Studies on triglyceride metabolism: Phosphatidate phosphohydrolase from guinea pig Harderian gland

Humble E, Berglund L. Studies on triglyceride metabolism: phosphatidate phosphohydrolase from guinea pig Harderian gland. Scand J Clin Lab Invest 1993; 493-498.

The guinea pig Harderian gland, located in the orbit, is characterized by a high production of lipids. However, little is known about the regulation of the metabolic pathways involved. In the present paper the properties of guinea pig Harderian gland phosphatidate phosphohydrolase, a key enzyme in triglyceride biosynthesis, was investigated. The enzyme was present both in the cytosolic and the microsomal fraction from the gland. Cytosolic phosphatidate phosphohydrolase was purified by hydroxylapatite chromatography. The enzyme was dependent on magnesium ions and inhibited in the presence of fluoride. The dependence on the substrate phosphatidate was investigated and the apparent Km for phosphatidate was about 0.6mM. Phosphatidate phosphohydrolase activity was influenced by different phospholipids. As is the case for the rat liver enzyme, phosphatidylethanolamine was found to stimulate the enzyme activity. The results indicate that Harderian gland phosphatidate phosphohydrolase has similar properties as the corresponding enzyme from rat liver, suggesting that it may be of regulatory importance.     

褪黑素对大鼠酒精性肝纤维化的作用

目的：观察褪黑素对酒精性肝纤维化的作用，并了解其是否有剂量依赖性。方法：实验于2004-03／12在解放军第四军医大学基础部病理学实验室进行。取SD雄性大鼠40只，随机分为正常对照组、模型组和褪黑素0．25．0．5，1．0ms／kg组5组（n=8）。①除正常对照组外，其他各组大鼠每天固定时间灌胃白酒-玉米油-吡唑混合液（酒的摄入量为10g／ks），连续12周复制酒精性肝纤维化大鼠模型。②造模成功后褪黑素各剂量组分别经尾静脉注射褪黑素0．25，0．5，1．0mg／（kg&;#183;d），正常对照组及模型组大鼠经尾静脉注射2．5mL／kg体积分数为0．02的乙醇，连续28d。③给药后颈椎脱臼处死大鼠，经苏木精-伊红染色观察肝组织的病理学变化．并检测大鼠肝匀浆液中超氧化物歧化酶和谷胱甘肽过氧化物酶的水平。结果：40只大鼠进入结果分析。①模型组大鼠肝小叶结构紊乱，有大量纤维组织沉积，炎症细胞浸润，肝细胞脂肪变性。褪黑素1．0mg／ks组纤维组织沉积减少，仅有少量炎症细胞的浸润。②超氧化物歧化酶活性：模型组显著低于正常对照组（P〈0．01）；褪黑素0．25，0．5，1．0mg／ks组显著高于模型组（P〈0．05，0．01），剂量越大，效果越好。③谷胱甘肽过氧化物酶活性：模型组显著低于正常对照组（P〈0.05）；褪黑素0.25，0.5，1．0mg／kg组显著高于模型组（P〈0．05），剂量越大，效果越好。结论：褪黑素对酒精性肝纤维化具有剂量依赖性的保护作用，其机制可能与增强肝脏超氧化物歧化酶和谷胱甘肽过氧化物酶等抗氧化酶的活性有关。     

