L-精氨酸对热应激大鼠胸腺细胞超微结构的影响

目的 探讨热应激对大鼠胸腺细胞超微结构的影响和L-精氨酸（L-Arg)对大鼠胸腺的保护作用。方法 观察通过灌胃补充不同浓度L-Arg的SD大鼠在常温和不同高温条件下热应激时胸腺细胞的超微结构变化。结果 各组在常温状态下,其胸腺结构基本一致;而在不同温度热应激状态下,各组大鼠胸腺均有不同程度的损伤。补充L-Arg组轻于未补充L-Arg组,低温组轻于高温组,而且胸腺细胞的超微结构变化随热应激后不同时间点而有所不同。结论 不同高温热应激均可造成胸腺结构及其细胞的损伤,温度越高损伤越重,足量的L-Arg对热应激大鼠胸腺有较好的保护作用。     

L-精氨酸对热应激大鼠胸腺和脾脏的影响

目的　探讨热应激对大鼠体重、胸腺指数、脾脏指数、呼吸、肛温的影响和补充L -精氨酸 (L -Arg)对热应激大鼠的保护作用。方法　采用三因素析因设计模型 ,将青春期SD雄性大鼠随机分为A、B、C3组 ,通过灌胃补充不同浓度的L -Arg ,观察在常温和不同高温条件下热应激时大鼠胸腺指数等相关指标的变化。 结果　在常温状态下 ,补充L -Arg组大鼠体重、胸腺指数、脾脏指数增加高于未补充组 (P <0 0 5 ) ,呼吸和肛温变化无显著性差异 (P >0 0 5 ) ;而在不同温度热应激状态下 ,各组大鼠体重、胸腺重量、脾脏重量均减轻 ,未补充L -Arg组低于补充L -Arg组 ,并且胸腺和脾脏重量减轻具有温度和热应激后时间依赖性 ;呼吸和肛温在一定范围内随温度的升高而增快和升高 ,但补充与未补充L -Arg组之间无显著性差异 (P >0 0 5 )。结论　补充适量的L -Arg可使大鼠在常温下体重、胸腺指数和脾脏指数有所增加 ,在热应激条件下 ,对防止胸腺和脾脏萎缩具有较好的作用     

L-精氨酸对热应激大鼠血清皮质醇变化的影响

目的 观察补充L-精氨酸对热应激大鼠血清皮质醇含量的变化，探讨L-精氨酸对热应激胸腺具有保护作用的可能机制。方法 青春期雄性SD大鼠，随机分为对照组、L-精氨酸灌胃组、维生素E饲料组，观察各组常温和41℃应激1，2h后及热应激后0，4，8h3个时间点的血清皮质醇的变化。结果 (1)高温应激后各组血清皮质醇含量均明显升高，其中热应激后4h升到最高，补充L-精氨酸组明显低于未补充组；(2)补充适量L-精氨酸可减轻热应激大鼠胸腺和脾脏的急性萎缩。结论 适量的L-精氨酸能够抑制热应激引起的血清皮质醇含量的显著升高及减小胸腺和脾脏指数，适量的L-精氨酸对热应激大鼠胸腺具有明显的保护作用，可以增强机体的免疫力。     

高温下补充精氨酸对小鼠体重,胸腺和脾脏重量的影响

初步观察高温下补充精氨酸对小鼠体重、胸腺和脾重量的影响。实验结果显示,短时间的热应激对体重影响不大,对胸腺和脾脏可造成急性萎缩;长时间受热(热习服9夭)则对体重和脾脏影响较大,对胸腺绝对重量也有明显影响。但补充适量精氨酸后,在热应激和热习服过程中,补充组小鼠体重生长率明显高于未补充组;胸腺重量在热习服过程中,补充组明显高于未补充组,脾脏重量4组间无明显差异。提示高温下补充适量精氨酸对保证体重正常生长,防止免疫器官急性萎缩具有较好作用。     

