马尾松松针提取物调节JNK3/caspase-3信号转导减轻大鼠脑缺血再灌注后氧化应激损伤

目的：探讨马尾松松针提取物（PNE）对大鼠脑缺血再灌注后氧化应激损伤的保护作用。方法：将SD雄性大鼠随机分为手术对照组、模型对照组、依达拉奉组、PNE小剂量组（200 mg/kg）、PNE中剂量组（400 mg/kg）、PNE大剂量组（800 mg/kg）,于造模前连续7 d及造模后6 h分别灌胃给药。其中,手术对照组和模型对照组灌胃给予等渗氯化钠溶液,依达拉奉组灌胃给予等渗氯化钠溶液的同时腹腔注射依达拉奉3 mg/kg,PNE各组灌胃给予各剂量PNE。通过大脑中动脉阻塞法建立脑缺血再灌注损伤大鼠模型,于再灌注24 h后测定各组大鼠神经功能缺损评分、脑组织含水量、脑梗死体积。采用苏木素-伊红染色观察大脑皮层及海马组织结构病理变化并统计正常神经细胞数;TUNEL法检测大脑皮层神经细胞凋亡率;试剂盒检测缺血侧脑组织一氧化氮、丙二醛含量与超氧化物歧化酶（SOD）活性;蛋白质印迹法检测大脑皮层c-Jun氨基末端激酶（JNK）3、磷酸化JNK3、B淋巴细胞瘤蛋白（Bcl）-2、Bcl-2相关X蛋白（Bax）、细胞色素C、胱天蛋白酶（caspase）-3的蛋白表达水平。结果：与模型对照组比较,PN...     

大鼠股直肌肌纤维型组成及分布研究

目的 探讨大鼠股直肌的肌纤维型组成和分布,以了解该肌功能.方法 取成年SD大鼠股直肌组织进行冰冻切片(8μm厚),采用Guth-Samaha肌球蛋白ATP酶组织化学染色法并稍做改良,对其进行肌纤维分型研究.结果 大鼠股直肌经肌球蛋白ATP酶组织化学染色后可明确分出2种肌纤维型,即白色的I型纤维(慢缩纤维)和深褐色的Ⅱ型纤维(快缩纤维),2种肌纤维在肌内呈棋盘样均匀分布;图像分析仪计数I纤维占(24.6±3.1)%,Ⅱ型纤维比例为(75.4±6.3)%,2者比较差异显著(P<0.01).结论 大鼠股直肌的肌纤维组成以Ⅱ型纤维为主,属于力量速度型肌.     

蒿甲醚抗SD大鼠原位脑胶质瘤血管生成的 实验

 目的探讨蒿甲醚（Artemether）抗SD大鼠原位脑胶质瘤血管生成作用。方法采用四甲基偶氮唑蓝(MTT)法测定不同浓度蒿甲醚对大鼠C6脑胶质瘤细胞株的生长抑制作用,计算半数抑制浓度(IC₅₀)。采用立体定位仪在SD大鼠大脑皮质层接种C6脑胶质瘤细胞（1×10⁶/μl）40只,雌、雄各半;随机分为5组,每组8只。在接种第3天后,各组采用灌胃给药法连续给药10天。于接种后的第20天解剖大鼠,经活体左心室灌注4%多聚甲醛,固定肿瘤的全脑标本。在大鼠脑部接种穿刺点做冠状切口,按垂直和水平方向测量肿瘤大小。肿瘤体积=a²bπ∕6(a为肿瘤的短径,b为肿瘤的长径)。全脑标本用4%多聚甲醛固定,肿瘤组织做病理观察,免疫组化方法检测移植瘤组织微血管密度。结果各实验组血管计数分别为Ⅰ组（39±4）,Ⅱ组（29±6）,Ⅲ组（12±8）,Ⅳ组（10±5）,生理盐水组为（52±7）。各实验组血管计数均明显少于生理盐水对照组,差异有统计学意义(分别P<0.05, P<0.01)。各实验组SD大鼠原位脑胶质瘤体积较对照组显著减小。结论在一定剂量范围内,蒿甲醚具有明显抑制SD大鼠原位脑胶质瘤血管生成作用;蒿甲醚抑制原位脑胶质瘤生长和转移的机制之一是透过血脑屏障抑制脑胶质瘤血管生成。     

