白藜芦醇对急性胰腺炎肺损伤大鼠树突状细胞的影响

目的 观察白藜芦醇（resveratrol,Res）对重症急性胰腺炎（SAP）肺损伤大鼠树突状细胞（DC）的影响.方法 36只SD大鼠随机分为三组：假手术组、SAP模型组、Res治疗组（Res 10 mg/kg）,每组各12只.各组SD大鼠于制模后12 h处死,行胰腺及肺组织病理学检查和评分.提取肺树突状细胞,流式细胞仪检测DC表型CD80表达,并检测IL-12的分泌水平.结果 Res组肺和胰腺组织病理学评分分别为（3.49±1.02）和（6.43±1.40）,而SAP组分别为（6.12±2.02）和（11.00±2.58）,Res组评分均显著降低（P＜ 0.05）.SAP组DC细胞表面分子CD80阳性表达率为（45.3±6.7）％,而Res组为（20.1±3.2）％,显著低于SAP组,差异有统计学意义（P＜0.05）;Res组和SAP组DC分泌IL-12浓度分别为（1 676.5±121.8） g/L和（4 436.4±169.8） g/L,Res组IL-12浓度显著低于SAP组,差异有统计学意义（P＜0.05）.结论 Res能显著减轻SAP时肺和胰腺组织损伤,其机制与抑制肺DC活化有关.     

Intranasal nerve growth factor bypasses the blood-brain barrier and affects spinal cord neurons in spinal cord injur y

The purpose of this work was to investigate whether, by intranasal administration, the nerve growth factor bypasses the blood-brain barrier and turns over the spinal cord neurons and if such therapeutic approach could be of value in the treatment of spinal cord injury. Adult Sprague-Dawley rats with intact and injured spinal cord received daily intranasal nerve growth factor administration in both nostrils for 1 day or for 3 consecutive weeks. We found an in-creased content of nerve growth factor and enhanced expression of nerve growth factor receptor in the spinal cord 24 hours after a single intranasal administration of nerve growth factor in healthy rats, while daily treatment for 3 weeks in a model of spinal cord injury improved the deifcits in locomotor behaviour and increased spinal content of both nerve growth factor and nerve growth factor receptors. These outcomes suggest that the intranasal nerve growth factor bypasses blood-brain barrier and affects spinal cord neurons in spinal cord injury. They also suggest exploiting the possible therapeutic role of intranasally delivered nerve growth factor for the neuroprotection of damaged spinal nerve cells.     

Green tea polyphenols protect spinal cord neurons against hydrogen peroxide-induced oxidative stress

Green tea polyphenols are strong antioxidants and can reduce free radical damage. To investigate their neuroprotective potential, we induced oxidative damage in spinal cord neurons using hydrogen peroxide, and applied different concentrations(50–200 μg/mL) of green tea polyphenol to the cell medium for 24 hours. Measurements of superoxide dismutase activity, malondialdehyde content, and expression of apoptosis-related genes and proteins revealed that green tea polyphenol effectively alleviated oxidative stress. Our results indicate that green tea polyphenols play a protective role in spinal cord neurons under oxidative stress.     

Hyperbaric oxygen therapy improves local microenvironment after spinal cord injury

Clinical studies have shown that hyperbaric oxygen therapy improves motor function in patients with spinal cord injury. In the present study, we explored the mechanisms associated with the recovery of neurological function after hyperbaric oxygen therapy in a rat model of spinal cord injury. We established an acute spinal cord injury model using a modification of the free-falling object method, and treated the animals with oxygen at 0.2 MPa for 45 minutes, 4 hours after injury. The treatment was administered four times per day, for 3 days. Compared with model rats that did not receive the treatment, rats exposed to hyperbaric oxygen had fewer apoptotic cells in spinal cord tissue, lower expression levels of aquaporin 4/9 mRNA and protein, and more NF-200 positive nerve fibers. Furthermore, they had smaller spinal cord cavities, rapid recovery of somatosensory and motor evoked potentials, and notably better recovery of hindlimb motor function than model rats. Our findings indicate that hyperbaric oxygen therapy reduces apoptosis, downregulates aquaporin 4/9 mRNA and protein expression in injured spinal cord tissue, improves the local microenvironment for nerve regeneration, and protects and repairs the spinal cord after injury.     