L-精氨酸对缓解呕吐毒素刺激大鼠损伤作用的研究

目的探讨补充精氨酸对低剂量呕吐毒素应激损伤的保护作用。方法 30只雄性SD大鼠随机分为空白对照组,1.0mg/kg bw呕吐毒素应激组和应激补充350 mg/kg bw精氨酸组。以观察精氨酸对呕吐毒素应激大鼠摄食与生长情况、脏器指数和血液各项指标的影响。结果在21d的试验期内,精氨酸能改善呕吐毒素应激造成的日增重下降,胸腺萎缩以及血清谷草转氨酶和丙二醛浓度升高的状态,达显著水平。结论精氨酸具有的营养及免疫调节双重作用,能在一定程度上缓解呕吐毒素应激损伤。     

精氨酸对热应激小鼠免疫功能的影响

目的　探讨精氨酸对热应激小鼠免疫功能的影响及可能机制。方法　将雄性小鼠随机分为给水组和给不同浓度精氨酸组 ,各组小鼠又分为常温组和热应激组 ,给药 1 4天后热应激组入 41℃± 0 5℃高温仓 2h后分别在 0 ,2 ,4,8,1 2 ,2 4h处死 ,测量各组小鼠胸腺指数、脾脏指数、淋巴细胞增殖活性、IL 2浓度及其受体的表达等指标的变化。结果　热应激后小鼠的各项免疫指标均有显著下降 ,其中在 2～ 8h降到最低 ;常温组小鼠补充适量精氨酸后淋巴细胞增殖活性、IL 2的浓度及IL 2R的表达均有显著性上升 ,而热应激后 3指标均显著降低 ,其中精氨酸浓度为 1 5mg/ g·体重时各指标的降低程度最少。结论　热应激 2～ 8h后 ,小鼠免疫功能受到的损伤最大 ;适量补充L 精氨酸可以对热应激损伤小鼠的免疫功能起到保护作用 ,补充 1 5mg/g·体重精氨酸能够最大限度的减少热应激对小鼠免疫功能的损伤。     

高温下补充精氨酸对小鼠血清氨基酸代谢的影响

观察了高温下补充精氨酸对小鼠血清氨基酸代谢的影响，结果显示，热应激时，补充精氨酸后，２１种游离氨基酸（ＦＡＡ）中有１８种ＦＡＡ有不同程度的下降，其中谷氨酰胺和甘氨酸下降显著（Ｐ＜０．０５）；在热习服期间补充精氨酸后，精氨酸增加１０．４％，组氨酸增加２３．６％，丝氨酸增加１８．８％，其它ＦＡＡ变化不大。血清尿素氮（ＳＵＮ）含量热应激时显著高于热习服（Ｐ＜０．０５），而补充精氨酸的两组均不同程度低于相应的对照组。提示，高温下补充精氨酸有减少热应激时蛋白质分解代谢的作用，防止氮的丢失，促进氮的储留。     

高温下精氨酸对一氧化氮和细胞增殖的影响

目的　探讨精氨酸对高温下血清一氧化氮 (NO)含量和淋巴细胞增殖活性的影响。方法　BALB/C小鼠 ,随机分为对照组、精氨酸补充组 [0 5 ,1 5 ,2 5 ,3 5 g/ (kg .bw) ],每组 35只 ,其中 5只为常温对照。 14d后 ,除常温对照外均放入 (41± 0 5 )℃动物高温仓热应激 12 0min ,结束后 0 ,2 ,4 ,8,12 ,2 4h共 6个时相分别眼眶采血 ,常温组在灌胃第 3,7,11,14d时采尾血。观察指标测定血清NO浓度、淋巴细胞增殖活性。结果　 (1)在常温下补充精氨酸后第 3d各实验组血清NO含量最高 ,第 7d后基本稳定 ,补充组各个时间点都高于未补充组 ,其中补充精氨酸 0 5 g/(kg .bw)组各个时间点明显高于其他补充组。 (2 )热应激后补充 0 5和 1 5 g/ (kg .bw)及未补充组血清NO浓度有先下降 (0～ 2h最低 )而后上升 ,4～ 8h基本稳定。而补充高浓度精氨酸的两组〔2 5和 3 5 g/ (kg .bw)〕热应激后持续上升 ,而且在 12h内 ,血清NO含量明显高于低浓度的两组和对照组。 (3)在热应激下补充精氨酸的各组刀豆蛋白(ConA)刺激指数高于对照组 ,补充精氨酸的各组 ,以 1 5 g/ (kg .bw)时ConA刺激指数达到最大。热应激后 ,小鼠淋巴细胞增殖活性受到抑制 ,其中 4～ 8h最低。结论　高温环境应激下小鼠对精氨酸的需要量增加 ,而血清NO含量的变     