褪黑素对大鼠酒精性肝纤维化的作用

目的:观察褪黑素对酒精性肝纤维化的作用,并了解其是否有剂量依赖性。方法:实验于2004-03/12在解放军第四军医大学基础部病理学实验室进行。取SD雄性大鼠40只,随机分为正常对照组、模型组和褪黑素0.25,0.5,1.0mg/kg组5组(n=8)。①除正常对照组外,其他各组大鼠每天固定时间灌胃白酒-玉米油-吡唑混合液(酒的摄入量为10g/kg),连续12周复制酒精性肝纤维化大鼠模型。②造模成功后褪黑素各剂量组分别经尾静脉注射褪黑素0.25,0.5,1.0mg/(kg·d),正常对照组及模型组大鼠经尾静脉注射2.5mL/kg体积分数为0.02的乙醇,连续28d。③给药后颈椎脱臼处死大鼠,经苏木精-伊红染色观察肝组织的病理学变化,并检测大鼠肝匀浆液中超氧化物歧化酶和谷胱甘肽过氧化物酶的水平。结果:40只大鼠进入结果分析。①模型组大鼠肝小叶结构紊乱,有大量纤维组织沉积,炎症细胞浸润,肝细胞脂肪变性。褪黑素1.0mg/kg组纤维组织沉积减少,仅有少量炎症细胞的浸润。②超氧化物歧化酶活性:模型组显著低于正常对照组(P<0.01);褪黑素0.25,0.5,1.0mg/kg组显著高于模型组(P<0.05,0.01),剂量越大,效果越好。③谷胱甘肽过氧化物酶活性:模型组显著低于正常对照组(P<0.05);褪黑素0.25,0.5,1.0mg/kg组显著高于模型组(P<0.05),剂量越大,效果越好。结论:褪黑素对酒精性肝纤维化具有剂量依赖性的保护作用,其机制可能与增强肝脏超氧化物歧化酶和谷胱甘肽过氧化物酶等抗氧化酶的活性有关。     

Superoxide production in the vasculature of lipopolysaccharide-treated rats and pigs

Sepsis is associated with increased production of reactive oxygen species (ROS); however, the metabolic sources of increased ROS are not well understood. We hypothesized that the recently described nonphagocytic NAD(P)H oxidase system could be an important source of the ROS superoxide anion (O2-) during sepsis, and the interaction of O2- with nitric oxide (NO) may contribute to sepsis-induced vascular Injury. To evaluate this issue, we measured O2- production before and after treatment with lipopolysaccharide (LPS) in rats, who are Inducible NO synthase producers (NOSII) and in pigs, who do not produce NOSII. LPS increased O2- production in aorta from rats from 0.38 +/- 0.07 nmol/mg/10 min to 1.18 +/- 0.23 nmol/mg/10 min, (P = 0.001) in rats, and 0.63 +/- 0.05 nmol/mg/10 min to 1.5 +/- 1.6 nmol/mg/10 min (P = 0.001) in carotid arteries from pigs. Components of NAD(P)H oxidase, including p22(phox), gp91(phox), p47(phox), p67(phox), mRNA and p22(phox), and gp91(phox) proteins were present in rat aorta and aorta and carotid arteries from pigs. Expression mildly increased in rats, but not in pigs. In rats, NADH and NADPH greatly increased O2- production with no difference in untreated versus LPS-treated rats. The addition of L-NAME increased NADH-dependant O2- production from 75 +/- 3 nmol/O2-/mg/10 min to 113 +/- 7 nmoVO2-/mg/10 min in LPS-treated rats, but had no effect in untreated rats. In pigs, the NADH-stimulated O2- production was 43 +/- 8 nmol/mg/10 min before and 63 +/- 4.3 nmol/mg/10 min after LPS even without L-NAME (P < 0.05). In contrast to LPS-treated rats, L-NAME markedly decreased NADH-stimulated O2- production (63 +/- 4 nmol/mg/10 min to 33 +/- 5.6 nmol/mg/10 min, P < 0.01). Luminol-enhanced chemiluminescence was also Increased in porcine carotid arteries after LPS treatment, which is consistent with peroxynitrite formation. Our results indicate that components of NAD(P)H oxidase are present in vessels of pigs and rats and there is substantial NADH-dependent O2- production that is increased after LPS. However, the behavior of NAD(P)H oxidase in NOSII-producing and nonproducing species differs with a reduction of O2- by NO in rats and NO-dependent production in pigs.     

