Plasma proinflammatory and anti-inflammatory cytokine and catecholamine concentrations as predictors of neurological outcome in acute stroke patients

Oto, Jun; Suzue, Atsuhiko; Inui, Daisuke; Fukuta, Yoshimichi; Hosotsubo, Kikumi; Torii, Mayumi; Saijo, Nagahiro; Nishimura, Masaji

doi:10.1007/s00540-008-0639-x

Cited by 51 publications

(42 citation statements)

References 28 publications

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“…16 Its role in CNS pathology, however, is less well understood. For example, IL-6 may mediate motor coordination deficits after TBI, 25 appears associated with poor neurological outcome following hemorrhagic stroke, 26 yet may also be involved in regenerative and repair processes. 16 In this study, we show that NE blunted ERK MAPK upregulation in juvenile males, but blocked upregulation in juvenile females after FPI.…”

Section: Discussionmentioning

confidence: 99%

Retracted:Norepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Blockade of ERK MAPK and IL-6 in Juvenile Pigs

Armstead

Riley

Vavilala

2016

Journal of Neurotrauma

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Traumatic brain injury (TBI) contributes to morbidity in children, and boys are disproportionately represented. Cerebral autoregulation is impaired after TBI, contributing to poor outcome. Cerebral perfusion pressure (CPP) is often normalized by use of vasoactive agents to increase mean arterial pressure (MAP). In prior studies of 1-to 5-day-old newborn piglets, we observed that norepinephrine (NE) preferentially protected cerebral autoregulation and prevented hippocampal necrosis in females but not males after fluid percussion injury (FPI). The ERK isoform of mitogen activated protein kinase (MAPK) produces hemodynamic impairment after FPI, but less is known about the role of the cytokine interleukin-6 (IL-6). We investigated whether NE protects autoregulation and limits histopathology after FPI in older juvenile (4-week-old) pigs and the role of ERK and IL-6 in that outcome by sex. Results show that NE significantly protects autoregulation and prevents reduction in cerebral blood flow (CBF) in both male and female juvenile pigs after FPI; co-administration of the ERK antagonist U 0126 with NE fully protects both indices of outcome. Papaverine induced dilation was unchanged by FPI and NE. NE blunted ERK MAPK and IL-6 upregulation in both males and females after FPI. NE attenuated loss of neurons in CA1 and CA3 hippocampus of males and females after FPI. These data indicate that NE protects autoregulation and limits hippocampal neuronal cell necrosis via blockade of ERK and IL-6 after FPI in both male and female juvenile pigs. These data suggest that use of NE to improve outcome after TBI is both sex and age dependent.

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Section: Discussionmentioning

confidence: 99%

Retracted:Norepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Blockade of ERK MAPK and IL-6 in Juvenile Pigs

Armstead

Riley

Vavilala

2016

Journal of Neurotrauma

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“…Several studies have reported that proinflammatory cytokines, including TNF-α and IL-1β are elevated in serum in the early phase of acute ischemic stroke [26,27].…”

Section: Discussionmentioning

confidence: 99%

Baicalin Inhibits TLR2/4 Signaling Pathway in Rat Brain Following Permanent Cerebral Ischemia

Yang

Shu

et al. 2010

Inflammation

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Recent work from our laboratory demonstrated that baicalin attenuates inflammatory reaction and cerebral ischemia injury in rats. Toll-like receptor 2 and 4 (TLR2/4) and the downstream nuclear factor-kappa B (NF-κB) signaling pathway, which mediate the inflammatory reaction, are involved in the pathophysiological processes of cerebral ischemia. In this study, we investigated whether baicalin inhibits TLR2/4 signaling pathway in a rat model of permanent focal cerebral ischemia. Adult Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (MCAO). Baicalin was administered by intraperitoneally injected twice at 2 and 12 h after the onset of ischemia. Cerebral infarct area and infarct volume were measured 24 h after MCAO. Expression of TLR2/4, NF-κB, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) were determined by RT-PCR or western blot. NO and PGE2 production in rat brain were measured 24 h after MCAO. Serum content of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) were detected by ELISA. Baicalin reduced cerebral infarct area and infarct volume. Baicalin reduced the expression of TLR2/4 and NF-κB, decreased the expression and activity of iNOS and COX-2 in rat brain. Baicalin also attenuated the serum content of TNF-α and IL-1β. Our results suggest that baicalin inhibits the TLR2/4 signaling pathway in cerebral ischemia, which may be a mechanism underlying the baicalin's neuroprotection.

