刺五加对甲醛染毒环境下运动大鼠血红蛋白含量的影响

探讨甲醛染毒对运动大鼠血红蛋白(HB)含量的影响及刺五加的保护作用.采用40只2月龄雄性Wistar大鼠,体重180±10g,随机分为对照组、模型组、刺五加组进行动式染毒,甲醛染毒剂量分别为0.8mg/m3、2.4mg/m3.每天染毒30min,每周6次,连续4周,刺五加的灌胃剂量为104.17mg/kg,测定运动大鼠HB含量.实验结果表明,模型组与对照组相比,模型组大鼠血HB含量均明显低于对照组(P0.05);刺五加组与模型组相比,刺五加组大鼠HB含量均明显高于模型组(P0.05).由实验得:甲醛可以造成运动大鼠HB含量降低,而灌服刺五加可以有效缓解其毒性.     

Spinal cord decompression reduces rat neural cell apoptosis secondary to spinal cord injury

Objective: To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design: We used an animal model of compressive spinal cord injury with incomplete paraparesis to evaluate neural cell apoptosis after decompression. Apoptosis and cellular damage were assessed by staining with terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate nick-end labelling (TUNEL) and immunostaining for caspase-3, Bcl-2 and Bax. Methods: Experiments were conducted in male Spragne-Dawley rats (n=78) weighing 300-400 g. The spinal cord was compressed posteriorly at T10 level using a custom-made screw for 6 h, 24 h or continuously, followed by decompression by removal of the screw. The rats were sacrificed on Day 1 or 3 or in Week 1 or 4 post-decompression. The spinal cord was removed en bloc and examined at lesion site, rostral site and caudal site (7.5 mm away from the lesion). Results: The numbers of TUNEL-positive cells were significantly lower at the site of decompression on Day l, and also at the rostral and caudal sites between Day 3 and Week 4 post-decompression, compared with the persistently compressed group. The numbers of cells between Day 1 and Week 4 were immunoreactive to caspase-3 and B-cell lymphoma-2 (Bcl-2)-associated X-protein (Bax), but not to Bcl-2, correlated with those of TUNEL-positive cells. Conclusion: Our results suggest that decompression reduces neural cell apoptosis following spinal cord injury.     

Extended exposure to environmental cues,but not to sucrose,reduces sucrose cue reactivity in rats

In the present study, we examined the effects of extinction of sucrose-predictive contextual cues and/or sucrose satiation on the expression of sucrose cue reactivity in a rat model of relapse. Context extinction was imposed by housing rats in their home cage or in the operant conditioning chamber for 17 h prior to testing. For sucrose satiation, rats were allowed unlimited access to water or sucrose for 17 h prior to testing. Cue reactivity was assessed after either one (Day 1) or 30 (Day 30) days of forced abstinence from sucrose self-administration. An abstinence-dependent increase in sucrose cue reactivity was observed in all conditions (“incubation of craving”). Context extinction dramatically reduced lever responding on both Day 1 and Day 30. Sucrose satiation had no significant effect on cue reactivity in any condition. These results demonstrate that the context in which self-administration occurs maintains a powerful influence over cue reactivity, even after extended forced abstinence. In contrast, the primary reinforcer has little control over cue reactivity. These findings highlight the important role of conditioned contextual cues in driving relapse behavior.     

莫诺苷对局灶性脑缺血-再灌注大鼠海马CyclinD1及CDK6的影响

目的：观察莫诺苷对局灶性脑缺血-再灌注大鼠细胞周期蛋白Cyclin D1及CDK6的影响。方法：用线栓法制备大鼠局灶性脑缺血-再灌注模型。将15只Sprague-Dawley（SD）大鼠随机分为假手术组,模型组,莫诺苷组（270、90、30 mg·kg-1）。利用免疫组化方法检测大鼠患侧海马Cyclin D1、CDK6表达。结果：与假手术组相比,模型组Cyclin D1及CDK6表达显著增加;给予莫诺苷治疗后,与模型组相比,莫诺苷（270、90 mg·kg-1）剂量组能显著降低大鼠Cyclin D1及CDK6的表达。结论：莫诺苷能通过降低脑缺血-再灌注后Cyclin D1及CDK6的表达而发挥神经保护作用。     

Effects of preweaning environmental enrichment on later problem-solving behavior in rats

