5-氟尿嘧啶区域动脉灌注对SAP大鼠炎性因子的影响

【目的】探讨5-氟尿嘧啶区域动脉灌注对重症急性胰腺炎(SAP)大鼠炎性因子的影响及其与胰腺病理损害程度的相关性。【方法】SD大鼠64只,随机分为假手术组(A组),SAP组(B组),5-氟尿嘧啶外周静脉注射组(C组),5-氟尿嘧啶区域动脉灌注组(D组)。测定各组大鼠的血清淀粉酶(Amy),各组动物血中白细胞介素-1(IL-1)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的含量及胰腺病理学变化。【结果】①制成SAP模型后,各组Amy水平显著上升,5-氟尿嘧啶治疗后可使Amy下降,其中5-氟尿嘧啶区域动脉灌注组下降更为明显。②5-氟尿嘧啶治疗可使血中IL-1、IL-6、TNF-α的含量显著降低(P<0.05),胰腺病理损害程度显著减轻(P<0.05),5-氟尿嘧啶区域动脉灌注组作用更强。【结论】①SAP时,应用5-氟尿嘧啶,可降低血中IL-1、IL-6、TNF-α的含量,减轻胰腺病理损害,是治疗SAP的方法之一。②区域动脉灌注是治疗SAP的增效途径。     

雄性大鼠肾上腺大部切除后骨质疏松生物力学研究

目的 研究雄性大鼠骨质疏松的骨生物力学特性.方法 基于切除肾上腺雄性大鼠骨质疏松模型,研究其股骨生物力学指标.结果 骨质疏松大鼠弯曲弹性模量、弯曲刚性系数及最大弯曲应力降低,弯曲韧性系数雄性大鼠升高.结论 骨质疏松雄性大鼠骨质综合生物力学水平降低,骨质抗应力性能降低,骨质韧性损失慢于或小于抗应力性能.     

TNF-α McAb对急性失血性休克大鼠肝脏的作用

目的探讨肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)在急性失血性休克大鼠肝损伤中的作用及TNF-α单克隆抗体的保护作用。方法将24只雄性SD大鼠随机均分为三组:对照组(A组)、休克+乳酸林格氏液复苏组(B组)和休克+TNF-α单克隆抗体复苏组(C组)。B和C组大鼠通过股动脉放血,制作急性失血性休克动物模型;B组用乳酸林格氏液复苏,C组用含TNF-α单克隆抗体(3mg/kg)的乳酸林格氏液复苏,而A组在同等条件下不进行失血。分别检测各组大鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、TNF-α水平和肝组织中MDA、SOD含量,并在光镜和电镜下观察各组大鼠肝组织的病理变化。结果 B、C组大鼠血清ALT、AST、TNF-α水平和肝组织中MDA含量较A组升高,SOD含量降低;C组ALT(343.63±35.61)U/L、AST(748.75±49.76)U/L、TNF-α(99.38±13.16)pg/mL、丙二醛(26.33±1.30)nmol/mgProt较B组ALT、AST、TNF-α、MDA含量降低,C组肝组织中SOD含量(510.14±47.44)U/mgProt较B组升高;在光镜、电镜下观察,C组肝组织损伤较B组减轻。结论 TNF-α可能是急性失血性休克肝损伤的重要因子之一,使用TNF-αMcAb复苏可以减轻失血性休克时大鼠肝损伤,具有一定的保护作用。     

葛仙汤治疗大鼠溃疡性结肠炎

目的:探讨葛仙汤对大鼠溃疡性结肠炎的治疗作用及其机制.方法:将SD大鼠按均衡随机原则分为正常对照组、模型对照组和葛仙汤低、中、高剂量组,采用大肠杆菌加乙酸免疫复合法造成大鼠溃疡性结肠炎模型.连续给药21 d,观察动物的一般情况,进行疾病活动指数(DAI)评估、结肠病理学评分(HS),检测血清中IL-6、IL-10含量.结果:葛仙汤低、中、高剂量3个治疗组DAI和HS均明显低于模型对照组(P<0.05或P<0.01),IL-6含量与模型对照组比较均明显减少(P<0.01);中剂量组IL-6含量明显低于高、低剂量组(P<0.05).3个治疗组IL-10均较模型对照组明显升高(P<0.01);中、低剂量组IL-10明显高于高剂量组(P<0.05).结论:低、中、高剂量葛仙汤均能缓解溃疡性结肠炎大鼠的症状,减轻其结肠病理损伤,促进溃疡面愈合,其中以中剂量效果为更好.     

