Measurement of interleukin-1 receptor antagonist in patients with systemic lupus erythematosus could predict renal manifestation of the disease.

Interleukin-1 receptor antagonist (IL-1Ra) is a good indicator of disease activity in patients with systemic lupus erythematosus (SLE). Glucocorticosteroids are the most frequently used drugs in SLE. Our goal was to compare IL-1Ra activity in SLE patients with and without renal involvement and to determine the effect of different dosage of glucocorticosteroids used in 17 patients with active SLE without nephritis, 7 patients with inactive lupus nephritis (LN), and 8 patients with active LN, along with 10 healthy controls. IL-1Ra levels were measured in the serum of SLE patients by Human Luminex [100] analyzer. Both in patients with active SLE without nephritis and in patients with LN, serum levels of IL-1Ra (p<0.001) were significantly higher compared with those in the controls. IL-1Ra was significantly higher in patients with active LN than in patients with inactive LN (p = 0.028). The use of methylprednisolone was significantly higher in the active LN group compared with the inactive LN group (p = 0.013). SLE patients with higher IL-1Ra are at lower risk for developing nephritis. The higher doses of glucocorticosteroids needed in active LN could be due to steroid resistance and IL-1Ra polymorphism. Measurement of IL-1Ra levels in SLE patients could help to predict future renal involvement.

A chronic Alzheimer's model evoked by mitochondrial poison sodium azide for pharmacological investigations.

Alzheimer's disease (AD) is a neurodegenerative disorder and accounts for 50-70% of all dementia cases affecting more than 12 million people worldwide. The primary cause of the disease is presently unknown; however, much evidence suggests the involvement of mitochondrial damage. Selective reduction of complex IV activity is present in post-mortem AD brains. Inhibition of this complex could be evoked by chronic sodium azide (NaN(3)) administration in animals. Partial inhibition of the mitochondrial respiratory chain produces free radicals, diminishes aerobic energy metabolism and causes excitotoxic damage creating a deleterious spiral causing neurodegeneration, a pathological process considered to underlie AD. In the present study SPRD rats were treated by various doses of NaN(3) (24-51 mg/kg per day) for 31 days via subcutaneously implanted osmotic minipumps. We have found the proper dose and duration of NaN(3) treatment which was able to cause easily detectable and reproducible cognitive changes. Animals receiving Na-azide doses under 45 mg/kg daily did not show cognitive deficits, but minor histopathological changes were already present. Doses above 45 mg/kg per day proved to be toxic in 4-week-long application causing mortality. NaN(3) dose of 45 mg/kg per day caused cognitive deficit in Morris water maze and passive avoidance tests and a decrease of spontaneous exploratory activity in open field. Histopathological but not biochemical changes were present: dendritic thickening, nerve cell loss, corkscrew-like dendrites and pycnotic nerve cells. The cognitive, behavioural and histopathological features were reproducible. The chronic Na-azide-induced mitochondrial poisoning is suitable for producing AD-like symptoms in rats and testing neuroprotective drug candidates by preventive or curative applications.