热应激对胸腺的损伤及精氨酸的保护作用

机体在热应激情况下，胸腺会发生一系列形态学和生理生化方面的改变，造成机体免疫功能障碍。单个氨基酸的药理学作用及其器官特异性作用的研究也是目前营养学研究的前沿课题之一。本综述了近年来有关热应激情况下胸腺、精氨酸的变化以及精氨酸对胸腺保护作用的可能机制的研究现状。     

补充L-精氨酸对热应激小鼠血清NO、NOS和T细胞亚群的影响

目的:通过补充不同剂量的L-精氨酸(L-Arg),探讨热应激后L-Arg对免疫功能的影响。方法:雄性成年NIH小鼠随机分为三组(A组:灌蒸馏水;B组:给L-Arg1.5mg/gbw;C组:给L-Arg2.5mg/gbw),每组各有6只为常温对照(不经过热应激处理),另36只为热应激后分6个时间点取样。给L-Arg14d后放入动物高温仓进行热应激,干球温度(41±0.5)℃,湿球温度(33.5±0.5)℃,相对湿度65%处理120min。结束后分别取样检测血清NO含量、NOS活性及胸腺T细胞亚群的变化。结果:常温下补充L-Arg组小鼠血清NO浓度、NOS活性及CD3+、CD4+细胞百分率、CD4+/CD8+比值均高于未补充组;而热应激后小鼠血清NO浓度、NOS活性、CD3+、CD4+细胞百分率、CD4+/CD8+比值补充组均明显高于未补充组,但CD8+细胞百分率则是补充组低于未补充组,而补充L-Arg的两组间无显著性差异。结论:热应激后4~8h小鼠免疫功能受损最严重。补充适量L-Arg可促进热应激小鼠NOS活性,提高体内NO水平,增加T细胞亚群数量及CD4+/CD8+比值。     

锌对热应激大鼠垂体POMC mRNA表达的影响

目的：通过锌对热应激大鼠垂体阿黑皮素原（ＰＯＭＣ）ｍＲＮＡ表达的影响研究，探讨锌对热应激大鼠的保护机理。方法：２０只ＳＤ雄性大鼠随机等分４组，即高锌高温暴露组（Ａ组）、中锌高温暴露组（Ｂ组）、低锌高温暴露组（Ｃ组）和正常锌室温对照组（Ｄ组）。在ＡＩＮ－９３Ｍ饲料配方基础上，以碳酸锌为锌源，配制成高锌、中锌、低锌和正常锌饲料，每公斤饲料锌含量测定值分别为９２．２ｍｇ、４５．６１ｍｇ、２１．７０ｍｇ和４５．６１ｍｇ。４组大鼠在室温下饲以相应饲料１４天后，将Ａ、Ｂ、Ｃ组大鼠置于高温室（Ｔｄｂ４０℃，Ｔｗｂ３０．８℃）中连续暴露３小时。用Ｎｏｒｔｈｅｒｎｂｌｏｔ杂交分析法（探针为地高锌标记的ＰＯＭＣｃＲＮＡ），观察垂体ＰＯＭＣｍＲＮＡ表达水平。结果：（１）高温应激可使大鼠垂体ＰＯＭＣｍＲＮＡ表达水平增高；（２）高锌摄入可使热应激大鼠垂体ＰＯＭ－ＣｍＲＮＡ表达水平升高，而低锌摄入则相反。结论：锌对热应激大鼠垂体ＰＯＭＣ基因有调控作用，作用环节可能在转录水平上     

Metabolism of L-ascorbic acid in rats under in vivo administration of mercury: effect of L-ascorbic acid supplementation.