亚高原地区大、小鼠生化指标正常参考值实验研究

目的 探讨亚高原地区SD大鼠和KM小鼠血液生化指标变化规律,确立参考值.方法 将2w龄SD大鼠和KM小鼠各60只,按饲养地区分为亚高原组(海拔1890 m)和平原组(海拔540 m),分别于4、6、10 w龄时检测血液生化指标,比较两组肝功能、肾功能、血脂及血糖的差异.结果 取得亚高原地区不同周龄、不同性别SD大鼠和KM小鼠的血液生化指标均值.亚高原组的肝功能指标普遍高于平原组,以谷丙转氨酶、谷草转氨酶、白蛋白的改变为主(P＜0.05);亚高原组肾功能指标也高于平原组(P＜0.05),特别是习服时间越长,改变越明显;亚高原组血脂指标高于平原组(P＜0.05);除平原组雄性KM小鼠血糖(GLU)高于亚高原组(P＜0.05)外,其余亚高原组大、小鼠GLU均高于平原组(P＜0.05).结论 建立了亚高原地区不同周龄、不同性别SD大鼠和KM小鼠的血液生化指标数据库,为该地区生物医学研究奠定了基础,也为亚高原地区KM小鼠和SD大鼠标准化鉴定和质量控制提供了可靠依据.     

Impact of the supine position versus left horizontal position on colonoscopy insertion: a 2-center,randomized controlled trial

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Phenotypic and metabolic aspects of prostatic epithelial cells in aged gerbils after antisteroidal therapy: Turnover in the state of chromatin condensation and androgen-independent cell replacement

The gerbil is a rodent considered a good model for studies of prostatic morphophysiology under different experimental conditions. Studies involving castration and steroidal blockers of aged gerbils showed that the glandular epithelium persists after long-term therapy, preventing the organ atrophy. Thus, the objective of this study was to evaluate the phenotypic characteristics and behavior of prostatic epithelial cells that remained after different periods of hormone ablation in aged gerbils. The identification of elements that influenced the survival of this cell type was performed by morphometric, nuclear phenotypes, ultrastructural and immune histochemical analysis. The most significant responses to treatment, by analyzing morphometric features, were observed during the first three time points (day 1, day 3, and day 7), after which there appeared to be an adjustment of the gland to the hormone ablation. All treatments led to changes in the state of chromatin condensation, DNA methylation pattern and phenotypic changes indicated cell senescence. Additionally, an increase in the basal cells seemed to guarantee self-renewal properties to the epithelium. These data indicate that changes occur at many levels, including gene expression and nuclear architecture in the epithelial cells, when aging and steroidal blockade are associated. These aspects are important when considering castration-resistant prostate cancer, a malignant tumor posing difficult therapeutic intervention.     

Reversal of slow growth and heartbeat through the restoration of mitochondrial function in clk-1-deficient mouse embryos by exogenous administration of coenzyme Q10

The longevity gene clk-1/coq7 encodes an enzyme that is essential for the biosynthesis of coenzyme Q (CoQ) in mitochondria and regulates the lifespan and behavioral timing in Caenorhabditis elegans and the chronological lifespan in fission yeast. However, whether the mammalian clk-1/coq7 ortholog (clk-1) regulates these phenotypes in mammals remains to be fully evaluated due to the embryonic lethality of clk-1-deficient (clk-1(-/-)) mice. To investigate whether clk-1 regulates biological functions, such as growth and heartbeat, through CoQ in mouse embryos, we cultivated the cells and hearts of clk-1(-/-) mouse embryos at embryonic day 10.5 (E10.5) for at least 10 days in the presence of fetal bovine serum. In embryonic cells, cardiomyocytes, and hearts, the growth and heart rates were significantly slowed in clk-1(-/-) compared with wild-type or heterozygous mouse tissues. Moreover, frequent apoptosis and a significant reduction in mitochondrial functions, including membrane potential and ATP production, were observed in the clk-1(-/-) cells and hearts. The slowed growth and heart rates and the reduced mitochondrial function of clk-1(-/-) embryonic cells and hearts in culture were almost completely rescued by the administration of exogenous CoQ(10). The results indicate that clk-1 regulates growth and heart rates through CoQ-mediated mitochondrial functions in mouse embryos.