利用体外碎石机低能量冲击波促进皮瓣成活的初步研究

目的:探讨利用体外碎石机低能量冲击波促进皮瓣成活的可行性及探索理想的实验条件。方法:应用X线定位系统的KDE-2001A型体外冲击波碎石机以0.18mJ/mm2能量冲击波治疗对20只大鼠背部皮瓣模型分为单纯皮瓣组和冲击波治疗组,进行同体成活率对比观察结果:冲击波治疗组坏死面积明显小于单纯皮瓣对照组;冲击波治疗组毛细血管分布明显密集于单纯皮瓣组。结论:0.18mJ/mm2能量冲击波亦可提高皮瓣成活率,以X线C型臂为定位系统的国内碎石机可满足实验要求。     

The effects of preweaning manganese exposure on spatial learning ability and p-CaMKIIα level in the hippocampus

BackgroundThe effects and mechanisms of preweaning Manganese (Mn) exposure on cognitive dysfunction remain unclear.ObjectiveThis study evaluated the effects of preweaning Mn exposure on spatial learning and memory as well as the protein expression of CaMKIIα and p-CaMKIIα.MethodsWe treated neonate rats with Mn²⁺ doses of 0 (control group), 10, 20 and 30 mg of Mn²⁺ per kg body weight (Mn-exposed groups) over postnatal day (PND) 1–21 by intraperitoneal injection. The ability of spatial learning and memory was tested on PND 22 using the Morris water maze (MWM), while the protein expressions of CaMKIIα and p-CaMKIIα in the hippocampus were evaluated by Western blotting. The levels of Mn in the blood and hippocampus were measured by inductively coupled plasma-mass spectrometry (ICP-MS).ResultsThe rats in Mn-exposed groups showed a significant delay in spatial learning ability on the third day of the MWM without dose-dependent differences, but there was no effect on the spatial memory ability. p-CaMKIIα, but not CaMKIIα protein expression significantly reduced in the Mn-exposed group.ConclusionThese findings suggested that the inhibition of p-CaMKIIα could be one of the mechanisms involved in the occurrence of Mn-induced cognitive impairments.     

Comparison of electroretinographic responses between two different age groups of adult Dark Agouti rats

AIM: To describe and compare the differences in electroretinographic responses between two different age groups of adult Dark Agouti (DA) rats and to better understand the effect of age on retinal histology and function.METHODS: The electroretinographic responses of two different age groups of adult DA rats were compared. Animals were divided into younger adult DA rats 10-12wk (n=8) and older adult DA rats 17-19wk (n=8). Full field electroretinography (ERG) was recorded simultaneously from both eyes after dark adaption and light adaption and parameters including the positive scotopic threshold response (pSTR), negative scotopic threshold response (nSTR), scotopic a-wave, b-wave, photopic a-wave, b-wave and photopic negative response (PhNR) were compared between groups.RESULTS: The older adult rats displayed lower stimulation thresholds of the STRs (pSTR and nSTR) and higher amplitudes of pSTR, scotopic a-wave and b-wave, photopic b-wave and PhNR amplitudes, with shorter implicit times. Photopic a-wave amplitudes were however higher in the younger adult rats.CONCLUSION:In summary, for the rod system, photoreceptor, bipolar cell and RGC activity was enhanced in the older adult rats. For the cone system, RGC and bipolar cell activity was enhanced, while photoreceptor activity was depressed in the older adult rats. Such age-related selective modification of retinal cell function needs to be considered when conducting ophthalmic research in adult rats.     