1.Rats toxicated with mercury showed drastic fall in growth rate and supplementation of L-ascorbic acid to these rats could not reverse this effect. The contents of L-ascorbic acid and of D-glucuronic acid in the urine of the toxicated animals were decreased which could be counteracted by subsequent L-ascorbic acid supplementation. 2. The concentration of L-ascorbic acid in the liver tissues of mercury toxicated rats was decreased markedly and administration of L-ascorbic acid to this group could raise the tissue reserve considerably. 3. Severe damages of the normal histological pattern of the kidney tissues of rats viz. cellular and glomerular degeneration were observed under mercury toxicity. 4. In the liver tissues of the mercury toxicated rats, the rate of L-ascorbic acid synthesis was reduced along with increased catabolism of L-ascorbic acid. Subsequent supplementation of L-ascorbic acid to these toxicated rats was, however, found to be effective in reversing these alterations almost to the basal level.     

Dietary iron supplements may affect stress adaptation and aggravate stress hyperglycemia in a rat model of psychological stress

ObjectiveIron supplementation is believed to decrease the risk of iron-deficiency anemia or low birth weight. In modern society, a majority of people are in a continual state of stress. Stress-induced hyperglycemia, known as transient hyperglycemia, may be a risk factor causing diabetes. To understand the role of iron in people under stress, it is necessary to evaluate the effect of iron supplementation on glucose or stress hyperglycemia.MethodsThe effect of a diet containing non-heme iron (80 or 320 mg/kg) on Sprague-Dawley rats and those under psychological stress was evaluated.ResultsCompared with control rats, a high-iron diet (320 mg/kg) increased blood glucose transiently in normal rats but induced hyperglycemia persistently in stressed rats throughout the experiment. Iron supplements further aggravated iron deposition and oxidative stress injury to the liver induced by the stress exposure. Glucose-related stress hormones were also affected by iron supplementation in stressed rats.ConclusionOxidative stress may be one of the main reasons for insulin resistance. Moreover, changes in stress hormones indicate that high-iron supplements may affect stress adaptation. Both are primary reasons for the hyperglycemia induced by iron supplementation in stressed rats. Gaining an insight into the mechanisms and correlations of these changes may be beneficial to human health and is important for the prevention of pathologic glycemia-related diseases.     

A comparison between tocopherol and tocotrienol effects on gastric parameters in rats exposed to stress

Rats exposed to stress developed various changes in the gastrointestinal tract and hormones. The present study was designed to compare the impact of tocopherol and tocotrienol on changes that influence gastric and hormonal parameters important in maintaining gastric mucosal integrity in rats exposed to restrain stress. These include gastric acidity, gastric tissue content of parameters such as malondialdehyde, prostaglandin (PGE(2)), serum levels of gastrin and glucagon-like peptide-1 (GLP-1). Sixty male Sprague-Dawley rats (200-250 g) were randomly divided into three equal sized groups, a control group which received a normal rat diet (RC) and two treatment groups each receiving a vitamin deficient diet with oral supplementation of either tocopherol (TF) or tocotrienol (TT) at 60 mg/kg body weight. Blood samples were taken from half the number of rats (non-stressed group) after a treatment period of 28 days before they were killed. The remaining half was subjected to experimental restraint-stress, at 2 hours daily for 4 consecutive days (stressed groups), on the fourth day, blood samples were taken and the rats killed. The findings showed that the gastric acid concentration and serum gastrin level in stressed rats were significantly (P<0.05) reduced compared to the non-stressed rats in the control and TF groups. However, the gastric acidity and gastrin levels in the TT group were comparable in stressed and non-stressed rats. These findings suggest that tocotrienol is able to preserve the gastric acidity and serum gastrin level which are usually altered in stressed conditions. The PGE(2) content and the plasma GLP-1 level were, however, comparable in all stressed and non-stressed groups indicating that these parameters were not altered in stress and that supplementation with TF or TT had no effect on the gastric PGE2 content or the GLP-1 level. The malondialdehyde, an indicator of lipid peroxidation was higher from gastric tissues in the stressed groups compared to the non-stressed groups. These findings implicated that free radicals may play a role in the development of gastric injury in stress and supplementation with either TF or TT was able to reduce the lipid peroxidation levels compared to the control rats. We conclude that both tocopherol and tocotrienol are comparable in their gastro-protective ability against damage by free radicals generated in stress conditions, but only tocotrienol has the ability to block the stress-induced changes in the gastric acidity and gastrin level.     