Two experiments investigated the importance of visual sensory modality in mediating enriched environmental effects during the preweaning period, and the importance of onset and duration of the enriched experience during the same period. Rat mothers and pups were exposed together in an enriched environment for either 7 or 11 days at different periods from Day 1 to Day 21. Also included was a group of rats which received only handling from Day 11 to Day 21 postpartum and another group in which the mothers were exposed to the enriched environment during the last trimester of pregnancy. Some rats were tested at 27 days of age, and others were tested at 64 days of age in the Hebb-Williams maze test. It was found that exposure in the enriched environment for a period of 7 days before the eyes opened improved rats’ problem-solving behavior above that of control rats and to the level of rats which received such experience after the eyes had opened. Handling of rats did not improve problem-solving behavior, nor did exposure during the gestation period. It was concluded that vision is not the most important factor in mediating effects during the preweaning period, since improvement in problem-solving behavior can occur before the visual system is fully developed. It was suggested that the beneficial enrichment effects might be mediated by the mother, who, in some way, transmits additional stimulation to the infant rat during this early stage of development.     

急性肺损伤大鼠肺中酸敏感离子通道的表达研究

目的:探讨在急性肺损伤(ALI)中酸敏感离子通道(ASIC3)的表达变化及其与ALI的关系。方法:24只雄性SD大鼠随机分为四组,LPS2h,4h,6h和对照组;以内毒素持续静脉注射复制大鼠急性肺损伤模型,急性肺损伤后2h、4h、6h时采集标本监测动脉血气、肺湿/干比、肺组织病理、免疫组化检测ASIC3在肺内的表达情况。结果急性肺损伤后4h,6h肺泡上皮细胞内ASIC3的表达明显高于对照组(P<0.05),LPS2h组和对照组相比无明显差异;肺的湿/干比LPS2h,4h和对照组相比无显著差异(P>0.05),LPS6h组明显高于对照组(P<0.05)。结论1大鼠肺泡上皮细胞和支气管粘膜上皮有ASIC3的表达;2急性肺损伤大鼠肺泡表面的ASIC3表达增多。     

GM1 stabilizes expression of NMDA receptor subunit 1 in the ischemic hemisphere of MCAo／reperfusion rat

INTRODUCTION GM1 ganglioside (GM1) is the main kind ofgangliosides in mammalia, and most abundant inbrain tissue (Duchemin et al., 2002). It was reportedthat GM1 could protect cerebral ischemia in vivo andin vitro, one protective mechanism of which is thatGM1 could reduce neural injury induced by toxicityof excitatory amino acid via N-methyl-D-aspartate receptor (NMDAR) (Kharlamov et al., 1993; Simon et al., 1993; Garofalo and Cue…     

大鼠脑弥漫性轴索损伤后早期病理学的研究

目的:探讨大鼠脑弥漫性轴索损伤(DAI)后早期轴索病理学改变及c-Fos蛋白的变化,为DAI的早期法医病理学鉴定寻找新的依据.方法:参照Mamarou的打击负荷伤模型,建立大鼠DAI动物模型.运用神经纤维特殊染色法观察轴索的病理学改变,并运用免疫组化SABC法观察c-Fos的变化.结果:嗜银染色于打击后1 h即可观察到...     

Effects of β-Aescin on the expression of nuclear factor-κB and tumor necrosis factor-α after traumatic brain injury in rats

To investigate the inhibiting effect of β-Aescin on nuclear factor-κB(NF-κB)activation and the expression of tumornecrosis factor-α(TNF-α)protein after traumatic brain injury(TBI)in the rat brain,62 SD rats were subjected to lateral corticalimpact injury caused by a free-falling object and divided randomly into four groups:(1)sham operated(Group A);(2) injured(Group B);(3)β-Aescin treatment(Group C);(4) pyrrolidine dithocarbamate(PDTC) treatment(Group D).β-Aescin was ad-ministered in Group C and PDTC treated in Group D immediately after injury.A series of brain samples were obtained directly 6h,24 h and 3 d respectively after trauma in four groups.NF-κB activation was examined by Electrophoretic Mobility Shift Assay(EMSA);the levels of TNF-α protein were measured by radio-immunoassay(RIA);the water content of rat brain was measuredand pathomorphological observation was carried out.NF-κB activation,the levels of TNF-α protein and the water content of ratbrain were significantly increased(P＜0.0     

