Effects of sleep deprivation on cellular immunity and interleukin-6 level in rats: increased dietary fat modulate sleep deprivation-induced immune change

Impairment of host defenses is chief among sleep deprivation outcomes, as evidenced by strikingly poor control over endogenous microorganisms. Interleukin [IL]-6 is a multifunctional cytokine. It is an inflammatory cytokine, which causes sickness manifestations. This cytokine might play a significant role in mediating the sleepiness and fatigue in the day after sleep deprivation. Leukocytosis has been a consistent finding in sleep deprivation inspite of the impaired immunity. Blood leukocyte differentials were performed to determine the cell types responsible for this finding of increased circulating white blood cell counts. Fatty acid composition of rodent diets can affect immune function as measured in vitro and in vivo and can modulates the immune response to different types of stress. This study was designed to investigate the effect of 4 days of sleep deprivation on the serum level of IL-6 and the differential count of white blood cells. Also to examine the effect of diet enriched with fat on the changes induced by sleep deprivation. Forty adult male albino rats were included in this study and were divided into 4 groups: Group I: [Control group] included 10 rats received standard rat chow and water and have normal sleep pattern, at -12 hours dark-light cycles. Group II: [Fat fed group] included 10 rats received standard rat chow enriched with corn oil and water, and have normal sleep pattern, at -12 hours dark-light cycles. Group III: [Sleep deprivation group] included 10 rats received standard rat chow and water, and was exposed to sleep deprivation. Group IV: [Fat fed and sleep deprived group] included 10 rats received standard rat chow enriched with corn oil and water, and was exposed to sleep deprivation in the same pattern as group III. Sleep deprivation was carried out by audio-visual mechanism. The results indicated decreased body weight, leukocytosis with neutrophilia and shift to the left, monocytosis and lymphopenia in sleep-deprived rats. The serum revealed an evolving pro-inflammatory state, as evidenced by high incidence of interleukin-6. Feeding the rats diet enriched with fat ameliorated the inflammatory state as evidenced by significant lower levels of IL-6 and partially corrected the change induced by sleep deprivation on the total and the differential blood count of WBCs. We can conclude that sleep deprivation has a considerable impact on the immune response. Nearly all of the immune-related events that emerged as responses to sleep deprivation have been implicated as a pro-inflammatory states that represents a risk factor for many diseases. Feeding sleep deprived rats a diet enriched in fatty acids ameliorated the effect of sleep deprivation on IL-6 secretion and partially attenuated the stimulation of inflammatory responses induced by sleep deprivation as indicated by partial correction of the body weight and WBCs count and composition

Effect of thyroid hormone on contractility and sarco/endoplasmic Reticulum Ca[2+] ATPase -1 [SERCA1] expression in adult rats; role in thermogenesis

Thyroid hormone is one of the main factors that determine skeletal muscle contractile properties and the slow-twitch vs. fast twitch muscle fiber phenotype. Sarcoplasmic reticulum Ca[2+] ATPase is one of the principal regulators of Ca[2+] homeostasis in the skeletal muscle cells. It has been previously shown that modification of thyroid hormone levels has a profound impact on cardiac function, predominantly through a direct regulation of the sarcoplasmic reticulum protein levels. The present study aimed to investigate the effects of thyroid hormone treatment for 4 weeks on slow twitch soleus muscle of rats via recording twitch tension, time to peak tension, and half relaxation time and determination of soleus muscle SERCA1 expression. 24 male rats of local strain were randomly divided into 2 groups [n=12], control euthyroid group and hyperthyroid group in which hyperthyroidism was induced by intra peritoneal [i.p] injection of L-troxin 200microg/kg B.W./day, for 4 weeks. The in-situ isometric measures were done for soleus muscle and twitch tension [TT], [expressed as screen units], time to peak tension [TPT], and half relaxation time, 1/2 Rt [expressed in milliseconds] were recorded. SERCA1 protein expression in rat soleus muscle was measured. Thyroid hormone treatment significantly reduced time to peak tension and half relaxation time and increased twitch tension. These contractile changes were accompanied with significant increase in expression of SERCA1 in soleus muscle of rats. Thyroid hormone stimulates the expression of SERCA1 in slow soleus muscle in rats, thereby speeding-up the contraction-relaxation cycle and this increases energy expenditure and these effects of thyroid hormone participate at least in part to thermogenic action of thyroid hormone

Comparative effect of antioxidants and l-arginine treatment on nerve conduction velocity and regeneration in streptozotocin-induced diabetic rats

Diabetic polyneuropathy [DPN] is the most common chronic complication of diabetes. In the last two decades it has become increasingly evident that underlying vascular and metabolic mechanisms emerged as a prominent pathogenetic factors for DPN. Oxidative stress is increased in both human and experimental diabetes and has been related to the development of diabetic neuropathy. Vascular factors include increased peripheral resistance also have been implicated in the pathogenesis of experimental diabetic neuropathy [EDN]. It seems still controversial, whether EDN is primarily of vascular or metabolic origin and the aim of the present study was to evaluate the possible contribution of two pathways to the development of such neural complications in type II diabetic animals. Ninety male albino rats were included. The animals groups were as follows: Group I: Control rats which were injected by intraperitoneal [i.p.] by vehicle solution alone, Group II: Diabetic rats not receiving any form of treatment [with fasting blood glucose level above 300mg/kg], Group III: Diabetic rats received daily subcutaneous insulin injection in a dose IIU/day, Group IV: Diabetic rats received intramuscular injection of Vitamin E in a dose 300mg/kg BW, three times/week, Group V: Diabetic rats received intramuscular injection of Vitamin E in a dose 600mg/kg BW, three times/week, Group VI: Diabetic rats received subcutaneous insulin [IIU/day], and intramuscular injection of Vitamin E [300mg/kg BW, three times/week], Group VII: Diabetic rats received subcutaneous insulin [IIU/day], and intramuscular injection of Vitamin E [600mg/kg BW, three times/week], Group VIII: Diabetic rats received daily intragastric L-arginine in a dose of 50mg/kg BW, Group IX: Diabetic rats received daily intragastric L-arginine in a dose of 50mg/kg BW, and subcutaneous insulin [IIU/day]. After 4 weeks, nerve conduction velocity studies were performed, serum glucose was measured, and sciatic nerves malondialdehyde [MDA], glutathione peroxidase [GTPx], endothelial nitric oxide synthase [eNOS] were measured. Diabetic rats had significant higher serum glucose levels, oxidative stress markers, lower eNOS, with delayed nerve conduction velocity [NCV] and lower amplitude of muscle contraction [AMC] as compared with the control group. Treating rats with insulin corrected serum glucose to control values. Treating rats with vitamin E significantly reduced oxidative stress markers, and corrected NCV and improved AC. L-arginine treatment had no effect on serum glucose, oxidative stress markers, but significantly improved NCV and AMC. It can be concluded that EDN is a multifactorial disease, caused by hyperglycemia, oxidative stress and vascular impairment. Conjugate treatment with vitamin E especially in higher doses [600mg/kg B. W.] with insulin could be of great value. Moreover correction of impaired nerve blood flow by drugs that induce NO has proved to be efficient in the protection against, and correction of EDN