Bone Marrow Stromal Cells Alleviate Secondary Damage in the Substantia Nigra After Focal Cerebral Infarction in Rats.

Transplantation of bone marrow stromal cells (BMSCs) is a promising therapy for ischemic stroke. Previously, we had reported that the secondary degeneration occurred in the ipsilateral substantia nigra (SN) after permanent distal branch of middle cerebral artery occlusion (dMCAO) in Sprague-Dawley rats. However, whether BMSCs have neurorestorative effects on the secondary damage in the SN after focal cerebral infarction has not known.

Inhibition of Cathepsins B Induces Neuroprotection Against Secondary Degeneration in Ipsilateral Substantia Nigra After Focal Cortical Infarction in Adult Male Rats.

Stroke is the leading cause of adult disability in the world. In general, recovery from stroke is incomplete. Accumulating evidences have shown that focal cerebral infarction leads to dynamic trans-neuronal degeneration in non-ischemic remote brain regions, with the disruption of connections to synapsed neurons sustaining ischemic insults.

Inhibition of Cathepsin B Alleviates Secondary Degeneration in Ipsilateral Thalamus After Focal Cerebral Infarction in Adult Rats.

Secondary degeneration in areas beyond ischemic foci can inhibit poststroke recovery. The cysteine protease Cathepsin B (CathB) regulates cell death and intracellular protein catabolism. To investigate the roles of CathB in the development of secondary degeneration in the ventroposterior nucleus (VPN) of the ipsilateral thalamus after focal cerebral infarction, infarct volumes, immunohistochemistry and immunofluorescence, and Western blotting analyses were conducted in a distal middle cerebral artery occlusion (dMCAO) stroke model in adult rats.

[A method for combining Fluoro-Jade B staining and immunofluorescent staining].

Objective: To explore a method for combining Fluoro-Jade B (FJB) staining with immunofluorescent staining in rats with focal cortical infarction.

Method: Permanent distal middle cerebral artery occlusion (dMCAO) was induced in rats by electrocoagulation. The rat models were randomized into two groups, and frozen sections of the brain tissues from each group were stained with FJB followed by immunofluorescent staining or in the reverse order.

Related expressional change of HIF-1α to the neuroprotective activity of exendin-4 in transient global ischemia.

Transient global ischemia induces selective hippocampal pyramidal neuronal death. Under conditions of severe ischemic hypoxia, hypoxia-inducible factor-1α (HIF-1α) induces apoptosis. Exendin-4 (Ex-4), the glucagon-like peptide-1 receptor (GLP-1R) agonist, provides neuroprotection against brain damage after cerebral ischemia.

Neuroprotective effects of overexpressed cyclophilin B against Aβ-induced neurotoxicity in PC12 cells.

Accumulated amyloid-β (Aβ) is a well-known cause of neuronal apoptosis in Alzheimer disease and functions in part by generating oxidative stress. Our previous work suggested that cyclophilin B (CypB) protects against endoplasmic reticulum (ER) stress. Therefore, in this study we examined the ability of CypB to protect against Aβ toxicity.

Voluntary exercise enhances survival and migration of neural progenitor cells after intracerebral haemorrhage in mice.

Primary Objective: This study explored the long-term effects of exercise on the proliferation, survival and migration of endogenous neural progenitor cells (NPCs) in the subventricular zone (SVZ) of the brain after intracerebral haemorrhage (ICH).

Research Design: ICH was induced by an injection of collagenase into the striatum. Animals in the voluntary running exercise group ran freely on a running wheel for 1, 3 and 6 weeks following the induction of ICH.

A novel method for olfactory bulbectomy using photochemically induced lesion.

We present the photochemically induced olfactory bulbectomy (P-bulbectomy) as a novel method to ablate the olfactory bulb thus inducing an animal model of depression. The photosensitizer Rose Bengal was injected through the tail vein and then the cool halogen light illuminated the skull region overlying of the olfactory bulb for 10 min. Two weeks after surgery, P-bulbectomy had completely removed olfactory bulb uniformly in all animals.

Voluntary exercise increases the new cell formation in the hippocampus of ovariectomized mice.

Voluntary exercise, such as running, can induce dramatic increases in adult hippocampal neurogenesis and improve learning and memory function. A recent report showed that exercise also improved memory problems in postmenopausal women. In this study, we examined whether voluntary running exercise could increase new cell formation in the hippocampus under menopausal conditions, modeled with ovariectomized (OVX) mice.