Immunohistochemical studies on the effect of Aloe vera on the pancreatic â-cells in neonatal streptozotocin-induced type-II diabetic rats

Aloe vera is used worldwide for several medical purposes as alternative medicine. There are positive and negative reports on the hypoglycaemic effects of this plant. From previous acute studies, Aloe leaf gel and pulp extracts lead to significant decreases in blood glucose in neonatal streptozotocin (n0-STZ)-treated type-II diabetic rats, whereas lowering of blood glucose during chronic treatment with the same extracts was statistically insignificant. Here we try to detect whether Aloe leaf gel and pulp extracts affect pancreatic â-cells. Using n0-STZ type-IIdiabetic rats, the immunoreactivity of â-cells of the islets of Langerhans did not differ among treatments of control, glibenclamide-, Aloe vera leaf pulp- and gel extract-treated rats. These results suggest that treatment of diabetic rats with Aloe vera gel or pulp or glibenclamide has no beneficial influence on the pancreatic â-cells in type II diabetes

Biallelic loss-of-function mutation in NIK causes a primary immunodeficiency with multifaceted aberrant lymphoid immunity

Primary immunodeficiency disorders enable identification of genes with crucial roles in the human immune system. Here we study patients suffering from recurrent bacterial, viral and Cryptosporidium infections, and identify a biallelic mutation in the MAP3K14 gene encoding NIK (NF- B-inducing kinase). Loss of kinase activity of mutant NIK, predicted by in silico analysis and confirmed by functional assays, leads to defective activation of both canonical and non-canonical NF- B signalling. Patients with mutated NIK exhibit B-cell lymphopenia, decreased frequencies of class-switched memory B cells and hypogammaglobulinemia due to impaired B-cell survival, and impaired ICOSL expression. Although overall T-cell numbers are normal, both follicular helper and memory T cells are perturbed. Natural killer (NK) cells are decreased and exhibit defective activation, leading to impaired formation of NK-cell immunological synapses. Collectively, our data illustrate the non-redundant role for NIK in human immune responses, demonstrating that loss-of-function mutations in NIK can cause multiple aberrations of lymphoid immunity

Protective effect of vanadyl sulfate on the pancreas of streptozotocin-induced diabetic rats

The aim of this study is to examine from a biochernical and histological perspective, whether vanadium has a protective effect on the pancreas of diabetic rats. Male, 6-6.5 months old, Swiss albino rats were divided into four groups. Group 1: control (intact) animals (n = 13). Group II: control rats given vanadyl sulfate (n = 5). Group III: streptozotocin-induced diabetic animals (n = 11). Group IV: streptozotocin-induced diabetic animals given vanadyl sulfate (n = 11). Vanadyl sulfate was given by gavage technique to rats in a dose of 100 mg/kg daily for 60 days, after experimental animals were made diabetic. On day 60, the pancreas tissue and blood samples were taken from the animals. In the streptozotocin-induced diabetic group, blood glucose levels significantly increased in contrast to the loss of body weight, but vanadyl sulfate in streptozotocin-diabetic rats reduced blood glucose levels and increased both blood glutathione levels and body weight. Tissue sections were immunostained using an insulin antibody. The control group given vanadyl sulfate was no different from the other intact control group considering the insulin immunoreactivity in B cells. In pancreatic islets of the diabetic group, a decrease in the number of immunoreactive B cells was observed in comparison to the control group. On the other hand, pancreatic islets of the diabetic group given vanadyl Sulfate showed a higher number of immunoreactive B cells in comparison to the diabetic group. According to the immunohistochemical and biochernical results obtained, it was concluded that vanadyl sulfate call regenerate B cells of endocrine pancreas in experimental diabetes. (c) 2005 Elsevier Ireland Ltd. All rights reserved

The effect of Z-FA.FMK on D-galactosamine/TNF-alpha-induced liver injury in mice

Cathepsin B is a cysteine proteinase, considered to have an important role in apoptosis, which is activated by D-galactosamine and tumor necrosis factor-alpha (D-GalN/TNF-alpha). Benzyloxycarbonyl-L-phenylalanine fluoromethyl ketone (Z-FA.FMK) is a cathepsin B inhibitor used in research on apoptotic pathways. The aim of this study was to investigate the role of Z-FA.FMK on apoptotic cell death, cell proliferation and liver damage induced by a D-GalN/TNF-alpha combination in mice. In the study, 1 h after administration of 8 mg/kg Z-FA.FMK by intravenous injection, D-GalN (700 mg/kg) and TNF-alpha (15 mu g/kg) were administered by a single intraperitoneal injection. In the group given D-GalN/TNF-alpha, the following results were found: Degenerative changes in the liver tissue, significant increase in the number of both TUNEL and activated caspase-3-positive hepatocytes, a decrease in the number of PCNA-positive hepatocytes, an increase in lipid peroxidation (LPO) levels and a decrease in glutathione (GSH) and DNA levels in the liver tissue. In contrast, in the group given D-GalN/TNF-alpha and Z-FA.FMK, a decrease in the damage of the liver tissue, a significant decrease in TUNEL and activated caspase-3-positive hepatocytes, a significant increase in the number of PCNA-positive hepatocytes, a decrease in the LPO levels, an increase in GSH and DNA levels in the liver tissue were found. As a result, microscopic and biochemical evaluations indicate that Z-FA.FMK plays a protective role against liver injury induced by D-GalN/TNF-alpha and it has an inverse effect on hepatocyte apoptosis and proliferation in BALB/c mice. Copyright (c) 2006 John Wiley & Sons, Ltd