Effect of treatment of rats with antidepressants on melatonin concentrations in the pineal gland and serum

The effect of administration of antidepressant drugs to rats on catecholamine-induced rises in the concentration of melatonin in the pineal gland and serum was studied. Increases in melatonin levels were produced by either the exogenous administration of different doses of L-isoproterenol or by exposure of rats to darkness. Repeated administration of either desmethylimipramine or nialamide reduced significantly the elevation in melatonin concentrations in the pineal gland produced by either L-isoproterenol or darkness. The rise in serum melatonin seen at night was also blunted significantly in rats treated repeatedly with these drugs. By contrast, the concentration of melatonin in either the pineal gland or serum was not reduced in rats given desmethylimipramine or nialamide acutely. In fact, daytime concentrations of melatonin both in the gland and in serum were significantly increased after either acute or repeated treatment with nialamide. The nialamide-induced increase in daytime concentrations of melatonin in the pineal gland was prevented if the rats were treated with propranolol. The diminished hormonal responsiveness produced by the repeated administration of antidepressants occurred at a time when the binding of [3H]dihydroalprenolol to pineal gland homogenates was reduced. Thus, a hormonal response to catecholamines regulated via beta adrenergic receptor activation is reduced by repeated antidepressant treatments in conjunction with the development of beta adrenergic receptor subsensitivity.     

Effects of melatonin on plasma oxidative stress in rats with streptozotocin induced diabetes.

The aim of this study was to evaluate the effect of single melatonin injection on plasma oxidative stress in rats with streptozotocin induced diabetes. Diabetes was induced after a single intraperitoneal dose of streptozotocin (60 mg/kg), while hyperglycemia was determined 10 days upon injection. Diabetic rats were divided into two groups. In the first group the injection of melatonin was applied intraperitoneally (20 mg/kg), while the second group received physiological solution. Twenty-four hours later the rats were killed and their blood was centrifuged. In the rat plasma the following parameters were evaluated: the glucose level, superoxide radical, lipid peroxidation, reduced glutathione, total antioxidant capacity, antioxidant enzymes and the aldose reductase activity. The injected melatonin decreased the superoxide radical in the rat plasma. Moreover, melatonin increased the total antioxidative capacity and the activity of antioxidative enzymes superoxide dismutase and glutathione peroxidase. These results indicate that melatonin is a strong scavenger, which may diminish negative effects of oxidative stress in diabetic rats 24 hours after its application The findings suggest that melatonin is also a strong antioxidant. It increases the antioxidant enzymes activity, inhibiting the release of superoxide radicals. A high total antioxidative capacity and the lower activity of aldose reductase enlarge melatonin scavenger capacity against reactive oxygen species in diabetic rats.     

褪黑素对急性脑出血小胶质细胞激活的影响

目的 探讨褪黑素对大鼠脑出血后小胶质细胞激活与超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量变化的影响.方法 130只雄性SD大鼠,随机(随机数字法)分为正常组、假手术组、脑出血模型组(模型组)、褪黑素干预组(褪黑素组);组内随机分为12 h、1d、2d、4d、7d共5个时间点,按Rosenberg法建立脑出血模型,褪黑素组每天腹腔注射1 mg/mL褪黑素10 mL/kg;透射电镜技术观察脑出血后出血侧皮层小胶质细胞形态;免疫组织化学方法观察脑组织OX42阳性细胞动态表达;黄嘌呤氧化法和硫代巴比妥酸比色法检测脑组织SOD活性及MDA含量.结果 透射电镜显示,脑出血后2d时皮层神经元肿胀,小胶质细胞活化,褪黑素组小胶质细胞活化不明显;脑出血后12 h时血肿周围可见大量OX42阳性小胶质细胞表达,1d时达到高峰,7d时仍有表达,各时间点褪黑素组OX42阳性细胞表达明显低于模型组(P＜0.05);脑出血后脑组织MDA含量(nmoL/mg prot)显著增加,7d时仍高于正常水平, (0.875 ±0.098) vs.(0.725±0.061),P＜0.05; SOD活性(U/mg prot)变化则与之相反,(70.46 ±3.12) vs.(85.86 ±4.95),P ＜0.05.与模型组比较,褪黑素组MDA含量显著降低(P＜0.05),SOD活性升高(P＜0.05).结论 褪黑素对脑出血后神经细胞损伤具有保护作用,其机制可能与褪黑素减轻脑出血导致的氧化应激反应、抑制小胶质细胞活化相关.     

