Cerebral inflammation

Microglia-associated induction of cerebral inflammation is a typical feature of thiamine deficiency. 

Chronic inflammation is considered to be a contributing factor in AD. Besides the low ACh levels in the brains of AD patients, decreased number of nicotinic (nAChR) and muscarinic acetylcholine receptors (mAChR) has been detected in AD patients brains as well as in experimental AD animals [24, 27]. In a recent publication, hupA has been shown to reduce both acute and chronic cerebral inflammation in rats, by a mechanism that is believed to be mediated through the nAChR [11]. 

Decreased cerebral blood flow, resulting from acute arterial occlusion, reduces oxygen and glucose delivery to brain tissue with subsequent lactic acid production, blood-brain barrier breakdown, inflammation, sodium and calcium pump dysfunction, glutamate release, intracellular calcium influx, free-radical generation, and finally membrane and nucleic acid breakdown and cell death. The degree of cerebral blood flow reduction following arterial occlusion is not uniform. Tissue at the... 

Ebselen is a seleno-oiganic that mimics glutathione peroxidase and inhibits iron-stimulated lipid peroxidation. It significandy reduced both inferct size and oedema progression in the middle cerebral artery exclusion (MCAO) focal model of stroke in tats (Matsui et al. 1990). Ebselen has also been shown to be an effective anti-inflammatory agent in a H202-dependent inflammation model in tats (Parnham 1991). 

A recent patent application from Roche [352] described a 2-amino-benzothiazole series. Roche claimed that compound (605) exhibited an IC50 value of 0.73 uM at CBi, and showed in excess of 10-fold selectivity over the CB2 receptor. The compounds were described as being of potential use in the treatment of a range of diseases, including CNS and psychiatric disorders, type-2 diabetes, gastrointestinal diseases, cardiovascular disorders, infertility disorders, inflammation, cancer, atherosclerosis, cerebral vascular incidents and cranial trauma. 

Plasma cell disorders Plasma cell disorders Inflammation-associated, familial Mediterranean fever Familial amyloidotic neuropathy, systemic senile amyloidosis Dialysis-associated amyloidosis Familial amyloidotic neuropathy, aortic amyloidosis Familial systemic amyloidosis Familial systemic amyloidosis Familial systemic amyloidosis Familial cerebral hemorrhage with amyloidosis Sporadic and familial Alzheimer s disease, familial cerebral hemorrhage with amyloidosis Spongiform encephalopathies C-cell thyroid tumors Insulinoma, type II diabetes Atrial amyloidosis Prolactinomas pituitary amyloidosis Iatrogenic amyloidosis Corneal amyloidosis ... 

Due to the numerous possible reactions and related biological consequences, inappropriate overproduction of NO can cause a series of disease states such as a variety of neurodegeneration diseases including inflammation, rheumatic disease, septic shock, diabetes melhtus, and cerebral ischemia. Therefore development of isoform-specific NOS inhibitors to regulate NO synthesis has been an active research area. 

K+ channels K-atp Rat brain Diabetes, asthma, cardiac arrythmia, angina, cardiac and cerebral ischemia, thrombosis, hypertension, incontinence, pain, neurogenic inflammation, epilepsy, stroke, hair growth Control of insulin release, vasodilatation, protection against cell ischemia... 

Acute exposure of rats to high concentrations (up to 40,000 ppm) has resulted in convulsions, pulmonary edema, respiratory arrest, and death. In rats repeatedly exposed at 600 ppm, death was attributed to renal papillary necrosis renal toxicity was not present in rabbits similarly exposed. Exposure of rabbits to 300 or 600 ppm resulted in convulsions and hyperactivity, moderate inflammation of nasal tissues, and some inflammation of the trachea or bronchi. Subchronic studies found that rats exposed at 3 00 ppm had mottled incisor teeth, minimal renal effects, pulmonary histiocytosis, inflammation of nasal tissues, and cerebral vacuolation. 

Adenosine 2a receptor ADORA2A Agonism Inhibition of platelet aggregation, anti-inflammation and neuroprotective effects, coronary vasodilation, decreased blood pressure, increased plasma renin activity and sleep induction. Antagonism Increased platelet aggregation, hypertension, nervousness (tremor, agitation), arousal, insomnia, cerebral and coronary vasodilation (in microvessels only). 

Many pathological conditions, including ischemia/reperfusion, inflammation, and sepsis may induce tissues to simultaneously produce both superoxide and nitric oxide. For example, ischemia allows intracellular calcium to accumulate in endothelium (Fig. 20). If the tissue is reperfused, the readmission of oxygen will allow nitric oxide as well as superoxide to be produced (Beckman, 1990). For each 10-fold increase in the concentration of nitric oxide and superoxide, the rate of peroxynitrite formation will increase by 100-fold. Sepsis causes the induction of a second nitric oxide synthase in many tissues, which can produce a thousand times more nitric oxide than the normal levels of the constitutive enzyme (Moncada et al., 1991). Nitric oxide and indirectly peroxynitrite have been implicated in several important disease states. Blockade of nitric oxide synthesis with N-methyl or N-nitroarginine reduces glutamate-induced neuronal degeneration in primary cortical cultures (Dawson et al., 1991). Nitroarginine also decreases cortical infarct volume by 70% in mice subjected to middle cerebral artery occlusion (Nowicki et al., 1991). Myocardial injury from a combined hy-... 

Scopolia tangutica Max. San Long Zhi (root) Hyoscyamine, scopolamine, anisodamine, anisodine.33-42 Treat shock caused by acute infectious diseases, cerebral thrombosis, acute spinal cord inflammation. 

Thiazolidinediones (TZDs) are potent synthetic agonists of PPARy and medicine for type 2 diabetes. TZDs were shown to induce neuroprotection after cerebral ischemia by blocking inflammation (Culman et al., 2007). Spinal cord injury (SCI), another type of neurodegenerative disease, also induces massive inflammation that precipitates secondary neuronal death. Park et al. (2007) analyzed the therapeutic efficacy of TZDs, pioglitazone, and rosiglitazone, after SCI... 

Maier C. M., Ahem K., Cheng M. L., Lee J. E., Yenari M. A., and Steinberg G. K. (1998) Optimal depth and duration of mild hypothermia in a focal model of transient cerebral ischemia effects on neurologic outcome, infarct size, apoptosis, and inflammation. Stroke 29, 2171-2180. 

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