Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Female C57BL/6 mice were decapitated and their brains were removed and cultured at either 37 or 33 degrees C for 48 h to investigate whether or not moderate hypothermia alters the cytokine reactions in the ischemic brain. The interleukin-6 and interleukin-1alpha levels in the culture media were significantly elevated in a time-dependent manner. The interleukin-6 levels after the incubation at 33 degrees C were significantly lower than those at 37 degrees C. The interleukin-1alpha levels at 33 degrees C were significantly higher than those at 37 degrees C. The interleukin-1alpha levels incubated with interleukin-6 antibody were significantly higher than those without IL-6 antibody. At 37 degrees C, the mRNA expression of interleukin-6 was observed from 2 to 48 h after incubation, but the same expression of interleukin-1alpha was only detected until 12 h. Accordingly, the ischemic brain incubated at 33 degrees C showed a decreased interleukin-6 production in comparison with that at 37 degrees C and the level of interleukin-6 showed negative feedback for the production of interleukin-1alpha. The temperature should, therefore, be carefully considered when evaluating the cytokine reaction for cerebral ischemia.
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PMID:Moderate hypothermia alters interleukin-6 and interleukin-1alpha reactions in ischemic brain in mice. 1194 85

Experimental and clinical data suggest an important role of iron in cerebral ischaemia. We measured infarct volume and analysed the oxidative stress, and also the excitatory and inflammatory responses to brain injury in a rat stroke model after an increased oral iron intake. Permanent middle cerebral artery occlusion (MCAO) was performed in ten male Wistar rats fed with a diet containing 2.5% carbonyl iron for 9 weeks, and in ten control animals. Glutamate, interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) were determined in blood samples before and at 2, 4, 6, 8, 24 and 48 h after MCAO, and thiobarbituric acid reaction substances (TBARS) were analysed at 48 h. Infarct volume was measured at 48 h by image analysis on brain slices stained with 1% TTC. Tissue iron was measured by atomic absorption spectrophotometry. Infarct volume was 66% greater in the iron fed rats than in the control group (178+/-49 mm(3) versus 107+/-53 mm(3), P<0.01). Significant higher levels of glutamate, IL-6 and TNF-alpha were observed in the group with iron intake (peak values were obtained at 6, 8 and 4 h, respectively). Iron-fed animals also showed significantly higher levels of TBARS than those receiving a normal diet (6.52+/-0.59 vs. 5.62+/-0.86 micro mol/l, P=0.033) Liver iron stores (3500+/-199 vs. 352+/-28 micro g Fe/g, P<0.0001), but not brain iron stores (131 vs. 139 micro g Fe/g, P=0.617), were significantly higher in the iron fed rats group. These results suggest that iron intake is associated with larger infarct volumes after MCAO in the rat. This effect seems to be associated with higher oxidative stress, excitotoxicity and inflammatory responses.
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PMID:Iron intake increases infarct volume after permanent middle cerebral artery occlusion in rats. 1236 98

Oxidative stress is a major source of injury from cerebral ischemia and reperfusion. We hypothesized that a catalytic antioxidant AEOL 10150 [manganese (III) meso-tetrakis (di-N-ethylimidazole) porphyrin] would attenuate changes in brain gene expression in a mouse model of transient middle cerebral artery occlusion (MCAO). C57BL/6J mice were subjected to either sham surgery or 60 min of right MCAO. AEOL 10150 or phosphate-buffered saline was given intravenously 5 min after onset of reperfusion (n = 6 per group). Six hours later, parenchyma within the MCA distribution was harvested. RNA from the six brains in each group was pooled and mRNA expression determined using an Affymetrix murine MG_U74A v. 2.0 expression microarray. Each experiment was performed three times. The largest changes in expression occurred in stress response and inflammatory genes such as heat shock protein, interleukin-6, and macrophage inflammatory protein-2. Treatment with AEOL 10150 attenuated only the increase in expression of inflammatory genes. This suggests that AEOL 10150 protects brain by attenuating the immune response to ischemia and reperfusion.
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PMID:A catalytic antioxidant (AEOL 10150) attenuates expression of inflammatory genes in stroke. 1237 26