褪黑素、维生素E对阿霉素所致大鼠心肌损伤的影响

目的研究褪黑素(MLT)、维生素(Vit)E对阿霉素(ADM)导致大鼠心肌损伤的影响。方法采用成年SD大鼠40只,随机分为空白对照组、ADM组、MLT+ADM组、VitE+ADM组、MLT+VitE+ADM组,每组各8只。实验30 d后Masson氏三色染色法进行左室胶原特异染色及半定量分析,计算胶原容积分数(CVF),并作HE染色,光镜下病理形态学观察,测定心肌超氧化物酶(SOD)活性及丙二醛(MDA)含量,测定Bcl-2/Bax蛋白的表达。结果与正常对照组大鼠比较,阿霉素组大鼠心肌MDA含量显著升高,而SOD活性显著降低,心肌细胞Bax/Bcl-2基因的蛋白阳性表达增高,心肌损伤。给予MLT、VitE治疗可明显降低心肌组织中MDA含量,并显著增强SOD活性,抑制心肌细胞Bcl-2/Bax基因的蛋白阳性表达心肌损伤减轻。2种抗氧化剂相比,MLT在大鼠心肌组织的抗氧化能力强于VitE,两者联用则抗氧化能力强于两者单独应用。结论MLT和VitE均可通过增强阿霉素诱导的心肌损伤大鼠的抗氧化能力和抑制氧化应激反应从而对心肌具有一定的保护作用,并且MLT的抗氧化能力强于VitE,联用MLT和VitE则抗氧化能力表现更明显。     

电针与褪黑素合用对大鼠应激性胃溃疡的影响

目的:观察电针与褪黑素合用对束缚-浸水应激大鼠胃溃疡指数、胃黏膜超氧化物歧化酶活性和丙二醛含量的影响,并与电针或褪黑素单独使用结果做比较。方法:实验于2004-10/2005-06在咸宁学院医学院生理教研室完成。①选用70只雄性SD大鼠,2～3月龄,体质量(250±30)g。将动物按随机抽签法分为5组:正常组、应激组、褪黑素 应激组、电针 应激组、电针 褪黑素 应激组。②正常组:不造模,不予处理。褪黑素 应激组、电针 应激组、应激组:分别于造模前30min腹腔注射褪黑素(Sigma公司产品,20mg/kg)、电针干预、腹腔注射含体积分数0.05乙醇的等体积生理盐水。电针 褪黑素 应激组:腹腔注射褪黑素(20mg/kg)后电针干预(用CDM1-2型双频针麻治疗仪电针刺激大鼠双侧后肢足三里穴位,电刺频率为4～16Hz,强度按1,2,3Ⅴ顺序增递电压,每个强度电针干预10min,共30min)再造模。③应激性溃疡模型制备:用乙醚轻度麻醉大鼠,将四肢及头部束缚于木板上。大鼠清醒后,将木板垂直浸于23℃水中,水面平胸骨剑突处。④浸水6h后处死大鼠剖腹,于胃幽门和贲门两处用线结扎,并向胃腔内注入40g/L甲醛溶液8～10mL。30min后沿大弯侧将胃剪开展平,观察溃疡发生情况。计算溃疡指数(损伤面的长度<1.0mm为1分;1.0～2.0mm为2分;2.0～3.0mm为3分;3.0～4.0mm为4分,>4.0mm将其分割若干段,每段按上法计算,溃疡宽度>1.0mm则分值×2,全胃得分之和为胃溃疡指数)。⑤取大鼠胃黏膜,制成组织匀浆液,取出上清液按南京建成生物工程研究所提供的试剂盒说明书检测超氧化物歧化酶活性、丙二醛含量。⑥组间计量资料差异比较采用t检验。结果:大鼠70只均进入结果分析,每组14只(进行胃溃疡指数计算7只,胃组织匀浆超氧化物歧化酶活性及丙二醛含量测定7只)。①胃溃疡指数:应激组明显高于褪黑素 应激组和电针 应激组(P<0.01),褪黑素 电针 应激组明显低于褪黑素 应激组和电针 应激组(P<0.01)。②胃黏膜超氧化物歧化酶活性:应激组明显低于正常组(P<0.01),褪黑素 应激组和电针 应激组明显高于应激组(P<0.01),明显低于电针 褪黑素 应激组(P<0.05,0.01)。③胃黏膜丙二醛含量:应激组明显高于正常组(P<0.01),褪黑素 应激组和电针 应激组明显低于应激组(P<0.01,0.05),明显高于电针 褪黑素 应激组(P<0.05)。结论:褪黑素或电针对应激性胃黏膜损伤有保护作用,该作用的发挥可能与抑制体内的过氧化反应有关,且电针与褪黑素合用对胃黏膜的保护作用更为显著。     

