Promotion of immune and glycaemic functions in streptozotocin-induced diabetic rats treated with un-denatured camel milk whey proteins

T cell mediated autoimmune diabetes is characterized by immune cell infiltration of pancreatic islets and destruction of insulin-producing β-cells. This study was designed to assess the effect of whey proteins (WP) on the responsiveness of lymphocytes in rats after four months of Streptozotocin (STZ)-induced Type 1 diabetes (T1D). A diabetic group was supplemented with WP daily for five weeks at a dose of 100 mg/kg. Ribonucleic acid (RNA) was extracted from stimulated lymphocytes in order to analyse gene expressions using real time PCR and RT-PCR. PCR results were confirmed with ELISA. The proliferation capacity of lymphocytes and their homing to the spleen were studied. Antigen-activated lymphocytes showed that diabetes impaired the mRNA expression of the protein kinase B (Akt1), Cdc42, and the co-stimulatory molecule, CD28, which are important for cell survival, actin polymerization and T cell activation, respectively. Accordingly, proliferation of lymphocytes was found to be suppressed in diabetic rats, both in vivo and in vitro. WP was found to restore Akt1, Cdc42 and CD28 mRNA expression during diabetes to normal levels. WP, therefore, served to activate the proliferation of B lymphocytes in diabetic rats both in vivo and in vitro. Although WP was found to up-regulate mRNA expression of both interleukin (IL)-2 and interferon gamma (IFN-γ), it suppressed the proliferation activity of almost all T cell subsets. This was confirmed by WP normalizing the structure and function of ß cells. Meanwhile, WP was found to down regulate the mRNA expression of Tumor necrosis factor-alpha (TNF-α) and its programmed cell death-receptor (Fas). Taken together, the results of this study provide evidence for the potential impact of WP in the treatment of immune impairment in T1D, suggesting that it serves to reverse autoimmunity by suppressing autoreactive T cells and down regulating TNF-α and Fas, resulting in improved pancreatic ß cell structure and function

Whey protein enhances normal inflammatory responses during cutaneous wound healing in diabetic rats

<p>Abstract</p> <p>Background</p> <p>Prolonged wound healing is a complication of diabetes that contributes to mortality. Impaired wound healing occurs as a consequence of excessive reactive oxygen species (ROS) production. Whey protein (WP) is able to reduce the oxygen radicals and increase the levels of the antioxidant glutathione. Thus, the aim of this study was to determine whether dietary supplementation with WP could enhance normal inflammatory responses during wound healing in diabetic rats. Animals were assigned into a wounded control group (WN), a wounded diabetic group (WD) and a wounded diabetic group orally supplemented with whey protein (WDWP) at a dose of 100 mg/kg body weight.</p> <p>Results</p> <p>Whey protein was found to significantly decrease the levels of malondialdehyde (MDA), nitric oxide (NO) and ROS. A significant restoration of the glutathione level was observed in WDWP rats. During the early wound healing stage, IL-1β, TNF-α, IL-6, IL-4 and neutrophil infiltration were significantly decreased in WD mice. WP supplementation was found to restore the levels of these inflammatory markers to the levels observed in control animals. In addition, the time required for wound healing was significantly prolonged in diabetic rats. WP was found to significantly decrease the time required for wound healing in WDWP rats.</p> <p>Conclusion</p> <p>In conclusion, dietary supplementation with WP enhances the normal inflammatory responses during wound healing in diabetic mice by restoring the levels of oxidative stress and inflammatory cytokines.</p

Aluminum-induced testosterone decrease results in physiological and behavioral changes in male mice

