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OBJECTIVE@#To determine whether resveratrol (Res) can correct osteoporosis induced in a rat model of male hypogonadism.@*METHODS@#Thirty-two rats were randomly divided into 4 groups, 8 in each group; 1) a control sham group: underwent a similar surgical procedure for induction of orchiectomy (ORCD) without ligation of any arteries or veins or removal of the testis and epididymis; 2) a control + Res-treated group (Con+Res): underwent sham surgery similar to the control, but was then treated with Res, as described below; 3) an ORCD-induced group: bilateral ORCD surgery as described above, and 4) a ORCD+Res-treated group: bilateral ORCD surgery followed by Res treatment. Res treatment began 4 weeks after ORCD and continued for 12 weeks. After 12 weeks, bone mineral density (BMD) and bone mineral content (BMC) were measured in the tibia and femur of each rat's right hind leg. Blood levels of bone turnover indicators such as deoxypyridinoline (Dpd), N-telopeptide of type I collagen (NTX I), alkaline phosphatase (ALP), and osteocalcin (OC), as well as receptor activator of nuclear factor kappa B (RANK) and osteoprotegerin (OPG) were assessed.@*RESULTS@#ORCD significantly decreased BMD (P<0.01) and significantly increased bone resorption, manifested by increased RANK. In addition, it inhibited serum levels of OPG and OC. Res treatment after ORCD effectively increased serum levels of bone formation markers such as OPG and OC, compared with testisectomized rats (P<0.05).@*CONCLUSION@#Res could ameliorate bone loss induced by male hypogonadism, possible via restoration of the normal balance between RANK and OPG.
Assuntos
Ratos , Masculino , Animais , Densidade Óssea , Resveratrol/farmacologia , Osteoporose , Osteoprotegerina/farmacologia , Remodelação Óssea , Hipogonadismo , Ligante RANK/farmacologiaRESUMO
Background@#The present study examined the effect of intermittent fasting (IF) on bone mineral content (BMC) and bone mineral density (BMD) and the markers of bone remodeling in a glucocorticoid-induced osteoporosis (GIO) rat model. @*Methods@#Forty male rats were allocated to 4 groups (N=10 per group): control group of normal rats; control+IF group (normal rats subjected to IF for 16-18 hr daily for 90 days); dexamethasone (DEX) group: (DEX [0.5 mg i.p.] for 90 days); and DEX+IF group (DEX and IF for 90 days). By the end of the experiment, BMD and BMC in the right tibia were measured. Serum levels of the following were measured: glucose; insulin; triglycerides (TGs); total cholesterol; parathyroid hormone (PTH); osteoprotegerin (OPG); receptor activator of nuclear factor-κB (RANK); bone-resorbing cytokines, including bone deoxypyridinoline (DPD), N-terminal telopeptide of collagen type I (NTX-1), and tartrate-resistant acid phosphatase 5b (TRAP-5b); and bone-forming cytokines, including alkaline phosphatase (ALP) and osteocalcin (OC). @*Results@#DEX administration for 90 days resulted in significantly increased serum levels of glucose, insulin, TGs, cholesterol, PTH, OPG, DPD, NTX-1, and TRAP-5b and significantly decreased BMD, BMC, and serum levels of RANK, OC, and ALP (all P<0.05). IF for 90 days significantly improved all these parameters (all P<0.05). @*Conclusions@#IF corrected GIO in rats by inhibiting osteoclastogenesis and PTH secretion and stimulating osteoblast activity.