脑室内注射胰岛素改善心肺复苏后大鼠神经功能及其机制的研究

目的：观察脑室内注射胰岛素对心肺复苏（CPR）后大鼠海马CA1区神经元Caspase-3mRNA表达、神经元凋亡及神经功能的影响。方法：将30只雄性SD大鼠随机分为对照组、复苏组及胰岛素组,并采用室颤法制备大鼠CPR模型。结果：①大鼠CPR后24 h和72 h胰岛素与复苏组相比胰岛素抑制促凋亡基因Caspase-3 mRNA表达,胰岛素与复苏组Caspase-3基因表达分别为（CPR 24 h）0.43±0.03,1.39±0.36,P=0.01;（CPR 72 h）0.63±0.06,1.08±0.05,P=0.001;②大鼠CPR后7 d,胰岛素组凋亡细胞计数（92.79±7.50/mm2）明显低于复苏组凋亡细胞计数（124.75±17.35/mm2）（F=5.853,P=0.02）;③大鼠CPR后24 h,胰岛素组神经功能评分明显高于复苏组[（70（64-72）,56（50-58）;P〈0.001]。结论：胰岛素抑制CPR后大鼠神经元Caspase-3mRNA的表达,从而抑制神经元凋亡,改善神经功能,保护神经系统。     

In case of obesity,longevity-related mechanisms lead to anti-inflammation

The exact mechanisms which contribute to longevity have not been figured out yet. Our aim was to find out a common way for prompting longevity by bringing together the well-known applications such as food restriction, exercise, and probiotic supplementing in an experimental obesity model. Experimental obesity was promoted in a total of 32 young (2 months old) and 32 aged (16 months old) male Wistar albino rats through 8-week cafeteria diet (salami, chocolate, chips, and biscuits). Old and young animals were divided into groups each consisting of eight animals and also divided into four subgroups as obese control, obese food restriction, obese probiotic-fed and obese exercise groups. Probiotic group diet contained 0.05 %w/total diet inactive and lyophilized Lactobacillus casei str. Shirota. The exercise group was subjected to treadmill running 1 h/day, at 21 m/min and at an uphill incline of 15 % for 5 days a week. Food restriction group was formed by giving 40 % less food than the others. The control group was fed regular pellet feed ad libitum. This program was continued for 16 weeks. Blood samples from all the groups were analyzed for fasting glucose, insulin, IGF-1, insulin-like growth factor binding protein 3 (IGFBP-3), interleukin (IL)-6, IL-12, malondialdehyde (MDA), fT3, TT3, fT4, TT4, and liver tissue MDA levels were measured. All applications showed anti-inflammatory effects through the observed changes in the levels of IGFBP-3, IL-6, and IL-12 in the young and old obese rats. While the interventions normally contribute to longevity by recruiting different action mechanisms, anti-inflammatory effect is the only mode of action for all the applications in the obesity model.     

丹酚酸B对非酒精性脂肪性肝炎大鼠肝细胞凋亡的影响

目的探讨丹酚酸B对非酒精性脂肪性肝炎(NASH)大鼠肝细胞凋亡的影响及对NASH的治疗作用。方法清洁级雄性SD大鼠60只,随机分为对照组、NASH模型组、丹酚酸B治疗组,每组20只。对照组以普通饲料喂养,其余2组以高脂饲料连续喂养12周复制NASH模型。第13周开始治疗组每天以浓度为1 mg/ml的丹酚酸B溶液20 ml/kg灌胃,模型组以20 ml/kg蒸馏水灌胃。治疗12周后,处死大鼠,取血及肝组织,计算肝指数,检测血清ALT、AST、甘油三酯(TG)、总胆固醇(TC),观察肝组织病理学变化,免疫组织化学法检测肝组织细胞色素C(Cyt C)、caspase-3蛋白的表达,逆转录-聚合酶链反应(RT-PCR)检测肝组织p53、Bax、Bcl-2 mRNA的表达。结果模型组大鼠肝指数、ALT、AST、TG、TC较对照组增高,肝组织炎症明显;Cyt C及caspase-3蛋白表达增加(P值均0.01);Bcl-2 mRNA表达降低,p53、Bax mRNA表达增高(P值均0.01)。治疗组与模型组相比肝指数、ALT、AST、TG、TC降低,炎症减轻;Cyt C及caspase-3蛋白表达减少(P值均0.01);Bcl-2 mRNA表达升高(P0.05),p53 mRNA表达降低(P0.05),Bax mRNA表达降低(P0.01)。结论丹酚酸B可通过调节Bcl-2、p53、Bax mRNA表达,降低Cyt C及caspase-3蛋白的表达,抑制肝细胞凋亡,对NASH起治疗作用。     

