Insulin deprivation decreases insulin degrading enzyme levels in primary cultured cortical neurons and in the cerebral cortex of rats with streptozotocin-induced diabetes.

Background: Many studies have indicated a relationship between diabetes and Alzheimer's disease (AD). However, the molecular mechanism underlying this association has not been clarified. Among several factors, insulin degrading enzyme (IDE), which plays roles in the degradation of both insulin and amyloid β (Aβ), has gained interest as a potential target in efforts to solve this puzzle.

Lack of insulin results in reduced seladin-1 expression in primary cultured neurons and in cerebral cortex of STZ-induced diabetic rats.

Several studies demonstrated that Diabetes mellitus (DM) enhances the risk for Alzheimer's disease (AD). Although hyperglycemia and perturbed function of insulin signaling have been proposed to contribute to AD pathogenesis, the molecular mechanisms behind this association is not clear yet. Seladin-1 is an enzyme catalyzing the last step in cholesterol biosynthesis converting desmosterol to cholesterol.

Effects of experimental diabetes on C/EBP proteins in rat hippocampus, sciatic nerve and ganglia.

Neurodegeneration is one of the most important complications of diabetes mellitus (DM). The exact mechanisms underlying neurodegeneration related to diabetic complications such as cognitive deficits and peripheral neuropathy are not clarified yet. Due to the fact that CCAAT/enhancer binding proteins (C/EBPs) have roles in cognitive functions, memory, synaptic plasticity, inflammation, lipid storage, and response to neurotrophic factors, it is possible to suggest that these transcription factors could have roles in neurodegeneration.

Megestrol acetate inhibits the expression of cytoplasmic aromatase through nuclear C/EBPβ in reperfusion injury-induced ischemic rat hippocampus.

Global ischemia after cardiac arrest, intraoperative hypoxia/hypotension, and hemorrhagic shock causes brain injury resulting in severe neurological and neurobehavioral deficits. Neurodegeneration can be prevented by local aromatase expression, and estrogen synthesis can be neuroprotective in ischemia/reperfusion. Therefore, aromatase, the enzyme that transforms androgens to estrogens, may be a potential target for the study of reperfusion injury after brain ischemia.

Diabetes alters aromatase enzyme levels in sciatic nerve and hippocampus tissues of rats.

Diabetes mellitus (DM) is associated with increased risk of impaired cognitive function. Diabetic neuropathy is one of the most common and important complications of DM. Estrogens prevent neuronal loss in experimental models of neurodegeneration and accelerate nerve regeneration.

Does tourniquet application alter the nitrergic responses of rabbit corpus cavernosum penis? A functional study.

Objective: To investigate the effects of short and long periods of tourniquet application on corporal nerves, endothelium and smooth muscle responses.

Methods: After the rabbits were anesthetized with xylazine (5 mg/kg) and ketamine hydrochloride (35 mg/kg), a standard rubber circular band was applied to the base of the penis. After waiting for 20, 40 and 60 min, the tourniquets were removed and the penil tissue was reperfused for 5 min.

Nicotine potentiates the nitrergic relaxation responses of rabbit corpus cavernosum tissue via nicotinic acetylcholine receptors.

The presence of neuronal nicotinic acetylcholine receptors in rabbit corpus cavernosum tissue and possible mechanisms underlying the potentiation of electrical field stimulation induced relaxation by nicotine were analyzed. In corpus cavernosum tissue strips nicotine (3 x 10(-5) M) and acetylcholine (10(-3) M) produced potentiation on electrical field stimulation (amplitude 50 V; frequency 4 Hz; width 0.8 ms) induced relaxation responses.

Impairment of endothelium- and nerve-mediated relaxation responses in the cavernosal smooth muscle of experimentally diabetic rabbits: role of weight loss and duration of diabetes.

The effects of short- and long-term experimental diabetes on corporal nerve, endothelium and smooth-muscle responses were investigated, and the reasons for possible alterations in corporal smooth muscle responses such as hyperglycaemia, duration of experimental diabetes and/or altered tissue weight were evaluated. Rabbits were injected with alloxan (125 mg/kg) to induce diabetes. Age-matched non-diabetic and diabetic (3 and 9 weeks) and weight-matched non-diabetic groups (9 weeks) were used as control.

Omeprazole-induced relaxation in rat aorta is partly dependent on endothelium.

We investigated the effect of omeprazole (1 x 10(-5)-3 x 10(-4)M), an inhibitor of H(+),K(+)-ATPase, on rat aortic rings pre-contracted with phenylephrine (10(-6)M). Omeprazole relaxed the tissue in a concentration-dependent manner. Either removal of the endothelium or incubation with nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 3 x 10(-5)M) significantly attenuated the relaxations.

Two new nitric oxide synthase inhibitors: pyridoxal aminoguanidine and 8-quinolinecarboxylic hydrazide selectively inhibit basal but not agonist-stimulated release of nitric oxide in rat aorta.

Structural modification at one of the guanidine nitrogens of L-arginine has led to the development of a number of compounds N(G)-monomethyl-L-arginine (L-NMMA), N(G)-nitro-L-arginine (L-NOARG), N(G)-nitro-L-arginine methyl ester (L-NAME) that competitively inhibit nitric oxide synthase (NOS). It was reported that another chemically related compound known as a glycation inhibitor, aminoguanidine also inhibits NOS. Recently, two new glycation inhibitors, structurally related to aminoguanidine (AG), pyridoxal aminoguanidine (PLAG) and 8-quinoline carboxylic hydrazide (8Q) were synthesized.

The spin trapping agent PBN stimulates H2 O2 -induced Erk and Src kinase activity in human neuroblastoma cells.

The spin-trap, alpha-phenyl-N-tert-butylnitrone (PBN) has been shown to have neuroprotective properties and may prevent oxidative injury in vivo and in cultured cells. Although PBN quenches reactive oxygen species, the direct mechanism of neuroprotective action is unknown. In the present study, we examined the effects of PBN on the regulation of the mitogen activated kinase Erk and as well as Src family tyrosine kinases, enzymes known to be activated by oxygen species such as H2O2.