Intensive brain injury, whatever its cause, is related with significant short-term and long-term morbidity and Mortality. Recently, stroke has been categorized as a medical emergency and several clinical trials have been done to find effectual therapies. A variety of insults can make worse the initial traumatic brainninjury and preventing or minimizing such insults represents a form of brain protection. Neuroprotective agents that can limit secondary tissue loss or recover behavioral results have been recognized in multiple animal models of acute brain injury.
“Rapid movement of the brain puts stress on blood vessels in the subarachnoid space, which causes them to rupture. The subarachnoid space, which is normally filled with cerebrospinal fluid, fills with blood. Compared to a subdural hematoma, bleeding in a subarachnoid hemorrhage is spread diffusely through the subarachnoid space, so it does not
Cerebral stroke, the second leading cause of death, each year affects nearly 15 million people above the age of 60 years, worldwide, is manifested through several mechanisms such as excitotoxicity, over production of free radicals, inflammation and apoptosis that cause severe brain damage and may ultimately lead to death. Since currently available stroke therapies are not much effective; therefore, it is an urgent need to test and develop some novel and more effective treatment strategies for the efficient management of cerebral stroke. Fortunately, recent reports showed that plant-derived flavonoids have potential neuroprotective actions against an array of neurodegenerative diseases including the stroke. For example, the standardized extracts
Pramipexole (PX) is a dopamine receptor agonist which has proved for its neuroprotective activity against cerebral ischemia. It shows its neuroprotective activity by having antioxidant [6], hypothermic and D3 receptor agonistic property in ischemic brain injury [7]. Hypothermia is the most promising neuroprotective strategy so far due to its lowering metabolic demand, reduction in calcium influx, suppression of inflammatory response and reduction in reactive oxygen species (ROS) generation [8]. Ischemic stroke produces excessive amount of ROS [9]. A drug like N-acetylcysteine (NAC) is well known for its quenching effect on ROS thereby it prevents cellular damage. Previous literature proved that NAC is neuroprotective for the reason that it has antioxidant property and neurovascular protective effects
Stroke is a severe medical condition and is the number five cause of death and leading cause of serious, long-term disability in America. There are three main kinds of stroke, ischemic which is caused by blood blots, hemorrhagic which is caused by ruptured blood vessels that cause brain bleeding, and transient ischemic attack (TIA) which is a “mini-stroke” caused by a temporary blood clot. It is well-known that brain cells die after a few minutes when they are no longer able to receive nutrients and/or oxygen from the blood or even when there is sudden bleeding in and around the brain. After the brain cells die, the part of the body that they control will no longer be able to function. The signs and symptoms depends on the
N-acetyl-cysteine (NAC), is a potent antioxidant which exerts its beneficial effects by modulating glutamatergic, neurotrophic and inflammatory pathways
The brain is split into different compartments, each of which has it’s own functions that it carries out (like: memory, judgment and movement). When brain cells in a particular compartment is damaged, it can’t carry out its functions as is normally would.
Resveratrol (3,4 ',5-trihydroxystilbene) is a naturally occurring phytochemical present in red wine, grapes, berries, chocolate and peanuts. Clinically, resveratrol has exhibited significant antioxidant, anti-inflammatory, anti-viral, and anti-cancer properties. Although resveratrol was first isolated in 1940, it was not until the last decade that it was recognised for its potential therapeutic role in reducing the risk of neurodegeneration, and Alzheimer 's disease (AD) in particular. AD is the primary cause of progressive dementia. Resveratrol has demonstrated neuroprotective effects in several in vitro and in vivo models of AD. Apart from its potent antioxidant and anti-inflammatory roles, evidence suggests that resveratrol also facilitates non-amyloidogenic breakdown of the amyloid precursor protein (APP), and promotes removal of neurotoxic amyloid beta (Aβ) peptides, a critical step in preventing and slowing down AD pathology. Resveratrol also reduces damage to neuronal cells via a variety of additional mechanisms, most notably is the activation of NAD+-dependent histone deacetylases enzymes, termed sirtuins. However in spite of the considerable advances in clarifying the mechanism of action of resveratrol, it is unlikely to be effective as monotherapy in AD due to its poor bioavailability, biotransformation, and requisite synergism with other dietary factors. This review summarizes the relevance of resveratrol in the pathophysiology of AD. It also highlights
Lab research has suggested that resveratrol might have some powers against the diseases of aging -- including Alzheimer's disease. But evidence from human studies has been lacking.
Scientists at Georgetown University have observed a relationship between resveratrol treatments and a protein called amyloid-beta40, which is a biomarker for Alzheimer’s. The results of this study were published Friday in the journal Neurology.
Both the control and aspirin groups were surgically inflicted with cerebral ischemia, WML models. Everyday for four weeks the control group was treated with ethanol and the aspirin group received varying doses of aspirin.
As aging is becoming a worldwide phenomenon, polyphenols have gained interest as potentially modifiable protective factors against neural diseases, such as dementia. The risk factors of cognitive function decline are not comprehensive, while the mechanisms may involve oxidative stress and inflammation. Epidemiological evidence shows that food contained flavonoid, which antioxidant and anti-inflammatory properties, is associated with a lower risk of neurodegenerative disorders and better cognitive evolution of the performance in the elderly(60). Although animal models are more properly used to investigate cellular and molecular mechanisms of the neuroprotective effects of Vaccinium berries, there
Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD
Emerging evidence indicates that free radicals are involved in the pathogenesis of several digestive system disorders as well as in the regulation of biological processes such as aging. Previous reports have indicated that opioids induce apoptosis via stimulating an oxidative stress pathway that is associated with the production of superoxide and nitric oxide (NO) [11]. NO, together with reactive oxygen species (ROS), has a pivotal role in the regulation of apoptosis and necrosis in various cells. Hsiao et al. investigated the role of NO and ROS in the morphine-induced apoptosis. They found that the morphine treatment enhanced apoptosis through both NO and ROS pathways [12]. The inducible nitric oxide synthase (iNOS) enzyme is one of the most important enzymes involved in the generation of NO from the amino acid L-arginine.
The blood-brain barrier (BBB) is a multifunctional interface separating the bloodstream from the brain interior. This barrier is crucial for maintaining brain homeostasis and allowing proper neuronal function, as well as for protecting the CNS from potentially harmful agents in the blood. The onset of BBB properties takes place during embryonic development as a microenvironment of neural stem cells, pericytes, and neurons provide developmental cues for induction of tight junctions and regulation of molecular permeability in developing endothelial cells. In adults, blood-brain barrier maintenance is a result of composite interactions between brain endothelial cells and resident neural cell types including astrocytes, pericytes, and neurons.