Clinical reports suggest close interactions between stressors, particularly those of long duration, and liver diseases, such as hepatic inflammation, that is proposed to occur via reactive oxygen species. In the present study we have used 21-day social isolation of male Wistar rats as a model of chronic stress to investigate protein expression/activity of liver antioxidant enzymes: superoxide dismutases (SODs), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GLR), and protein expression of their upstream regulators: glucocorticoid receptor (GR) and nuclear factor kappa B (NFkB). We have also characterized these parameters in either naive or chronically stressed animals that were challenged by 30-min acute immobilization. We found that chronic isolation caused decrease in serum corticosterone (CORT) and blood glucose (GLU), increase in NFkB signaling, and disproportion between CuZnSOD, peroxidases (CAT, GPx) and GLR, thus promoting H2O2 accumulation and prooxidative state in liver. The overall results suggested that chronic stress exaggerated responsiveness to subsequent stressor at the level of CORT and GLU, and potentiated GLR response, but compromised the restoration of oxido-reductive balance due to irreversible alterations in MnSOD and GPx., J. Djordjevic ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Chronic stress is a crucial public issue that occurs when a person
is repetitively stimulated by various stressors. Previous
researches have reported that chronic stress induces
spermatogenesis dysfunction in the reproductive system, but its
molecular mechanisms remain unclear. The nectin protein family,
including nectin-1 to nectin-4, is Ca2+-independent
immunoglobulin-like cell adhesion molecules, that are widely
expressed in the hippocampus, testicular tissue, epithelial cells
and other sites. Nectin-3 contributes to the sperm development
at the late stage, and the abnormal expression of nectin-3
impairs spermatogenesis. Some recent studies have
demonstrated that stress induces a decrease in nectin-3
expression in the hippocampus via corticotropin-releasing
hormone (CRH) to corticotropin-releasing hormone receptor 1
(CRHR1) pathway. Here, we tested whether chronic stress also
caused a reduction in nectin-3 expression in the testis. We
established a chronic social defeat stress paradigm, which
provides naturalistic and complex chronic stress in male C57BL/6
mice. After 25 days of chronic social defeat stress, the mice
showed weight loss, thymic atrophy and some other typical
symptoms of chronic stress (e.g. anxiety-like behavior and social
avoidance behavior). We found gonad atrophy, testicular
histological structure changes and semen quality reductions in
the stressed mice. The stressed male mice significantly spent
more time to impregnate the female mice than the control male
mice. Moreover, nectin-3 protein levels in stressed mice were
significantly decreased in the testes compared with those in
control mice. In addition, we found that the CRHR1 expression
level was increased in the testes of stressed mice. Therefore, we
demonstrated a decreased level of nectin-3 expression and
an increase in CRHR1 expression in the testis after exposure to
chronic stress, which may provide a potential therapeutic target
for the spermatogenesis dysfunction induced by chronic stress.
Stress serves as a risk factor in the etiology of hypertension. The present study was designed to decipher the effect and mechanism of chronic stress on the progression of pressure overload-induced cardiac dysfunction. We used abdominal aortic constriction (AAC) to induce pressure overload with or without chronic restraint stress to establish the animal models. Echocardiographic analysis showed pressure overload-induced cardiac dysfunction was worsened by chronic stress. Compared with the AAC rats, there is a significant increase in cardiac hypertrophy, injury, apoptosis and fibrosis of the AAC + stress rats. Furthermore, we found the secretion of norepinephrine (NE) increased after the AAC operation, while the level of NE was higher in the AAC + stress group. Cardiomyocytes and cardiac fibroblasts isolated from neonatal rats were cultured and separately treated with 1, 10, 100 μM NE. The higher concentration NE induced more cardiomyocytes hypertrophy and apoptosis, cardiac fibroblasts proliferation and collagen expression. These results revealed that high level of NE-induced cardiomyocytes hypertrophy and apoptosis, cardiac fibroblasts proliferation and collagen expression further contributes to the effect of chronic stress on acceleration of pressure overloadinduced cardiac dysfunction., W. Liu, X. Wang, Z. Mei, J. Gong, X. Gao, Y. Zhao, J. Ma, F. Xie, L. Qian., and Obsahuje bibliografii