人参根总皂甙对热应激小鼠免疫功能保护作用的机制初探

小鼠在45℃高温环境15 min.末梢血T淋巴细胞百分数和淋巴细胞占白细胞百分数均下降.血清皮质酮升高。应激前15 min lP人参根总皂甙(GRS)50、100 mg·kg~(-1)可防止末梢血T淋巴细胞百分数的降低,但不能抑制血清皮质酮的升高。GRS50mg·kg~(-1)ip可防止末梢血中淋巴细胞占白细胞百分数的降低。GRS50 mg·kg~(-1)、利血平0.5 mg·kg~(-1)或水杨酸毒扁豆碱0.3 mg·kg~(-1)ip均可消除热应激对小鼠迟发超敏反应的抑制作用。     

Cytochrome P-45011 beta in rat brain

The presence of cytochrome P-45011 beta in rat brain was studied by immunohistochemistry using polyclonal rabbit antibodies raised against purified bovine adrenocortical P-45011 beta, which is involved in the steroid 11 beta-hydroxylation and glucocorticoid formation. The results showed that cytochrome P-45011 beta immunoreactivity is selectively localized to the tracts of myelinated fibers throughout the brain. The specificity of immunohistochemical stainings with P-45011 beta antibodies was established by control tests including nonimmune rabbit immunoglobulin Gs and P-45011 beta antibodies absorbed with purified antigen. Western immunoblots of homogenates from different brain areas with P-45011 beta antibodies, together with biochemical enzymatic assays for cytochrome P-45011 beta monooxygenase activity in these homogenates, confirmed the selective localization of this enzyme observed with immunohistochemistry. Cytochrome P-45011 beta and 11 beta-hydroxylase activity were detected in a homogenate from the cortical white matter (brain area rich in myelinated fibers) as in that from the rat adrenal, but were not detectable in a homogenate from the cerebral cortex (brain area poor in myelinated fibers). Furthermore, quantitation of the P-45011 beta bands on the immunoblots by the areal density revealed that the cortical white matter contains approximately 1.4 pmol of cytochrome P-45011 beta/mg of tissue protein, the value of which was about one sixth of the corresponding value estimated in the rat adrenal. This relatively high content of cytochrome P-45011 beta was also reflected in a relatively high level of 11 beta-hydroxylase activity measured in a homogenate of this brain area by biochemical enzymatic assays using [4-14C]-11-deoxycorticosterone.(ABSTRACT TRUNCATED AT 250 WORDS)     

损毁下丘脑不同脑区对折断腿骨所致血浆皮质酮变化的影响

清醒sprague-Dawley雄性大鼠64只,以折断胫腓骨造成应激。观察非内侧基底下丘脑脑区损毁对应激前(Bo)、后(Bs)血浆皮质酮变化的影响。以Bs/Bo及Bs-Bo的值衡量应激反应的大小。根据所损毁脑区的部位及范围将动物分为6组:假手术组、室旁核损毁组、室旁核部分损毁组、室旁核少量损毁组、下丘脑前部—视前区损毁组、下丘脑后部损毁组。用统计学方法比较了6组动物的Bs/Bo及Bs-B0值,以及根据4例室旁核完全损毁动物仍保持有应激反应的事实,我们得出结论:(1)在清醒大鼠的损伤性应激反应中,下丘脑室旁核较其他非基底内侧下丘脑区具有较重要的作用。(2)室旁核以外的促肾上腺皮质激素释放因子神经元可能也参与应激反应。     

三种氨基酸对兔血浆皮质酮浓度的影响

侧脑室注射甘氨酸使健康家兔和烧伤家兔血浆皮质酮浓度降低;注射L—谷氨酸和L—天冬氨酸使健康家兔血浆皮质酮浓度升高,但不能使烧伤后升高的血浆皮质酮浓度发生改变。提示这三种氨基酸作为神经递质参与下丘脑—垂体—肾上腺皮质轴的调控。烧伤刺激通过下丘脑引起内分泌紊乱,这种紊乱与L—谷氨酸和L—天冬氨酸失控有关。     

Effect of Tripterygium Vilfordii on Adrenal Cortex in Rat with Adjuvant Arthritis

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Effect of water restrictions on the physiological parameters,psychological behavior and brain c-Fos expression in rat

