Omega-3 polyunsaturated fatty acids ameliorate neuroinflammation and mitigate ischemic stroke damage through interactions with astrocytes and microglia.

Omega-3 polyunsaturated fatty acids (PUFA n3) provide neuroprotection due to their anti-inflammatory and anti-apoptotic properties as well as their regulatory function on growth factors and neuronal plasticity. These qualities enable PUFA n3 to ameliorate stroke outcome and limit neuronal damage. Young adult male rats received transient middle cerebral artery occlusion (tMCAO).

Hypoxia-induced gene expression of aquaporin-4, cyclooxygenase-2 and hypoxia-inducible factor 1α in rat cortical astroglia is inhibited by 17β-estradiol and progesterone.

17β-Estradiol (E2) and progesterone (P) are neuroprotective in acute brain injury by attenuating neuropathophysiological processes and regulating local glial function. Besides controlling brain-intrinsic immune responses, astrocytes are cellular targets for sex steroids in health and disease and typically resist to hypoxic damage. In this in vitro study, we aimed at uncovering astroglia-specific reactions to sublethal hypoxic conditions and astroglia-specific effects of both sex steroid hormones on these parameters.

Regulation of hypoxia-induced inflammatory responses and M1-M2 phenotype switch of primary rat microglia by sex steroids.

Microglia cells are the primary mediators of the CNS immune defense system and crucial for the outcome of shaping inflammatory responses. They are highly dynamic, moving constantly, and become activated by neuronal signaling under pathological conditions. They fulfill a dual role by not only regulating local neuroinflammation but also conferring neuronal protection.

Comparison of infarct volume and behavioral deficit in Wistar Kyoto and spontaneously hypertensive rat after transient occlusion of the middle cerebral artery.

Rodent models of focal cerebral ischemia are important tools in experimental stroke research. Such models have proven instrumental for the understanding of injury mechanisms in cerebral stroke and helped to identify potential new therapeutic options. A plethora of neuroprotective substances have been shown to be effective in preclinical stroke research but failed to prove effectiveness in subsequent clinical trials.

Sex steroid hormone-mediated functional regulation of microglia-like BV-2 cells during hypoxia.

17β-estradiol (E2) and progesterone (P) are neuroprotective hormones in different neurological disorders and in particular under hypoxic conditions in the brain. Both hormones dampen brain-intrinsic immune responses and regulate local glial cell function. Besides astrocytes which are functionally regulated in a manifold and complex manner, especially microglial cells are in the focus of steroid-mediated neuroprotection.

Long-term cerebral cortex protection and behavioral stabilization by gonadal steroid hormones after transient focal hypoxia.

Sex steroids are neuroprotective following traumatic brain injury or during neurodegenerative processes. In a recent short-term study, we have shown that 17β-estradiol (E) and progesterone (P) applied directly after ischemia reduced the infarct volume by more than 70%. This protection might primarily result from the anti-inflammatory effects of steroids.

Solulin reduces infarct volume and regulates gene-expression in transient middle cerebral artery occlusion in rats.

Background: Thrombolysis after acute ischemic stroke has only proven to be beneficial in a subset of patients. The soluble recombinant analogue of human thrombomodulin, Solulin, was studied in an in vivo rat model of acute ischemic stroke.

Methods: Male SD rats were subjected to 2 hrs of transient middle cerebral artery occlusion (tMCAO).

Nrf2 expression by neurons, astroglia, and microglia in the cerebral cortical penumbra of ischemic rats.

Experimental animal studies have demonstrated that oxidative stress plays an essential role during ischemic stroke. In addition to oxidizing macromolecules leading to cell injury, oxidants are also involved in cell death/survival signal pathways and cause mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2) represents one of the major regulators implicated in the endogenous defense system against oxidative stress.

Gonadal steroids prevent cell damage and stimulate behavioral recovery after transient middle cerebral artery occlusion in male and female rats.

17β-estradiol (E) and progesterone (P) are neuroprotective factors in the brain preventing neuronal death under different injury paradigms. Our previous work demonstrates that both steroids compensate neuronal damage and activate distinct neuroprotective strategies such as improving local energy metabolism and abating pro-inflammatory responses. The current study explored steroid hormone-mediated protection from brain damage and restoration of behavioral function after 1h transient middle cerebral artery occlusion (tMCAO).

TTC staining of damaged brain areas after MCA occlusion in the rat does not constrict quantitative gene and protein analyses.

In models of ischemic stroke, TTC (2,3,5-triphenyltetrazolium chloride) staining is commonly applied for the fast and reliable visualization of hypoxic brain tissue and for defining the size of cerebral infarction and penumbra. Deciphering molecular processes of pathogenesis within the penumbra is of particular interest for the development of therapeutic strategies. The aim of this study was to assess whether TTC-stained tissues can easily and in a reliable quantitative manner be processed for further molecular and biochemical analyses.

Cuprizone effect on myelination, astrogliosis and microglia attraction in the mouse basal ganglia.

Multiple sclerosis is the leading cause of neurological disability in young adults affecting more than two million people worldwide. Although multiple sclerosis is generally considered as white matter disease, distinct pathological alterations are also found in the grey matter. Involvement of basal ganglia seems to be related to a set of symptoms such as fatigue, impaired cognition, and movement disturbance.

The cuprizone animal model: new insights into an old story.

Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease that affects the central nervous system and represents the most common neurological disorder in young adults in the Western hemisphere. There are several well-characterized experimental animal models that allow studying potential mechanisms of MS pathology. While experimental allergic encephalomyelitis is one of the most frequently used models to investigate MS pathology and therapeutic interventions, the cuprizone model reflects a toxic experimental model.

Selective regulation of growth factor expression in cultured cortical astrocytes by neuro-pathological toxins.

Astrocytes are integrated in the complex regulation of neurodegeneration and neuronal damage in the CNS. It is well-known that astroglia produces a plethora of growth factors which might be protective for neurons. Growth factors prevent neurons from cell death and promote proliferation and differentiation of precursor cells.

Early formation of a GFAP-positive cell population in the ventricular zone during chicken brain development.

It is believed that neurons are generated near the surface of the embryonic cerebral ventricles, whereas glial cell proliferation occurs at sites distant to the ventricles. There is still uncertainty concerning the developmental stages when glial and neuronal cell lines diverge in the proliferative zone. The purpose of this study was to determine whether at early stages of chicken brain development during neurogenesis, cells from the astrocytic lineage are present in relevant amounts, where they are located in the neural tube, and to what extent brain regional differences exist.

Cuprizone treatment induces distinct demyelination, astrocytosis, and microglia cell invasion or proliferation in the mouse cerebellum.

Demyelination of the cerebellum is a well-known phenomenon in human multiple sclerosis (MS). Concordantly, patients with MS frequently developed symptoms deriving from cerebellar lesions, i.e.