Interleukin-4 Aggravates LPS-Induced Striatal Neurodegeneration In Vivo via Oxidative Stress and Polarization of Microglia/Macrophages.

The present study investigated the effects of interleukin (IL)-4 on striatal neurons in lipopolysaccharide (LPS)-injected rat striatum in vivo. Either LPS or PBS as a control was unilaterally injected into the striatum, and brain tissues were processed for immunohistochemical and Nissl staining or for hydroethidine histochemistry at the indicated time points after LPS injection. Analysis by NeuN and Nissl immunohistochemical staining showed a significant loss of striatal neurons at 1, 3, and 7 days post LPS.

Impact of Several Types of Stresses on Short-term Memory and Apoptosis in the Hippocampus of Rats.

Purpose: Stress has a deteriorating effect on hippocampal function. It also contributes to symptom exacerbation in many disease states, including overactive bladder and interstitial cystitis/bladder pain syndrome. We investigated the effects of various types of stresses (restraint, noise, and cold) on short-term memory and apoptosis in relation with corticotropin-releasing factor (CRF) expression.

Treadmill exercise and wheel exercise enhance expressions of neutrophic factors in the hippocampus of lipopolysaccharide-injected rats.

Brain inflammation plays a pivotal role in the pathogenesis of chronic neurodegenerative disorders, including Alzheimer's disease and Parkinson's disease. We investigated the effects of treadmill exercise and wheel exercise on spatial learning ability in relation with long-term potentiation (LTP) using lipopolysaccharide-induced brain inflammation in the rats. Brain inflammation was induced by an injection of LPS into the cerebral ventricle.

Depression-like state in maternal rats induced by repeated separation of pups is accompanied by a decrease of cell proliferation and an increase of apoptosis in the hippocampus.

Stressful experiences, such as an unsatisfactory mother-infant relationship after delivery, can induce depressive disorders, and it is well-known that stressors impair memory function. The hippocampus plays a crucial role in memory processes. In the present study, we determined whether a depressed-like state induced by repeated separation of pups affects the memory capability of the maternal rats.

Interleukin-13 enhances cyclooxygenase-2 expression in activated rat brain microglia: implications for death of activated microglia.

Brain inflammation has recently attracted widespread interest because it is a risk factor for the onset and progression of brain diseases. In this study, we report that cyclooxygenase-2 (COX-2) plays a key role in the resolution of brain inflammation by inducing the death of microglia. We previously reported that IL-13, an anti-inflammatory cytokine, induced the death of activated microglia.

Prevention of nitric oxide-mediated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease in mice by tea phenolic epigallocatechin 3-gallate.

In animal models of Parkinson's disease (PD), the toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is mediated by oxidative stress, especially by nitric oxide (NO). Inhibition of NO synthase (NOS) activity in the brain produces a neuroprotective effect against PD induced by MPTP Green tea containing high levels of (-)-epigallocatechin 3-gallate (EGCG) was administered to test whether EGCG attenuates MPTP-induced PD in mice through the inhibition of NOS expression. Both tea and the oral administration of EGCG prevented the loss of tyrosine hydroxylase (TH)-positive cells in the substantia nigra (SN) and of TH activity in the striatum.

Prothrombin kringle-2 activates cultured rat brain microglia.

Microglia, the major immune effector cells in the CNS, become activated when the brain suffers injury. In this study, we observed that prothrombin, a zymogen of thrombin, induced NO release and mRNA expression of inducible NO synthase, IL-1beta, and TNF-alpha in rat brain microglia. The effect of prothrombin was independent of the protease activity of thrombin since hirudin, a specific inhibitor of thrombin, did not inhibit prothrombin-induced NO release.

Interleukin-13 and -4 induce death of activated microglia.

When the brain suffers injury, microglia migrate to the damaged sites and become activated. These activated microglia are not detected several days later and the mechanisms underlying their disappearance are not well characterized. In this study, we demonstrate that interleukin (IL)-13, an anti-inflammatory cytokine, selectively induces cell death of activated microglia in vitro.