Although the function of fever is still unclear, it is now beyond doubt that body temperature influences the outcome of brain damage. An elevated body temperature is often found in stroke patients and denotes a bad prognosis. However, the pathophysiologic basis and treatment options of elevated body temperature after stroke are still unknown. Cerebral ischemia rapidly induced neuronal interleukin-6 (IL-6) expression in mice. In IL-6-deficient mice, body temperature was markedly decreased after middle cerebral artery occlusion (MCAO), but infarct size was comparable to that in control mice. If body temperature was controlled by external warming after MCAO, IL-6-deficient mice had a reduced survival, worse neurologic status, and larger infarcts than control animals. In cell culture, IL-6 exerted an antiapoptotic and neuroprotective effect. These data suggest that IL-6 is a key regulator of body temperature and an endogenous neuroprotectant in cerebral ischemia. Neuroprotective properties apparently compensate for its pyretic action after MCAO and enhance the safety of this endogenous pyrogen.
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PMID:Regulation of body temperature and neuroprotection by endogenous interleukin-6 in cerebral ischemia. 1267 17

Stroke is the second most common cause of death in developed countries. Carotid plaque disruption and distal embolization of atheromatous debris are the most common pathogenic mechanisms for cerebral ischemia from carotid atherosclerotic disease. Morphologic composition of the atherosclerotic plaque, rather than the stenotic severity, appears to be central in determining the risk of both plaque rupture and subsequent thrombosis. Histologic features of vulnerable plaques include a large lipid core, a thin fibrous cap, intraplaque hemorrhage, and an increased number of inflammatory cells, mostly monocyte-macrophages. Due to the catastrophic implications of thrombus formation and embolization on the arterial plaque, detection before major neurologic events occur is now a major goal of cardiovascular clinicians and researchers. New detection imaging techniques such as intravascular thermography, optical coherence tomography, photonic spectroscopy, and elastography have been developed in order to document atherosclerotic lesion composition. This review will focus on the new possibilities under investigation for vulnerable atherosclerotic carotid plaque detection by means of the serologic markers of plaque instability. New markers, such as pregnancy-associated protein A, P-selectin, interleukin-6 and interleukin-12, metalloproteinases, lipoprotein(a), and oxidation products have been reviewed. Most of the promising serologic markers in this article are still in a nascent phase of development and remain to be validated in clinical settings. However, these biohumoral markers, and their potential combination of techniques, may hold promise for the future characterization of the vulnerable plaque and moreover of the vulnerable patient.
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PMID:[Unstable carotid plaque: biochemical and cellular marker of vulnerability]. 1284 77

The onset of cerebral ischaemia triggers a cascade of proinflammatory molecular and cellular events. Clinical studies suggest that the strength of this acute response is important in early and late clinical outcomes, early clinical worsening, and extent of brain damage. Variables that are predictors of adverse stroke outcome include erythrocyte sedimentation rate, and levels of C-reactive protein (CRP), interleukin-6, tumour necrosis factor-alpha and intercellular adhesion molecule-1. Current data indicate that inflammation serves to fuel atherosclerosis and can act as the link between atherosclerosis and atherothrombosis. Growing evidence indicates that platelets act as prominent players in the inflammatory component of these disease processes. Thus, upon activation, platelets release a series of cytokines and growth factors and express CD40 ligand, which interacts with the CD40 receptor on other major cell types involved in atherosclerosis/atherothrombosis. In healthy volunteers, CD40L expression in platelets is not significantly inhibited by acetylsalicylic acid (ASA) alone, but is inhibited after treatment with the ADP-receptor antagonist clopidogrel or with clopidogrel plus ASA. Of a range of potential inflammatory biomarkers that have been reported in the literature, the best studied is CRP. Such biomarkers may have clinical utility for refined identification of patients at high risk for atherothrombosis in different arterial beds and for monitoring of therapeutic agents in clinical trials.
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PMID:Role of inflammation in stroke and atherothrombosis. 1473 Feb 51

