Effect of Jiawei Sini Decoction on glucocorticoid receptor in thymocytes of chronic psychological stress rats

AIM: To observe the effect of Jiawei Sini Decoction (JWSND) on glucocorticoid receptor (GCR) in thymocytes of chronic psychological stress rats. METHODS: The rats were randomly divided into 4 groups, control group (C), model group (M), group treated by JWSND C₁, group treated by ginsenosides C₂. The number of thymocyte GCR sites and the GCR nuclear thanslocation rate were detected by radioimmunoassay. RESULTS: Compared with the control group, in the model group, the thymocyte weight index lowered significantly ( P<0.05 ), and the GCR nuclear thanslocation rate was increased significantly ( P<0.01 ), but the number of thymocyte GCR sites was unchanged. Compared with the model group, thymus gland weight indexes of C₁ and C₂ were increased significantly ( P<0.05 ), while the GCR nuclear thanslocation rate lowered significantly ( P<0.01 ). Moreover, no significant difference was found in all indexes between C₁ and control group. CONCLUSION: The inhibitory effect of glucocorticoid on the thymus could be significantly reversed by JWSND via suppressing the thanslocation of GCR from cytoplasm to nucleus in chronic psychological stress rats.     

Stress: An inevitable component of animal translocation

As the number and diversity of animal species meriting conservation intervention increases, improving the success of translocation efforts is vital and understanding the role of physiological stress in translocation failure is essential. Though the short-term acutestress response is critical for survival in the wild, chronic stress results in pathology and occurs when the physiological stress response system is pushed beyond the normal capacity and becomes dysregulated. As this review discusses, translocation may inevitably lead to a state of chronic stress; however, this translocation-induced stress does not doom an animal to post-release failure or preclude translocation as a conservation tool. Rather, because chronic stress in translocated animals may actually be the norm rather than the exception, “stress” can be considered a predictable factor to incorporate into translocation planning. In terms of translocation failure, we argue that the role of stress is an indirect one. Translocation-induced chronic stress increases the overall vulnerability of the individuals and, as a result, decreases the probability that the population will become self-sustaining. In this review, we further propose techniques to potentially decrease the total number and magnitude of stressor exposures throughout the translocation procedure in order to diminish the incidence of chronic stress-related pathology. Aspects of the translocation activities, such as capture techniques and care procedures during captivity, can be adjusted to accomplish this. Though stress may be an inevitable component of translocation, reducing the impact and time course of chronic stress on the physiology and behavior of translocated animals will increase the likelihood of translocation success as measured by the formation of a new, self-sustaining population     

High urinary corticoid/creatinine ratios in cats with hyperthyroidism

Measurement of the urinary corticoid : creatinine (C : C) ratio provides an assessment of cortisol secretion over a period of time. Therefore, this test is a very sensitive measure of adrenocortical function. The stress of the diagnostic procedure and nonadrenal disease may increase the urinary C : C ratio. In addition, diseases such as hyperthyroidism may influence the metabolic clearance of cortisol. To evaluate the effect of thyroid hormone excess, urinary C : C ratios were measured in 32 cats with hyperthyroidism and 45 healthy household cats. In 7 cats, urinary C : C ratios were measured both before and after treatment for hyperthyroidism. With data from the healthy cats, the reference range for the urinary C : C ratio was determined to be 8.0 to 42.0 X 10(-6). The urinary C : C ratios in the cats with hyperthyroidism (median, 37.5 x 10(-6); range, 5.9-169.5 x 10(-6)) were significantly (P = .001) higher than those in the healthy cats (median, 16 x 10(-6); range, 4.8-52.5 x 10(-6)). In 15 cats with hyperthyroidism, the urinary C : C ratios exceeded the upper limit of the reference range. Treatment for hyperthyroidism led to a marked decrease in urinary C : C ratios. The results of this study demonstrate that the urinary C : C ratio may be abnormally high in cats with hyperthyroidism, probably because of increased metabolic clearance of cortisol and activation of the pituitary-adrenocortical axis by disease. Although the clinical features of hyperthyroidism and hyperadrenocorticism in cats are different, hyperthyroidism should be ruled out when cats are suspected of hyperadrenocorticism on the basis of abnormally high urinary C : C ratios.     