Leukotriene D4 activates a chloride conductance in hepatocytes from lipopolysaccharide-treated rats.

Endotoxin (LPS) can cause hepatocellular injury under several circumstances, and leukotrienes have been implicated as a contributing factor. Since ion channel activation has been associated with cytotoxicity, the aim of this study was to determine the circumstances under which LPS and/or leukotrienes activate ionic conductances in hepatocytes. LPS treatment of rats increased Cl- conductance in hepatocytes from 232+/-42 to 1236+/-134 pS/pF. Voltage dependence and inhibitor specificity of this conductance were similar to that of a swelling-activated Cl- conductance, and internal dialysis with nucleoside analogues suggested control by an inhibitory G protein. The lipoxygenase inhibitor nordihydroguaiaretic acid, the specific leukotriene D4 (LTD4) receptor antagonist MK-571, and the 5-lipoxygenase activating protein inhibitor MK-886 all significantly inhibited the conductance. Intracellular dialysis with LTD4 (1.5 microM) elevated intracellular Ca2+ from 143+/-6.5 to 388+/-114 nM within 6 min and stimulated an outwardly rectifying conductance from 642+/-159 to 1669+/-224 pS/pF (n = 9, P < 0.001). In hepatocytes prepared from untreated rats, this concentration of intracellular LTD4 neither raised intracellular Ca2+ nor activated the conductance. The LTD4 response could be induced in normal hepatocytes by culture with either conditioned medium from LPS-treated macrophages or purified TNF-alpha. In conclusion, intracellular LTD4 activates a chloride conductance in hepatocytes isolated from rats treated with LPS or primed in vitro with TNF-alpha. Changes in the hepatocellular accumulation of leukotrienes therefore mediate channel activation and may contribute to liver injury during sepsis and other inflammatory conditions.     

