The Positive Impact of Vitamin D on Glucocorticoid-Dependent Skeletal Muscle Atrophy.

(1) The study aimed to investigate whether vitamin D supplementation would positively affect rats with glucocorticoids-induced muscle atrophy as measured by skeletal muscle mass in two experimental conditions: chronic dexamethasone (DEX) administration and a model of the chronic stress response. (2) The study lasted 28 consecutive days and was performed on 45 male Wistar rats randomly divided into six groups. These included two groups treated by abdominal injection of DEX at a dose of 2 mg/kg/day supplemented with vegetable oil (DEX PL; = 7) or with vitamin D 600 IU/kg/day (DEX SUP; = 8), respectively, and a control group treated with an abdominal injection of saline (CON; = 6).

The Electrical Stimulation of the Bed Nucleus of the Stria Terminalis Causes Oxidative Stress in Skeletal Muscle of Rats.

Recent studies indicate that activation of hypothalamus-pituitary-adrenocortical axis (HPA) plays the crucial role in stress response, while several lines of evidence mark the bed nucleus of the stria terminalis (BST) as a major mediator of the HPA axis responses to stress. The purpose of this study was to investigate the influence of the corticosterone flux induced by the electrical stimulation of BST on markers of free radical damage of lipids and proteins and antioxidant enzyme activity in skeletal muscle of rats. The male Wistar rats were used and assigned to one of three groups: sham-operated (SHM; = 6), two-week (ST2; = 6), and four-week stimulated (ST4; = 5) groups.

The effects of ryanodine receptor (RYR1) mutation on natural killer cell cytotoxicity, plasma cytokines and stress hormones during acute intermittent exercise in pigs.

Stress susceptibility has been mapped to a single recessive gene, the ryanodine receptor 1 (RYR1) gene or halothane (Hal) gene. Homozygous (Hal(nn)), mutated pigs are sensitive to halothane and susceptible to Porcine Stress Syndrome (PSS). Previous studies have shown that stress-susceptible RYR1 gene mutated homozygotes in response to restraint stress showed an increase in natural killer cell cytotoxicity (NKCC) accompanied by more pronounced stress-related hormone and anti-inflammatory cytokine changes.

The effects of ryanodine receptor 1 (RYR1) mutation on plasma cytokines and catecholamines during prolonged restraint in pigs.

In the current study, plasma cytokines, including interleukin (IL) 1, IL-2, IL-6, IL-10, IL-12, interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) and catecholamines (adrenaline and noradrenaline) were evaluated during 4h restraint and recovery phase in 60 male pigs. Blood samples were collected from three groups of pigs representing different RYR1 genotypes, namely NN homozygotes (wild-type), Nn heterozygous and nn homozygous (mutant). The 4h restraint evoked an increase in plasma cytokine concentrations in each of the RYR1 genotype groups.

Natural killer cell cytotoxicity, cytokine and neuroendocrine responses to opioid receptor blockade during prolonged restraint in pigs.

This study evaluated porcine natural killer cell cytotoxicity (NKCC), plasma cytokines including interleukin (IL) 1β, IL-6, IL-10, IL-12 and tumor necrosis factor-α and plasma stress-related hormones including prolactin (PRL), growth hormone (GH), β-endorphin (BEND), ACTH and cortisol (COR) during a 4h restraint and recovery phase after saline or naloxone (1mg/kg BW) administration. The restraint preceded with saline altered NKCC and IL-12 concentration (an early from 15 to 60 min increase followed by a decrease) and increased other measured cytokines and hormones concentrations. Naloxone pretreatment blocked the suppressive effects of the restraint on NKCC and IL-12 and altered IL-10, IL-6, TNF-α, PRL and ACTH concentrations.