L-精氨酸对脂多糖诱导免疫应激大鼠血清生化指标和肝脏的影响

目的探讨外源性精氨酸对动物机体在免疫应激状态下的保护作用。方法以腹腔注射大肠杆菌内毒素(LPS)的方式复制免疫应激动物模型。将SD大鼠32只随机分成4组:正常对照组;生理盐水配对组;免疫应激组(LPS组);L-精氨酸+LPS组(L-Arg+LPS组)。结果腹腔注射LPS 4mg/kg.bw,可以使大鼠产生免疫应激。L-Arg+LPS组大鼠血清中Arg浓度非常显著高于其余各组(P<0.01),与对照组相比,L-Arg+LPS组和LPS组血液中谷丙转氨酶(ALT)活性非常显著(P<0.01),L-Arg+LPS组和LPS组血清中总的一氧化氮合酶(T-NOS)活性显著增高(P<0.05),NO浓度和诱导型一氧化氮合酶(iNOS)活性达到非常显著(P<0.01)。免疫组化显示:L-Arg+LPS组的大鼠肝组织内皮型一氧化氮合酶(eNOS)表达呈强阳性,其他组未见eNOS表达;而LPS组肝组织iNOS表达呈中度阳性,L-Arg+LPS组iNOS表达呈痕迹反应,对照组和配对组均无iNOS表达。L-Arg+LPS组和LPS组分别与对照组相比,肝细胞凋亡极显著增多(P<0.01),但L-Arg+LPS组细胞凋亡数显著低于LPS组(P<0.05),对照组和配对组之间差异不显著。结论对免疫应激大鼠添加精氨酸后,可抑制由iNOS催化生成NO而导致的肝脏组织炎症及肝细胞凋亡,缓减免疫应激对大鼠机体的损害作用。     

谷氨酰胺对应激大鼠学习记忆的影响及其机制的研究

目的　观察谷氨酰胺 (Gln)对应激大鼠学习记忆的影响 ,并对其机制进行探讨。方法　Wistar大鼠 30只 ,随机分为三组 : 组为对照组 , 组为应激组 , 组为应激 +Gln组。其中 、 组饲以普通饲料 , 组给予补充 2 % Gln的饲料。以光电刺激作为应激条件 ,在 组和 组大鼠建立应激模型 ,用 Y-迷宫法对大鼠的学习记忆能力进行测定 ,并分别用放射性配基结合法、放射免疫法、荧光分光光度计法测定大鼠小脑中 γ-氨基丁酸 (GABA)受体、脑中胆囊收缩素 (CCK)、还原型谷胱甘肽 (GSH)的含量。结果　与 组相比 , 组大鼠在 Y-迷宫实验中的逃避时间延长 ,而 组与 组则无显著差异 ; 组大鼠小脑中 GABA受体水平、CCK含量均升高 ,而 GSH含量则降低 ,给予 Gln后可从一定程度上逆转上述改变。结论　心理应激可影响大鼠的学习记忆能力 ,而 Gln则有一定的改善作用 ,其机制可能是通过减轻应激所致的脑中GABA受体水平、CCK和 GSH含量的异常改变而发挥此作用