两种含胶原凝胶的人工肝生物反应器的功能比较

目的改进中空纤维型人工肝生物反应器。方法将大鼠肝细胞与胶原溶液混合并注入中空纤维反应器管外腔,待混合物在管外腔中形成胶原凝胶将肝细胞悬浮其中,构成胶原凝胶混悬肝细胞反应器(Ⅰ组);另将大鼠肝细胞混悬液注入涂有胶原层的中空纤维反应器管外腔,构成胶原涂层加肝细胞反应器(Ⅱ组)。两组反应器均由管内腔循环灌注培养液,置孵箱培养9 d,每24 h换液一次,每48 h取灌注液检测白蛋白(Alb)、尿素、乳酸脱氢酶(LDH)浓度,以检验反应器的肝细胞功能。采用统计软件SPSS 13.0进行统计学分析,计量数据以均数±标准差(x±s)表示,两组资料比较用配对t检验。结果Ⅰ组和Ⅱ组的Alb值均在灌注第3天达峰值,分别为(1.41±0.08)和(0.65±0.05)g/L,3~9 d各时间点Alb值Ⅰ组均明显高于Ⅱ组(P值均0.01)。Ⅰ组和Ⅱ组的尿素值分别在灌注第5天和3天达峰值,分别为(1.73±0.14)和(1.56±0.18)mmol/L,5~9 d各时间点尿素值Ⅰ组均明显高于Ⅱ组(P值均0.01)。Ⅰ组和Ⅱ组的LDH值在灌注第9天达峰值,分别为(32.03±9.13)和(70.17±25.28)U/L,1~9 d各时间点LDH值Ⅰ组均明显低于Ⅱ组(P值均0.01)。提示胶原凝胶混悬肝细胞反应器(Ⅰ组)比胶原涂层加肝细胞反应器(Ⅱ组)有更好的肝细胞合成代谢功能,肝细胞酶漏出也更少。结论胶原凝胶混悬固定肝细胞更适用于构建中空纤维型人工肝生物反应器。     

肝衰竭大鼠胃窦胆碱能和氮能神经分布的变化分析

目的观察肝衰竭大鼠胃排空及胃窦肌间神经丛胆碱能和氮能神经的变化。方法 40只Wistar大鼠随机分为肝衰竭模型组和对照组,采用葡聚糖蓝-2000为标志物观察大鼠胃排空的变化,应用乙酰胆碱酯酶(AchE)和还原型辅酶Ⅱ硫辛酰胺脱氢酶(NADPH-d)组织化学染色及肌间神经丛全层铺片技术,观察肝衰竭大鼠胃窦肌间神经丛胆碱能和氮能神经的变化,并进行定量分析。计量资料以均数±标准差(x±s)表示,组间比较采用t检验。结果肝衰竭组大鼠胃排空明显减弱(163.00±25.68 vs 100.00±18.93,P0.01),胃窦肌间神经丛胆碱能阳性神经元数量减少,神经纤维变细,分布较稀疏,明显低于对照组(t=3.201,P0.01);氮能神经阳性神经元数量及神经纤维分布明显高于对照组(t=2.912,P0.01)。结论肝衰竭大鼠胃功能的减退与胃窦肌间神经丛胆碱能神经分布减少及氮能神经分布增加有关。