Na(+), K(+)-ATPase content in skeletal muscle of dogs with pituitary-dependent hyperadrenocorticism

Several hormones regulate Na⁺, K⁺-ATPase content in the muscle cell membrane, which is essential for maintaining muscle cell excitability. Chronic glucocorticoid excess is associated with muscle weakness and reduced endurance. We hypothesized that chronic glucocorticoid excess affects Na⁺, K⁺-ATPase content in canine skeletal muscle, and contributes to reduced endurance and muscle weakness associated with pituitary-dependent hyperadrenocorticism (PDH) in dogs. Therefore, Na⁺, K⁺-ATPase content in skeletal muscle was evaluated before and after hypophysectomy and hormone replacement (cortisone and l-thyroxin) in dogs with PDH (n = 13), and in healthy controls (n = 6). In addition, baseline and exercise-induced changes in plasma electrolyte concentrations and acid–base balance were evaluated before and after hypophysectomy in dogs with PDH. Na⁺, K⁺-ATPase content of gluteal muscle in dogs with PDH was significantly lower than in control dogs (201 ± 13 pmol/g versus 260 ± 8 pmol/g wet weight; P < 0.01). Similar differences were found in palatine muscle. After hypophysectomy and on hormone replacement, Na⁺, K⁺-ATPase was increased (234 ± 7 pmol/g wet weight). Both plasma pH and base excess in dogs with PDH (7.44 ± 0.01; 1.7 ± 0.6 mmol/l, respectively) were significantly higher (P < 0.05) than after hypophysectomy and hormone replacement (7.41 ± 0.01; −0.2 ± 0.4 mmol/l, respectively). Exercise induced respiratory alkalosis, but did not result in hyperkalemia in dogs with PDH. In conclusion, chronic glucocorticoid excess in dogs with PDH is associated with decreased Na⁺, K⁺-ATPase content in skeletal muscle. This may contribute to reduce endurance in canine PDH, although dogs with PDH did not exhibit exercise-induced hyperkalemia. Na⁺, K⁺-ATPase content normalized to values statistically not different from healthy controls after hypophysectomy and hormone replacement.     

Infection, immunity and the neuroendocrine response

The Central Nervous (CNS) and Immune Systems (IS) are the two major adaptive systems which respond rapidly to numerous challenges that are able to compromise health. The defensive response strictly linking innate to acquired immunity, works continuously to limit pathogen invasion and damage. The efficiency of the innate response is crucial for survival and for an optimum priming of acquired immunity. During infection, the immune response is modulated by an integrated neuro-immune network which potentiates innate immunity, controls potential harmful effects and also addresses metabolic and nutritional modifications supporting immune function. In the last decade much knowledge has been gained on the molecular signals that orchestrate this integrated adaptive response, with focus on the systemic mediators which have a crucial role in driving and controlling an efficient protective response. These mediators are also able to signal alterations and control pathway dysfunctions which may be involved in the persistence and/or overexpression of inflammation that may lead to tissue damage and to a negative metabolic impact, causing retarded growth.This review aims to describe some important signalling pathways which drive bidirectional communication between the Immune and Nervous Systems during infection. Particular emphasis is placed on pro-inflammatory cytokines, immunomodulator hormones such as Glucocorticoids (GCs), Growth hormone (GH), Insulin-like Growth Factor-1 (IGF-1), and Leptin, as well as nutritional factors such as Zinc (Zn).Finally, the review includes up-to-date information on this neuroimmune cross-talk in domestic animals. Data in domestic animal species are still limited, but there are several exciting areas of research, like the potential interaction pathways between mediators (i.e. cytokine-HPA regulation, IL-6-GCS-Zn, cytokines-GH/IGF-1, IL-6-GH-Leptin and thymus activity) that are or could be promising topics of future research in veterinary medicine.     

Effects of glucocorticoid on miRNA-155 expression in CD4+T cells of asthmatic mice

AIM:To investigate the effects of glucocorticoid on the regulation of microRNA-155 (miRNA-155) expression in the CD4⁺ T cells of asthmatic mice. METHODS:The ovalbumin (OVA)-induced asthma mouse model was established and the mice were treated with glucocorticoid. The effects of glucocorticoid on the pulmpnary histopathological changes, the expression of miRNA-155 in the lung tissues and CD4⁺T cells, and the levels of cytokines in the bronchoal-veolar lavage fluid (BALF) were evaluated. RESULTS:The results of RT-qPCR showed that the expressions of miRNA-155 in the lung tissues and CD4⁺T cells from the spleen of asthmatic mice were significantly increased, and the level of miRNA-155 in the CD4⁺T cells was significantly increased with the increase in the allergen exposure time (P<0.01). HE and PAS staining showed that OVA significantly increased inflammatory cell infiltration as compared with control group, and the peribronchial and perivascular inflammation and mucus secretion of proliferative goblet cells were significantly reduced after glucocorticoid treatment. Glucocorticoid treatment inhibited the increase in the proportion of CD4⁺ CD8^- cells in the spleen and decreased the accumulation of CD4⁺ T cells in the lung tissues of asthmatic mice (P<0.01). After glucocorticoid treatment, the levels of interleukin-4 (IL-4), IL-5 and IL-13 in BALF were decreased, while the level of interferon-γ was increased significantly (P<0.01). CONCLUSION:Glucocorticoid reduces the accumulation of CD4⁺ T cells and inhibits the expression of miRNA-155 in the lung tissues and spleen CD4⁺ T cells of asthmatic mice.