Increased systemic low-grade inflammation in high altitude native rats mediated by adrenergic receptors.

OBJECTIVE: To compare the serum levels of inflammatory mediators in high altitude (HA) native rats, and to search for the possible underlying mechanism(s). METHODS: The study was carried out between January and April 2013. Fifty male rats from the same genetic pool were bred at either a HA or low altitude (LA) area. The study was carried out in 2 stages. In the first stage, serum levels of inflammatory markers, adhesive molecules, lipid profiles, catecholamines, magnesium (Mg+2), and lipid peroxidation were compared between theses 2 groups. In the second stages, inflammatory response and lipid peroxidation were analyzed in HA native rats after treatment with either alpha (Prazosin) or beta (propranolol) adrenergic blockage. RESULTS: The HA native rats showed significant increases in the serum levels of inflammatory cytokines, lipid profiles, as well as a significant increase in the urinary norepinephrine with a concomitant decrease in the serum levels of Mg+2 and increased lipid peroxidation. Blockage of the beta and alpha adrenergic receptors of the HA rats caused partial or complete decreases in both inflammatory and oxidative stress mediators. CONCLUSION: Living under HA conditions results in an increased systemic inflammatory reaction; an effect that is mediated through the sympathetic nervous system mainly via alpha-adrenergic receptors and could be attributed to low Mg+2 levels.

Resveratrol reverses cadmium chloride-induced testicular damage and subfertility by downregulating p53 and Bax and upregulating gonadotropins and Bcl-2 gene expression.

This study was performed to investigate the protective and therapeutic effects of resveratrol (RES) against CdCl2-induced toxicity in rat testes. Seven experimental groups of adult male rats were formulated as follows: A) controls+NS, B) control+vehicle (saline solution of hydroxypropyl cyclodextrin), C) RES treated, D) CdCl2+NS, E) CdCl2+vehicle, F) RES followed by CdCl2 and M) CdCl2 followed by RES. At the end of the protocol, serum levels of FSH, LH and testosterone were measured in all groups, and testicular levels of TBARS and superoxide dismutase (SOD) activity were measured. Epididymal semen analysis was performed, and testicular expression of Bcl-2, p53 and Bax was assessed by RT-PCR. Also, histopathological changes of the testes were examined microscopically. Administration of RES before or after cadmium chloride in rats improved semen parameters including count, motility, daily sperm production and morphology, increased serum concentrations of gonadotropins and testosterone, decreased testicular lipid peroxidation and increased SOD activity. RES not only attenuated cadmium chloride-induced testicular histopathology but was also able to protect against the onset of cadmium chloride testicular toxicity. Cadmium chloride downregulated the anti-apoptotic gene Bcl2 and upregulated the expression of pro-apoptotic genes p53 and Bax. Resveratrol protected against and partially reversed cadmium chloride testicular toxicity via upregulation of Bcl2 and downregulation of p53 and Bax gene expression. The antioxidant activity of RES protects against cadmium chloride testicular toxicity and partially reverses its effect via upregulation of BCl2 and downregulation of p53 and Bax expression.