电针与褪黑素合用对大鼠应激性胃溃疡的影响

目的：观察电针与褪黑素合用对束缚-浸水应激大鼠胃溃疡指数、胃黏膜超氧化物歧化酶活性和丙二醛含量的影响，并与电针或褪黑索单独使用结果做比较。 方法：实验于2004-10／2005-06在咸宁学院医学院生理教研室完成。①选用70只雄性SD大鼠，2～3月龄，体质量（250&;#177;30）g。将动物按随机抽签法分为5组：正常组、应激组、褪黑索＋应激组、电针＋应激组、电针＋褪黑素＋应激组。②正常组：不造模，不予处理。褪黑紊＋应激组、电针＋应激组、应激组：分别于造模前30min腹腔注射褪黑索（Sigma公司产品，20mg／kg）、电针干预、腹腔注射含体积分数0．05乙醇的等体积生理盐水。电针＋褪黑素＋应激组：腹腔注射褪黑素（20mg／kg）后电针干预（用EDM1-2型双频针麻治疗仪电针刺激大鼠双侧后肢足三里穴位，电刺频率为4-16Hz，强度按1,2，3V顺序增递电压。每个强度电针干预10min，共30min）再造模。③应激性溃疡模型制备：用乙醚轻度麻醉大鼠，将四肢及头部束缚于木板上。大鼠清醒后，将木板垂直浸于23℃水中，水面平胸骨剑突处。④浸水6h后处死大鼠剖腹，于胃幽门和贲门两处用线结扎，并向胃腔内注入40g／L甲醛溶液8—10mL。30min后沿大弯侧将胃剪开展平，观察溃疡发生情况。计算溃疡指数（损伤面的长度〈1．0mm为1分；1．0-2．0mm为2分；2．0～3.0mm为3分；3．04．0mm为4分。〉4．0mm将其分割若干段。每段按上法计算，溃疡宽度〉1.0mm则分值X^2，全胃得分之和为胃溃疡指数）。⑤取大鼠胃黏膜，制成组织匀浆液，取出上清液按南京建成生物工程研究所提供的试剂盒说明书检测超氧化物歧化酶活性、丙二醛含量。⑥组间计量资料差异比较采用t检验。 结果：大鼠70只均进入结果分析，每组14只（进行胃溃疡指数计算7只，胃组织匀浆超氧化物歧化酶活性及丙二醛含量测定7只）。①胃溃疡指数：应激组明显高于褪黑素＋应激组和电针＋应激组（P〈0．01），褪黑素＋电针＋应激组明显低于褪黑素＋应激组和电针＋应激组（P〈0．01）。②胃黏膜超氧化物歧化酶活性：应激组明显低于正常组（JP〈0．01）。褪黑紊＋应激组和电针＋应激组明显高于应激组（P〈0．01），明显低于电针＋褪黑索＋应激组（P〈0.05，0．01）。③胃黏膜丙二醛含量：应激组明显高于正常组（P〈0．01）。褪黑素＋应激组和电针＋应激组明显低于应激组（P〈0．01，0．05），明显高于电针＋褪黑素＋应激组（P〈0．05）。 结论：褪黑素或电针对应激性胃黏膜损伤有保护作用，该作用的发挥可能与抑制体内的过氧化反应有关，且电针与褪黑素合用对胃黏膜的保护作用更为显著。     

A simplified radioimmunoassay for melatonin and its application to biological fluids. Preliminary observations on the half-life of plasma melatonin in man

A simplified and rapid radioimmunoassay (RIA) for melatonin is presented. Melatonin is extracted from seru, plasma or urine and RIA is performed by using [3H]melatonin as the tracer. The standard curve covers the range 0.2--4.3 nmol/l. By increasing the sample volume the range can be extended to 0.06 nmol/l. The intra-assay variability is 7% (relative standard deviation = rsd) and the inter-assay variability is 10% (rsd). The recovery of melatonin added to calf serum is 96%. The long term variability of the assay (43 assays on aliquots of one serum sample during 6 months) is 13.5% (rsd). The serum levels in man after one oral dose of 430 mumol melatonin have been measured. The peak value, 620 nmol/l, was noted after 0.5 h and the melatonin concentration was still above the normal range at 24 h (2.1 nmol/l).     

Effect of melatonin on cadmium-induced hepatotoxicity in male Sprague-Dawley rats.

Effect of melatonin on toxicity of cadmium (Cd) was studied in male SD rats co-administered daily Cd (1 mg/kg b.w., s.c.) with melatonin (10 mg/kg b.w., i.p.) for 15 days. Cd alone injection decreased GSH concentrations in the liver and RBC by 35% and 43% compared with those in saline-treatment group, but not in the kidney and whole brain. The activity of GSSG-reductase was significantly decreased in the liver of Cd alone injected rats, while melatonin given in combination with Cd failed to prevent the Cd-induced decreased activity of hepatic GSSG-reductase. However, the hepatic GSH concentration decreased by Cd alone was restored by melatonin treatment, and the melatonin also ameliorated Cd-induced histopathological changes in the liver. Therefore, data indicate that melatonin restores the reduction of hepatic GSH level induced with Cd regardless of GSSG-reductase activity, and suggests that melatonin may ameliorate Cd-induced hepatotoxicity.     