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To test the hypothesis that the neurohormone, melatonin, differentially activates the release of the proinflammatory cytokines, such as, interleukin-1 beta [IL-1 beta] and tumor necrosis factor-alpha [TNF-alpha], as well as inducing leukocyte mobilization into the peripheral blood in response to a sterile tissue injury. This study was conducted between November 2011 and September 2012 at the Department of Physiology, College of Medicine, King Khalid University, Abha, Kingdom of Saudi Arabia. Sterile tissue injury of either skin injury or gastric ulceration was induced in equal numbers in Wistar albino rats aged 7-8 weeks [150-200 g] [20 each], with each group being equally divided into melatonin treated or vehicle-treated. Melatonin treatment and sterile tissue injuries significantly [p<0.05] increased the plasma levels of IL-1 beta and TNF- alpha compared to baseline levels. However, higher levels of IL-l beta compared with TNF- alpha were obtained only with melatonin treatment. Furthermore, melatonin treatment significantly increased [p<0.05] total leukocyte counts before the induction of skin injury and gastric ulceration, and remained elevated for a longer period than injured, but vehicle-treated rats. In addition, our methods of inducing skin injury or gastric ulceration caused an increase in leukocyte levels in the blood circulation [p<0.05]. Melatonin differentially stimulated plasma IL-1 beta and TNF- alpha, and increased blood leukocyte counts before and after sterile tissue injuries. It is worth pursuing further investigation into the therapeutic effect of melatonin in inflammatory disease that involves leukocyte recruitment to sites of injury
Assuntos
Animais de Laboratório , Melatonina/farmacologia , Citocinas , Leucócitos , Ratos Wistar , Interleucina-1beta , Fator de Necrose Tumoral alfa , Tecidos/lesõesRESUMO
To study the effect of chronic exposure to native high altitude [HA] on blood pressure, and to investigate the underlying mechanism of action. This study was carried out between February and April 2011. A total of 20 male rats were divided into 2 groups [n=10 rats]. The low altitude [LA] group were rats born and lived in an LA environment at King Saud University, College of Pharmacy, Riyadh, Kingdom of Saudi Arabia [KSA], and the HA group were rats born in the same LA area, then acclimatized to HA area in Physiology Department, King Khalid University, College of Medicine, Abha, KSA for 90 days. At the end of day 90, hematocrit, plasma renin activity, aldosterone, norepinephrine and vasopressin levels were determined in both groups. Invasive arterial blood pressure was also measured, and fractional excretion of sodium [FENa], and potassium [FE[K]] were calculated. The quantitative real time-polymerase chain reaction of renin was carried out in the kidneys of both rat groups. When compared to LA native rats, HA rats exhibited a significant increase in systolic and diastolic blood pressure with a significant increase in renin plasma activity as well as an increase in the levels of aldosterone, norepinephrine, and vasopressin. Furthermore, HA rats showed a significant increase in renin expression in their kidneys, as well as decreased FENa. Data shows that prolonged exposure to HA results in elevated blood pressure precipitated by the activation of the renin-angiotensin-aldosterone system
RESUMO
The habit of khat chewing represents a major socio-economic problem in many countries but research into its hepato-renal toxic effects has produced contradictory results. To evaluate the subacute effects of Khat [Catha edulis] extract on hepatic and renal functions in white albino rats. Randomized experimental animal study. Physiology laboratory, medical school of King Khalid University. Twenty white albino rats aged between 14 and 16 weeks were included in the study. The rats were assigned randomly into two groups, ten each. Treated rats received orally administered hydro-ethanol extract of Catha edulis for four weeks. Control rats received corresponding amounts of normal saline. There was statistically significant increase in the activities of hepatic enzymes in treated rats compared to the control group. In addition, serum urea, bilirubin and phosphorus concentrations were significantly increased compared to a decreased serum total protein and albumin concentrations. Oral administration of the extract induced lipid peroxidation and oxidative stress in hepatic and renal tissues as shown by significant increases in lipid peroxidation biomarkers thiobarbituric acid reactive substances [TBARS] and significant decreases in levels of superoxide dismutase [SOD], catalase [CAT] and glutathione [GSH]. Histological examination of Catha edulis treated rats revealed marked hepato-renal pathological changes compared to the control group. These results indicate that orally administered Catha edulis extract exerts severe hepato-nephro toxicity and the mechanism of this damage may be related to oxidation, increased lipid peroxidation, and generation of free radicals inside these tissues