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“…3). As discussed above, hyperglycemia of diabetes or insulin deficiency-induced generation of ROSs and toxicity to vascular endothelial cells, and/or increased non-enzymatic glycosylation (NEG) of functional proteins (e.g., vascular or extracellular collagen, albumin, hemoglobulin) have been implicated in type-II diabetes complications (e.g., cardiovascular diseases, stroke, retinopathy, nephropathy, neuropathy, hypertension, high serum cholesterol-LDL, or atherosclerosis) [6,18,20,52,82,84,151,190,192,[195][196][197][198][199]. Circulating high glucose levels may induce additional oxidative stress in insulin-independent tissues (e.g., vasculature, retina, RPE, kidney, brain) by modifying or competing with transport, metabolism, and function of important solutes/metabolites or regenerative pathways in ascorbate (vitamin C)-semidehydroascorbate (SDA), pyridoxal phosphate-pyridoxine (vitamin B6), myo-inositol transport and/ or post-modifications of functional proteins, or alterations of NADP ?…”

Section: Metabolic Factors In Agingmentioning

confidence: 99%

“…3) [1,45,50,52,66,74,82,151,[183][184][185][186][187][188][189][190][191][192]. For example, age-associated hormonal alterations in thymic atrophy and associated declines in the genesis of subsets of T cells have been linked to immunoscenescence and chronic diseases [133,[183][184][185][186][187].…”

Section: Hormones and Growth Factorsmentioning

confidence: 99%

“…Detailed discussion on the role of various hormones or growth factors on organ system functions under normal or diseased conditions is beyond the scope of this communication. Suffice to note that hormones such as gonadal steroids (e.g., estrogen or progerstrone) or insulin play important roles in the reproductive systems, regulation of fluid homeostasis and/or metabolic pathways, immune responses to stress, as well as the physiology, function, and remodeling of bone, neuronal function, myelination, and neurogeneration of brain and CNS and/or membrane-associated fatty acid metabolism [20,21,131,[183][184][185][186][187][188][189][190][191][192][193][194]. For example, estrogen withdrawal has been associated with increased production of proinflammatory cytokines and alterations of bone resorption and remodeling and changes in essential fatty acid metabolism in many chronic diseases such as osteoporosis or atherosclerosis [21,184,[186][187][188].…”

Section: Hormones and Growth Factorsmentioning

confidence: 99%

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Inflammation, Aging, and Cancer: Tumoricidal Versus Tumorigenesis of Immunity

Khatami

2009

Cell Biochem Biophys

100

168

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Acute inflammation is a highly regulated defense mechanism of immune system possessing two well-balanced and biologically opposing arms termed apoptosis ('Yin') and wound healing ('Yang') processes. Unresolved or chronic inflammation (oxidative stress) is perhaps the loss of balance between 'Yin' and 'Yang' that would induce co-expression of exaggerated or 'mismatched' apoptotic and wound healing factors in the microenvironment of tissues ('immune meltdown'). Unresolved inflammation could initiate the genesis of many age-associated chronic illnesses such as autoimmune and neurodegenerative diseases or tumors/cancers. In this perspective 'birds' eye' view of major interrelated co-morbidity risk factors that participate in biological shifts of growth-arresting ('tumoricidal') or growth-promoting ('tumorigenic') properties of immune cells and the genesis of chronic inflammatory diseases and cancer will be discussed. Persistent inflammation is perhaps a common denominator in the genesis of nearly all age-associated health problems or cancer. Future challenging opportunities for diagnosis, prevention, and/or therapy of chronic illnesses will require an integrated understanding and identification of developmental phases of inflammation-induced immune dysfunction and age-associated hormonal and physiological readjustments of organ systems. Designing suitable cohort studies to establish the oxido-redox status of adults may prove to be an effective strategy in assessing individual's health toward developing personal medicine for healthy aging.

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Plasma proinflammatory and anti-inflammatory cytokine and catecholamine concentrations as predictors of neurological outcome in acute stroke patients

Abstract: In ischemic stroke, plasma cytokines and catecholamines were not predictors of neurological outcome at 1 month. In hemorrhagic stroke, high levels of IL-6 in the early phase indicated a poor neurological outcome.

Cited by 51 publications

References 28 publications

Retracted:Norepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Blockade of ERK MAPK and IL-6 in Juvenile Pigs

Retracted:Norepinephrine Protects Cerebral Autoregulation and Reduces Hippocampal Necrosis after Traumatic Brain Injury via Blockade of ERK MAPK and IL-6 in Juvenile Pigs

Baicalin Inhibits TLR2/4 Signaling Pathway in Rat Brain Following Permanent Cerebral Ischemia

Inflammation, Aging, and Cancer: Tumoricidal Versus Tumorigenesis of Immunity

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