外源性褪黑素对睡眠作用的Meta分析

目的综合评价褪黑素对失眠干预的效果。方法在Cochrane图书馆、Medline、Embase、中国生物医学文献数据库、中国知识资源总库等相关数据库,对1991至2007年的英文相关文献进行检索。纳入的研究应该包括至少6个没有严重致残全身性疾病的成人受试者;随机双盲;包含安慰剂对照的临床试验;包括至少这三个结果指标(睡眠潜伏期、总睡眠时间、睡眠效率)中的一个。使用Revman软件4.2.10进行Meta分析。结果共纳入13个RCT,其方法学质量的Jadad评分≥3分。Meta分析显示:①褪黑素和安慰剂的睡眠潜伏期比较共纳入9个RCT(238例),褪黑素组睡眠潜伏期缩短12.84 min(95%CI 7.84,17.85)(P<0.01)。②褪黑素和安慰剂的总睡眠时间的比较共纳入7个RCT(233例),褪黑素组总睡眠时间延长7.60 min(95%CI-5.49,20.69)(P>0.05)。③褪黑素和安慰剂的睡眠效率的比较共纳入8个RCT(286例),睡眠效率提高5.15%(95%CI 2.47,7.83)(P<0.01)。结论外源性褪黑素干预能提高睡眠质量,对失眠有治疗作用。     

Thermographic observations on rats with experimental neuropathic pain.

Infrared thermographic images were obtained from the plantar hind paws of rats with an experimental nerve injury that produces signs of neuropathic pain. Thermograms confirmed that the experimental neuropathy produces signs resembling those of patients with neuropathic pain. The hind paws on the nerve-damaged side were abnormally hot, abnormally cold, or apparently normal 8-16 days post injury, a variability that is seen clinically in neuropathic pain patients. Abnormally cold hind paws became warm as soon as the injured sciatic nerve was transected, indicating that the underlying vasoconstriction was mediated by neural impulse activity. Xylazine (Rompun), a sympatho-inhibitory alpha 2-adrenoceptor agonist that normally increases cutaneous temperature, caused the hind paw on the control side to warm, as anticipated, while causing paradoxical cooling of abnormally hot hind paws, and even of 'normal temperature' paws on the nerve-injured side. These findings shed light on possible mechanisms underlying abnormal deviations of skin temperature as a symptom of nerve injury. The findings also attest to the usefulness of the experimental animal model of neuropathic pain and of the thermographic method.     

六味地黄丸对OLETF鼠胰腺形态学改变的影响

目的:研究六味地黄丸对自发性2型糖尿病鼠(otsukalong-evanstokushimafattyrats,OLETF鼠)胰腺形态学改变的影响。方法:OLETF鼠40只,随机分为六味地黄丸干预组和对照组,LETO(long-evanstokushimaotsuka)鼠10只作为正常对照组。干预组从8周龄起以六味地黄丸2.4g/(kg·d)灌胃给药,其余两组以等量蒸馏水灌胃。每周监测体重,定期OGTT试验检测血糖,胰腺切片HE染色观察组织学改变。结果:OLETF鼠体重和血糖显著高于LETO鼠。随病程进展,OLETF鼠对照组胰岛早期表现为肥大增生,晚期破坏、纤维化程度明显高于LETO鼠。干预组胰岛结构保存明显好于对照组,且干预组负荷后血糖显著低于对照组。结论:六味地黄丸能有效地保护OLETF鼠胰腺的组织形态结构并改善其糖代谢能力。     