1 Introduction Exposure to hostile stressors causes a series of coor- dinated responses in the body, such as alterations of neu- roendocrine secretion, immune reaction and behavioral manifestation to maintain homeostasis stability and sur-vival of the organisms. Stressors are divided into two main categories: physical, or systemic, and psychological, or emotional / processive. Each stressor might activate a spe- cific central pathway to induce a special neuroendocrine response, even cause stre…     

不同时辰刺激大鼠的交叉上核对血浆中皮质酮含量的影响

应用拉丁方设计，在不同体重组的大鼠，于不同时辰，对交叉上核采取不同强度的刺激，用放射免疫法测定外周血中皮质酮的含量。其结果显示：各体重组间无显著性差异，不同时辰血浆皮质酮的平均含量各组呈现基本相同的节律性变化，无论何时辰刺激交叉上核使之兴奋，均可显著提高血浆皮质酮的含量。完全损毁交叉上核后７２小时血浆皮质酮含量和正常对照组无显著性差异，且其节律性也没有出现明显变化。     

Corticosterone release in response to repeated, short episodes of neonatal isolation : evidence of sensitization

Repeated isolation of neonatal rats produces persistent changes in physiology and behavior. In Experiment 1, we examined changes in plasma corticosterone (CORT) levels as a possible mechanism for the effects of isolation. Pups that were isolated from their mother and the nest for 1 h per day on postnatal days (PND) 2–9 were compared to control litters of pups that were either nonhandled or handled but not isolated. On PND 2, compared to nonhandled pups, handled pups had elevated CORT levels that returned to baseline levels within 30 to 60 min of return to the home cage. No significant elevation of CORT levels were found in handled pups on PND 9. The CORT levels of isolated pups were over twice those of nonhandled pups on PND 2 and four times those of nonhandled pups on PND 9. In Experiment 2, we investigated whether the increased CORT release in response to isolation on PND 9 was the result of the pups treatment on the previous six days as against an effect of maturation. Plasma CORT levels were measured in rat pups that were either isolated, handled or nonhandled on PNDs 2–8 during the conditions of isolation, handling and nonhandling on PND 9. There were no differences among the groups in basal plasma levels of CORT. Handling on PND 9 did not result in elevated CORT levels in any of the groups. All three groups showed a significant increase in plasma CORT levels after isolation on PND 9. However, the CORT response to isolation of pups previously isolated on PND 2–8 were significantly higher than pups that were either handled or nonhandled on PNDs 2–8. Thus, daily episodes of isolation potentiate the hypothalamic-pituitary-adrenal response to stress.     

Cocaine-induced Increase in Cortical Acetylcholine Release: Interaction with the Hypothalamo—Pituitary—Adrenal Axis

An influence on drug-taking behaviours of the stress-related hypothalamo-pituitary-adrenal (HPA) axis and its final hormonal mediator, corticosterone, has previously been demonstrated. A role for cortically projecting cholinergic neurons in these behaviours can also be proposed. The experiments presented here examine the effect of the drug of abuse cocaine (15 mg/kg) on the release of acetylcholine (ACh) in the cortex of freely moving rats, using the technique of in vivo microdialysis. To assess a possible modulatory influence of the HPA axis via its final hormonal mediator corticosterone, the cocaine-induced effect on cortical ACh release in intact rats was compared to that in adrenalectomized (ADX) rats, which thus lacked their endogenous source of corticosterone, and in ADX rats in which the cocaine-induced corticosterone peak and/or the basal circadian concentrations of serum corticosterone were simulated by replacement treatments. The results reported here demonstrate that cortical ACh release is greatly increased by cocaine in intact rats; ADX prolongs the return to basal levels of cortical ACh, and the chronic replacement of circadian levels of corticosterone normalizes this effect. In contrast, during the plateau period of cocaine-induced increased cortical ACh release, where no effect of ADX is evident, rats with chronic replacement of corticosterone show an attenuated cocaine-induced cortical ACh release, and the acute replacement of the cocaine-induced corticosterone secretion further attenuates this response. These results demonstrate that cocaine stimulates cortically projecting cholinergic neurons, and that the HPA hormone corticosterone modulates this interaction in a complex manner which merits further investigation.