2猪流感病毒诱导的小鼠肺损伤过程中上述自由基可能发挥重要作用。