Recently, there has been much controversy on the role of testosterone on social and aggression behaviors. This work aimed to determine the effect of testosterone decrease, induced by aluminum exposure on the level of aggression. Male Swiss-Webster strain mice were classified into three groups. The first (control group) received distilled water, while the second and third groups were administrated 300 and 600 mg/kg aluminum chloride, respectively, by oral route for 20 days. Thereafter, they were subjected to “standard opponent” test. A significant decrease in testosterone levels in the treated groups was obtained at both the low and high doses of aluminum. Expectedly, significant decreases were observed in the social contacts, threat, attack and number of fights of both treated groups in a dose dependant manner. All blood parameters revealed a dose dependent significant decrease as well. A significant decrease in both serotonin and dopamine levels was simultaneously obtained with the decrease of testosterone level especially at the high dose of aluminum. In contrast, at the high dose, acetylcholine recorded significantly high value. In conclusion, aluminum-induced testosterone decrease resulted in a significant decline in aggression, several blood parameters and levels of neurotransmitters.Keywords: Aluminum, Swiss-Webster mice, standard opponent test, social behavior, testosteron

Bioactivity of Samsum ant (Pachycondyla sennaarensis) venom against lipopolysaccharides through antioxidant and upregulation of Akt1 signaling in rats

BACKGROUND: This study aimed at investigating the oxidative stress ameliorating effect, lipids profile restoration, and the anti-inflammatory effect of Samsum Ant Venom (SAV) in induced endotoxemic male rats, injected with bacterial lipopolysaccharides (LPS). RESULTS: Results revealed that LPS significantly increased the oxidative stress indications in LPS-injected rats. A significant increase of both malondialdehyde (MDA), and advanced oxidative protein products (AOPP), as well as a significant suppression of glutathione were all detected. Treatment with 100 μg/kg dose of SAV significantly restored the oxidative stress normal indications and increased the total glutathione levels. Treatment of the LPS-rats with 100 μg/kg dose of SAV showed a clear anti-inflammatory function; as the histological architecture of the hepatic tissue was partially recovered, along with a valuable decrease in the leukocytes infiltrated the hepatic tissues. Treatment of some rat groups with 600 μg/kg dose of SAV after LPS injection induced a severe endotoxemia that resulted in very high mortality rates. SAV versus the effects of LPS on AKT1, Fas, TNF-α and IFN-γ mRNA expression. SAV was found to significantly lower Fas gene expression comparing to the LPS group and restore the level of IFN-γ mRNA expression to that of the control group. CONCLUSION: In conclusion, SAV, at the dose of 100 μg/kg body weight, maintained and restored the oxidative stability, the anti-inflammatory, and the hypolipidemic bioactivity in rats after induced disruption of these parameters by LPS injection. This improvement by SAV was mediated by upregulation of AKT1

Antioxidant Potential of Spirulina platensis

The present study aimed to examine the protective role of Spirulina platensis (S. platensis) against arsenic-induced testicular oxidative damage in rats. Arsenic (in the form of NaAsO2 at a dose of 6.3 mg/kg body weight for 8 weeks) caused a significant accumulation of arsenic in testicular tissues as well as a decrease in the levels of testicular superoxide dismutase (SOD), catalase (CAT), reduced glutathione, and zinc. Moreover, it significantly decreased plasma testosterone, luteinizing hormone (LH), triiodothyronine (T3), and thyroxine (T4) levels and reduced sperm motility and sperm count. Arsenic (AS) led to a significant increase in testicular malondialdehyde (MDA), tumour necrosis factor alpha (TNF-α), nitric oxide (NO), and sperm abnormalities. S. platensis at a dose of 300 mg/kg was found to attenuate As-induced oxidative stress, testicular damage, and sperm abnormalities by its potent antioxidant activity. S. platensis may represent a potential therapeutic option to protect the testicular tissue from arsenic intoxication

Lead Nitrate Induced Histopathological Alterations in the Liver and Intestine of African Catfish Clarias gariepinus Exposed to Sublethal Concentrations