褪黑素对全肝缺血再灌注大鼠肺细胞凋亡的影响及相关机制

目的 探讨褪黑素对全肝缺血再灌注大鼠肺组织细胞凋亡的影响作用及相关机制.方法 30只SD大鼠随机分3组:褪黑素治疗组,缺血再灌注组与假手术对照组.阻断肝门30 min后开放血流,建立大鼠全肝缺血再灌注模型.褪黑素组与缺血再灌注组分别于肝门阻断前15 min和再灌注前10 min静脉注射褪黑素溶液或相同剂量溶剂,于再灌注1 h处死动物.假手术组不阻断肝门,于上述各相应时间点注射溶剂与处死动物.留取肺脏组织,原位末端转移酶(TUNEL)法检测细胞凋亡、PCR法检测Bcl-XL与Bax mRNA表达,考马斯亮兰法检测肺泡灌洗液(BALF)总蛋白含量,同时进行肺组织病理学检查.结果 与缺血再灌注组相比,褪黑素组病理学改变减轻;BALF总蛋白含量、细胞凋亡指数(AI)与Bax mRNA表达显著降低(P＜0.01);而Bcl-XL mRNA表达及Bcl-XL/Bax比值显著增加(P＜0.01).结论 褪黑素可能通过影响Bcl-XL/Bax比值来抑制大鼠全肝缺血再灌注后肺细胞凋亡.     

益寿康乐液对大鼠去势后交配能力及性腺指数的作用

目的:通过中药复方制剂益寿康乐液对大鼠去势后交配能力的实验研究,探讨益寿康乐液与生殖有关变化的关系。方法:实验大鼠按照随机数字表法将54只SD大鼠随机分为7组,每组又分为六七个小组,分别观察其去势后性腺指数,交配能力及阴茎勃起潜伏期的差异。结果:去势大鼠精囊、前列腺指数,去势模型组为52.1±7.5,益寿康乐液3.5g/kg组为67.4±18.6(P<0.01,t=8.03,2.41);提肛肌指数,去势模型组为92.1±18.7,益寿康乐液组为118.1±22.4(P<0.01,t=9.13,2.87),增加雄性大鼠捕捉次数和射精次数。结论:益寿康乐液可明显促进性腺发育,提高交配能力,缩短阴茎勃起潜伏期。     

Effects of melanotropic peptides on fetal adrenal gland.

Adrenal glands from early, mid, and late fetuses of rabbit, guinea pig, and rat, and from newborn animals of each species, were incubated for 1-4 h with and without 0.1 nM-1 microM ACTH, alpha- or beta-melanocyte-stimulating hormone (alpha MSH or beta MSH). The effects of the peptides were measured on production of glucocorticoids, and on incorporation of labeled thymidine or leucine into DNA or protein, respectively. The findings were similar in all three species. ACTH stimulated synthesis of glucocorticoids throughout fetal life. Potency increased progressively, as reflected by declining minimal effective dose and rising maximal response. In early and mid fetus alpha MSH and beta MSH caused a modest glucocorticoid steroidogenic effect. ACTH and alpha MSH stimulated DNA and protein synthesis in the early and mid fetal gland. alpha MSH was more potent than ACTH in these respects, minimal effective dose being generally 10 times less and maximal response 25-200% greater. The effects diminished or disappeared in the late fetal and newborn gland. These data indicate that alpha- and beta MSH possess steroidogenic or growth-promoting properties, or both, for the fetal adrenal gland.     

Effects of inorganic nitrates on thyroid gland activity and morphology in female rats

The present study was undertaken to determine the effects of intake of inorganic nitrates in drinking water on thyroid gland activity and morphology in female rats. During 5 months of treatment, nitrates 50, 150 and 500 mg/L induced a significant dose-dependent decrease in bodyweight gain, compared with the control rats. At the end of the experiment, nitrates 150 and 500 mg/L induced hypertrophy of the thyroid gland, accompanied by an increase in the size of the thyroid follicles and hyposecretion of thyroid hormones T3 (triiodothyronine) and T4 (tetraiodothyronine). We concluded that a high nitrate intake in water influenced thyroid gland activity and morphology and might be considered to be a goitrogenic factor.