细胞色素P450CYP81A6基因在水稻中的表达:组织特异性、蛋白质亚细胞定位以及对除草剂的响应(英文)

目的:分析CYP81A6基因在苯达松及甲磺隆处理下的诱导表达模式,解释该基因与两种除草剂代谢相关的可能原因。创新点:从两种除草剂降解途径中产生的小分子物质的结构相似性出发,通过基因诱导表达的特点分析,解释CYP81A6和两种除草剂降解相关的原因。方法:通过实时定量聚合酶链反应(PCR)来分析基因表达的特点;利用CYP81A6启动子与GUS报告基因构建的载体来分析组织特异性表达;通过亚细胞定位来确定CYP81A6发挥功能的场所。结论:CYP81A6基因受苯达松及甲磺隆诱导,在不同的时间点开始上调,说明了甲磺隆的降解中间产物可以诱导这个基因的表达;CYP81A6是组成型表达,在根、茎、叶中均有表达;亚细胞定位结果证明CYP81A6是一个内质网上的蛋白。     

中药复方对戊四氮致痫大鼠海马神经元caspase-3表达的影响

目的：观察戊四氮（PTZ）致痫大鼠海马神经元caspase-3表达以及中药复方AAP的脑保护作用.方法：144只健康成年雄性Wistar大鼠随机分为对照组（CK组）、模型组（PTZ组）、中药大剂量组（AAPl组）、中药中剂量组（AAPm组）、中药小剂量组（AAPs组）和丙戊酸钠组（VPA组）;每组各6只.CK组和PTZ组分别给予生理盐水（4mL/kg.d）灌胃;中药各组分别给予中药复方大、中、小剂量（10.26g/kg、5.13g/kg、2.56g/kg）灌胃,每天1次;VPA组腹腔注射VPA（20mg/kg.d）.造模第一天,除CK组外,其余各组大鼠均腹腔注射戊四氮（PTZ）75mg/kg,观察记录大鼠行为学变化;于致痫后12h、2d、5d、7d相应时间点取材,制备脑标本;免疫组化检测caspase-3表达.结果：致痫后,除CK组外,其余各组海马区caspase-3阳性表达增强;7天,与PTZ组相比,AAPl组、AAPm组和AAPs组海马CA3区caspase-3阳性表达减弱（P〈0.05）.结论：caspase-3参与致痫大鼠海马神经元凋亡过程;AAP能降低caspase-3表达,减少神经元凋亡,有神经保护作用.     

Expressions of cardiac sympathetic norepinephrine transporter and β1-adrenergic receptor decreased in aged rats

Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovascular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine (NE) transporter (NET) on presynaptic membrane is a predominant component to eliminate released NE in the synaptic cleft and maintains the sensitivity of the β-adrenergic receptor (β-AR). In the present study, we investigated NET and β1-AR mRNA levels and sympathetic nerve density in cardiac sympathetic ganglion and left ventricular myocardium in 2- and 16-month-old rats with Northern blot analysis and immunohistochemistry. The expression levels of NET mRNA, NET protein and β₁-AR mRNA in the ganglia or myocardia of 16-month-old rats were markedly reduced by 67%, 26%, and 43%, respectively, in comparison with those in 2-month-old rats. Our results also show that aging induces a strong decrease of the catecholaminergic nerve fiber density. Project supported by the Postdoctoral Fellow Foundation of the Science and Technology Committee of Shanghai (No. 98–10) and the Natural Science Foundation of Chinese People’s Armed Police Force (Nos. WKH2006-5 and WKH2008ZO4), China     

Expressions of cardiac sympathetic norepinephrine transporter and β1-adrenergic receptor decreased in aged rats

Evidence suggests that the deterioration of communication between the sympathetic nervous system and cardiovas-cular system always accompanies the aging of human and animals. Cardiac sympathetic norepinephrine (NE) transporter (NET) on presynaptic membrane is a predominant component to eliminate released NE in the synaptic cleff and maintains the sensitivity of the β-adrenergic receptor (β-AR). In the present study, we investigated NET and β1-AR mRNA levels and sympathetic nerve density in cardiac sympathetic ganglion and leff ventricular myocardium in 2- and 16-month-old rats with Northern blot analysis and immunohistochemistry. The expression levels of NET mRNA, NET protein and β1-AR mRNA in the ganglia or myocardia of 16-month-old rats were markedly reduced by 67%, 26%, and 43%, respectively, in comparison with those in 2-month-old rats. Our results also show that aging induces a strong decrease of the catecholaminergic nerve fiber density.     