反式白藜芦醇对β－淀粉样肽致痴呆大鼠的保护作用

目的：观察反式白藜芦醇（ TR）对β－淀粉样肽（Aβ25－35）致痴呆大鼠海马旁回的保护作用。方法先将SD大鼠分为3,20月龄2大组,然后再分为假手术组、模型组、低与高剂量实验组。用Aβ25－35制痴呆模型后,实验组灌胃给TR 10,40 mg? kg－1? d－1,假手术组、模型组均给予0．9％NaCl（1 mL／100 g）,连续10 d。用实时定量PCR法检测8组大鼠海马及皮质半胱氨酸蛋白酶－3（caspase－3）、DNA聚合酶γ的表达。结果模型组与假手术组的caspase－3、DNA聚合酶γ表达水平比较差异有统计学意义（ P＜0．01）,说明造模成功。 TR对caspase－3、DNA聚合酶γ表达水平的下调非常显著（ P＜0．01）。模型组3月龄较20月龄大鼠的caspase－3表达量明显增高（ P＜0．05）。实验组3月龄与20月龄大鼠caspase－3表达量差别有统计学意义（ P＜0．05）。结论 TR对损伤的大鼠海马周围皮层神经元有保护作用。     

纤维蛋白封闭剂对SD大鼠连续腹腔注射给药14天的毒性研究

目的 评价SD大鼠连续腹腔注射纤维蛋白封闭剂的安全性。方法 SD大鼠雌雄分别按体质量随机分4组,即空白对照组、纤维蛋白封闭剂低剂量组、中剂量组和高剂量组,每组20只,雌雄各半。3个给药组的给药剂量分别为85.5、171.0和342.0mg/kg,每天腹腔注射给药,连续14d,恢复期28d,进行一般症状、血液学、血液生化和病理组织学等指标检测。结果 与空白对照组相比,纤维蛋白封闭剂中、高剂量组大鼠第14天的白细胞计数显著升高,纤维蛋白原显著降低,中、高剂量组大鼠脾脏的脏器重量有增加趋势。组织病理学检查发现部分高剂量动物腹腔出现残留药物引起的纤维肉芽组织包裹。上述变化指标在恢复期结束时基本可恢复。结论大鼠腹腔注射纤维蛋白封闭剂85.5~342.0mg/kg,安全剂量为85.5mg/kg,毒性剂量为171.0mg/kg。毒性靶系统或靶部位为血液系统、免疫系统和给药局部,毒性作用可逆。     

Dimethylarsinic acid (DMAV) changed the expressions of proliferative related factors and secretion of inflammatory cytokines in rat bladder

Dimethylarsinic acid (DMA^V), the major urinary metabolite of inorganic arsenic, is a urinary bladder carcinogen and bladder tumor promoter in adult rats. Increased urothelial cellular proliferation has been considered as an earlier phenotype in DMA^V‐induced bladder carcinogenesis. The present study examined the ultrastructural changes of bladder epithelial cells and expressions of proliferation factors, as well as the secretion of inflammatory cytokines in rats exposed to DMA^V for 10 weeks by transmission electron microscopy (TEM), qRT‐PCR, immunohistochemical staining and ELISA methods. The results showed that DMA^V administered in the drinking water produced urothelial cytotoxicity and ultrastructural changes in rats. PCNA, cyclin D1 and COX‐2 mRNA expressions and immunoreactivities were elevated in bladder urothelium. In addition, 200 ppm DMA^V treatment increased the transforming growth factor‐beta 1 (TGF‐β1) secretion and decreased tumor necrosis factor‐alpha (TNF)‐α level in the urine of rats. These data suggest that chronic inflammation, bladder epithelium lesions and proliferation might be the basic process of the chronic toxicity effects in DMA^V‐treated rats. Copyright © 2014 John Wiley & Sons, Ltd.