552-557Studies were carried out on the liver and intestine tissue of Clarias gariepinus after exposure to sublethal concentrations of LC50 lead nitrate for 20 days. Fish were distributed into four groups, control (0 mg/L, LC50 of Pb(NO3)2) and three groups exposed to 20, 40 and 60% of the LC50 of Pb(NO3)2 (16.12, 32.24 and 48.37 mg/L respectively). Section of hepatic and intestine tissues showed the normal structure for control group. However, treated hepatic tissues of fish exhibited altered its characteristic architecture, with remarkably high vacuolation in hepatocytes and hepatoctolysis. Also, central vein was dilated and increased hemorrhage in the sections of almost samples from treated fish. Increased number of fibroblasts and Kuppffer cells were observed in the examined sections from treated fish when compared to the control. Therefore, fish treated with 60% LD50 of Pb(NO3)2 observed the proliferation of fibrous in connective tissue particularly near sinusoids and substituting liver parenchyma. Therefore, intestinal sections from the different treated fish groups revealed an evident harmful to intestinal tissue, especially in enterocytes and structures of villi. Also, disturbed longitudinal and circular muscularis were observed, to abnormally dilated, lamina propria, was infiltrated with a huge numbers of inflammatory leukocytes. Mucous secreting goblet cells proliferated and multiplied in all exposed fish

Toxico-histological Effects of Sublethal Concentrations of Lead Nitrate on the Gills of the African Catfish, Clarias gariepinus

This study aimed to investigate the effects of subleathal lead doses on the histological architecture of gills in the freshwater African catfish, Clarias gariepinus. Results revealed three stages of changes after exposure to three doses of lead nitrate. The changes were mild in fish exposed to 16.12 mg/L of Pb (NO3)2 (stage I 20% of LC50) and severe in case of 40% of LC50 (stage II, 32.24 mg/L) and 60% of LC50 (stage III 48.37% mg/L) in comparison to control. The histological examination revealed normal architecture of gills in control fish. Normal gills were characterized with primary gill lamellae with a central hyaline cartilage. However, three-stage changes were observed after exposure to the three doses of lead nitrate. In stage I, a cartilaginous matrix appeared along with loosening of the epithelial lining of the cartilaginous core and abundant vascular spaces were observed on the secondary gill lamellae. An extra cartilaginous matrix, loosening of the epithelial lining of the cartilaginous core, de-shaped gill lamellae, and degeneration of the secondary gill lamellae were noted in stage II. Lesions in the gill pattern in stage III were represented by shortening of the tips of secondary gill lamellae, damaged gill lamellae, a cartilaginous matrix, and hyperplasia. This indicated that lead exposure resulted in severe histopathological changes in the gills in a dose-dependent manner

Possible Causes of Ileal Injury in Two Models of Microbial Sepsis and Protective Effect of Phytic Acid

Background: Sepsis related-multiple organ dysfunction is associatedwith ileum injury. We aimed to determine the causes ofileal injury in two models of microbial sepsis resulted from infectionwith Aeromonas hydrophila or its endotoxin. We alsoevaluated the protective effect of phytic acid.Methods: Thin sections of ileum from 60 Swiss male mice incontrol, bacteria-infected or lipopolysaccharides (LPS) andbacteria-infected or LPS-infected co-administered with phyticacid were subjected to histopathological and TdT-mediateddUTP nick-end labeling (TUNEL) assay for apoptotic cellsdetection while ultra thin sections were stained with uranylacetate and lead citrate for cytological changes examination.Also, ileum images were exposed to the image analysis softwareto determine some related morphometric measures.Results: Necrosis and apoptosis were observed in ileum injuryin both examined sepsis models. The ileum injury was moresevere in LPS model. Phytic acid showed the ability to attenuateileum injury in Aeromonas hydrophila and its endotoxinmodels of sepsis after four weeks administration where itssupplementation significantly minimized the histopathologicaland cytological complications and morphometric alterationsresulted from the injury.Conclusion: The protective effects of phytic acid may becaused by increased mucous secretion, decreased apoptoticindex, attenuating the inflammatory and lymphocytic cellscount or increasing the renewal of the crypt cells and villousepithelial cells proliferation