天麻素对模型大鼠海马Caspase-3表达的影响

目的：观察天麻素对癫痫大鼠海马Caspase-3表达的影响及其脑保护作用。方法：120只健康成年雄性Wistar大鼠随机分为对照组、PTZ（戊四氮）组、VPA（丙戊酸钠）组、Gb（天麻素大剂量）组和Gs（天麻素小剂量）组（n=24）。对照组和PTZ组分别以生理盐水（4mL/kg·d）灌胃;VPA组给予丙戊酸20mg．kg^-1,Gb组和Gs组分别给予天麻素200mg．kg^-1和100mg．kg^-1;每天1次,连续7天。造模第一天,除对照组大鼠外,余者均腹腔注射戊四氮75mg／kg,记录动物行为学变化。于致痫后12h、2d、5d和7d相应时间点取材,制备脑标本,免疫细胞化学术检测caspase-3表达。结果：致痫后12h,P11Z组Caspase-3有微量表达,其余各组几乎无表达;2—7d。PTZ组Caspase-3表达增加。与PTZ组比较,Gb组、Gs组及VPA组Caspase-3阳性表达降低,差异显著（P〈0．05）;与VPA组比较,Gb组和Gs组Caspase-3表达无显著差异（P〉0．05）。结论：天麻素能降低致痫大鼠海马神经元Caspase-3表达;可能通过抑制神经元凋亡发挥脑保护作用。     

大鼠神经胶质瘤和嗜铬细胞瘤中P2X受体表达特征的研究

目的：采用实时荧光定量聚合酶链式反应（polymerase chain reaction,PCR）技术,研究P2X受体在大鼠神经胶质瘤和嗜铬细胞瘤及原代培养皮层神经元和星形胶质细胞上的表达差异。方法：取新生1-2 d SD大鼠大脑皮层,分离纯化神经元和星形胶质细胞,并采用实时荧光定量PCR技术,比较P2X受体在大鼠胶质瘤C6细胞、大鼠肾上腺嗜铬细胞瘤PC-12细胞、星形胶质细胞和皮层神经元上的表达差异。结果：C6细胞P2X2、P2X3和P2X5表达水平显著高于星形胶质细胞,P2X4、P2X6和P2X7表达水平显著低于星形胶质细胞,PC-12细胞P2X1、P2X2、P2X3和P2X6表达水平显著高于皮层神经元,P2X5和P2X7表达水平则显著低于皮层神经元。此外,还发现P2X2、P2X5和P2X6在C6和PC-12细胞上的表达水平存在显著差异。结论：大鼠胶质瘤和嗜铬细胞瘤细胞表达多种P2X受体,且与原代培养细胞存在表达差异,提示核苷酸介导的信号传递系统可能作为潜在的肿瘤治疗靶点。     

益智仁对束缚应激致大鼠海马神经元NMDA受体亚基NR2B表达的调节作用

为了研究益智仁对束缚应激致大鼠海马神经元NMDA受体亚基NR2B表达的调节作用,将30只SD大鼠随机等分为正常对照组、模型对照组和益智仁治疗组。模型对照组、益智仁治疗组大鼠每日束缚1次,连续3周。益智仁治疗组束缚前给予益智仁水提取物灌胃。采用免疫组织化学方法,观察益智仁水提取物对束缚应激大鼠海马神经元NMDA受体亚基NR2B表达的调节作用。结果显示NR2B阳性产物呈深棕色或棕褐色,主要沉积在CA1区和CA3区锥体细胞的细胞膜周边。与正常对照组比较,模型对照组的NR2B阳性产物明显增多(P﹤0.01);益智仁治疗组与模型对照组比较,NR2B阳性产物明显减少(P﹤0.05)。实验结果提示益智仁能够降低束缚应激大鼠海马CA1区和CA3区NMDA受体亚基NR2B的表达。     

立体定向血肿抽吸对大鼠脑出血细胞凋亡的影响

[目的]探讨大鼠脑出血双侧纹状体区细胞凋亡的时程变化规律和早期立体定向血肿抽吸术干预治疗对细胞凋亡的影响.[方法]雄性Sprague-Dawley(SD)大鼠80只,随机分成正常对照组,假手术组,脑出血自然恢复组,6 h血肿抽吸组,12 h血肿抽吸组以及24 h血肿抽吸组.采用立体定向注入Ⅶ型胶原酶建立脑出血模型.采用原位末端标记法检测出血周边组织细胞的凋亡.[结果]①大鼠脑出血周边组织12 h出现凋亡细胞,3d凋亡细胞达峰值,11 d仍有凋亡细胞表达.②血肿抽吸术干预后出血周边组织凋亡细胞数与脑出血组对应时间点比较显著下降(P<0.05).③6 h血肿抽吸组与24 h血肿抽吸组比较细胞凋亡数明显低于24 h血肿抽吸组,差异有显著性(P<0.05).[结论]立体定向血肿抽吸术干预治疗大鼠脑出血可明显影响细胞凋亡的表达,脑出血各种临床治疗的“时间窗”应为出血后12 h之内.早期(6 h)立体定向血肿抽吸术治疗可以显著减少脑出血后细胞凋亡.     

刺五加对甲醛致运动大鼠心肌氧化损伤的保护作用实验研究

目的：通过实验观察甲醛对运动大鼠心肌组织抗氧化系统的影响及服用刺五加后的作用,探讨甲醛对运动大鼠的心肌组织毒性及刺五加的保护作用。方法：采用人为模拟不同程度甲醛染毒环境进行动式染毒,甲醛剂量分别为0.8 mg/m3,2.4 mg/m3。每天染毒30 min,每周6次,连续4周,刺五加的灌胃剂量为104.17 mg/kg,测定运动大鼠心肌组织的超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-PX）、过氧化氢酶（CAT）的活力和丙二醛（MDA）的含量。结果：染毒组与对照组相比,2.4 mg/m3剂量染毒运动组大鼠心肌组织 CAT、GSH-PX、SOD活性明显低于对照组（P〈0.01）,MDA含量明显高于对照组（P〈0.01）。服药染毒运动组与染毒运动组相比,0.8mg/m3剂量染毒服药组大鼠心肌组织CAT、GSH-PX、SOD活性明显高于染毒运动组（P〈0.01）,MDA含量明显低于染毒运动组（P〈0.01）。结论：甲醛可以降低染毒大鼠心肌组织抗氧化酶的活性,造成心肌组织氧化性损伤,而灌服中药刺五加可以有效缓解其毒性。     

Regulation of autophagy by tea polyphenols in diabetic cardiomyopathy

Objective

To investigate the effect of tea polyphenols on cardiac function in rats with diabetic cardiomyopathy, and the mechanism by which tea polyphenols regulate autophagy in diabetic cardiomyopathy.

Methods

Sixty Sprague-Dawley (SD) rats were randomly divided into six groups: a normal control group (NC), an obesity group (OB), a diabetic cardiomyopathy group (DCM), a tea polyphenol group (TP), an obesity tea polyphenol treatment group (OB-TP), and a diabetic cardiomyopathy tea polyphenol treatment group (DCM-TP). After successful modeling, serum glucose, cholesterol, and triglyceride levels were determined; cardiac structure and function were inspected by ultrasonic cardiography; myocardial pathology was examined by staining with hematoxylin-eosin; transmission electron microscopy was used to observe the morphology and quantity of autophagosomes; and expression levels of autophagy-related proteins LC3-II, SQSTM1/p62, and Beclin-1 were determined by Western blotting.

Results

Compared to the NC group, the OB group had normal blood glucose and a high level of blood lipids; both blood glucose and lipids were increased in the DCM group; ultrasonic cardiograms showed that the fraction shortening was reduced in the DCM group. However, these were improved significantly in the DCM-TP group. Hematoxylin-eosin staining showed disordered cardiomyocytes and hypertrophy in the DCM group; however, no differences were found among the remaining groups. Transmission electron microscopy revealed that the numbers of autophagosomes in the DCM and OB-TP groups were obviously increased compared to the NC and OB groups; the number of autophagosomes in the DCM-TP group was reduced. Western blotting showed that the expression of LC3-II/I and Beclin-1 increased obviously, whereas the expression of SQSTM1/p62 was decreased in the DCM and OB-TP groups (P<0.05).

Conclusions

Tea polyphenols had an effect on diabetic cardiomyopathy in rat cardiac function and may alter the levels of autophagy to improve glucose and lipid metabolism in diabetes.