Interleukin-6 (IL-6) is a potent, pleiotropic cytokine that plays a central role in host defense and acute inflammatory responses, exhibiting pro- and anti-inflammatory activities. However, little is known about the effect of acupuncture on IL-6 in inflammatory responses caused by cerebral ischemia-reperfusion. The objective of present study was to investigate the influence of electroacupuncture (EA) on IL-6 mRNA expression in ischemic rat brain, by means of reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. Data showed that EA stimulation significantly upregulated IL-6 mRNA levels in rat cortex and striatum following cerebral ischmia-reperfusion (P<0.05 vs. cerebral ischemia group, respectively), but nothing for sham-EA treatment. The result suggests that EA may partially participate in the regulation of inflammatory processes, and the mechanism of neuroprotective action of EA is implicated in modulation of IL-6 gene expression in cerebral ischemic injury.
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PMID:Expression of interleukin-6 mRNA in ischemic rat brain after electroacupuncture stimulation. 1499 53

Altered hypothalamo-pituitary-adrenal axis was reported in stroke patients; however, mechanisms responsible for this phenomenon are barely understood. Acute cerebral ischemia triggers interleukin-6 (IL-6) release into blood. Circulating IL-6 can stimulate hypothalamo-pituitary-adrenal axis. The goal of our study was to assess a relationship between serum IL-6 and cortisol in acute ischemic stroke. Twenty two patients with ischemic stroke and 17 controls were included. Serum samples were collected on the 2nd day of stroke at 6:00, 10:00 18:00, 22:00 h and at the same time points in control group. Cytokines and cortisol levels were measured using ELISA method. Serum IL-6 and cortisol levels were higher in stroke patients than in controls. Cortisol displayed diurnal variations in both stroke patients and controls. In contrast with control subjects, serum IL-6 levels did not display diurnal variations in stroke patients. In stroke patients, but not in controls, IL-6 level correlated significantly with cortisol level and morning serum IL-6 level independently predicted evening/night cortisol level. In conclusion, brain ischemia could stimulate IL-6 release in blood and in this way modulate hypothalamo-pituitary-adrenal axis.
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PMID:Serum interleukin-6 predicts cortisol release in acute stroke patients. 1505 41

Cerebral ischemia triggers interleukin-6 (IL-6) release into blood. IL-6 is a key mediator of acute phase reaction. Markers of acute phase reaction (C-reactive protein, fibrinogen, fever) have been linked to poor prognosis in stroke patients. Interleukin-6 soluble receptor (sIL-6R) can potentiate IL-6 pro-inflammatory activity. The aim of this study was to investigate the relationship between IL-6 and sIL-6R in stroke patients. Serum cytokine levels were measured in 18 stroke patients and 13 controls using the ELISA method. On the second day of stroke, IL-6 levels were significantly higher in stroke patients than in controls; sIL-6R levels did not differ significantly between groups. Three months after stroke, IL-6 levels did not differ significantly between groups; sIL-6R levels were significantly decreased in stroke patients when compared with that in controls and with levels in acute phase of stroke. Decreased sIL-6R early after stroke might reflect a regulatory mechanism attenuating inflammatory response.
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PMID:Serum interleukin-6 soluble receptor in relation to interleukin-6 in stroke patients. 1545 42

The aim of the present study was to ascertain whether the possible occurrence of overproduction of inducible nitric oxide synthase (iNOS)-dependent nitric oxide (NO) in the brain and inflammatory cytokines in the peripheral blood exhibited during heat stroke can be reduced by prior administration of Shengmai San, a Chinese herbal medicine. Aminoguanidine, an iNOS inhibitor, was evaluated at the same time as a reference (positive control). Urethane-anesthetized rats were exposed to heat stress (ambient temperature of 43 degrees C) to induce heat stroke. Control rats were exposed to 24 degrees C. Mean arterial pressure and cerebral blood flow after the onset of heat stroke were all significantly lower than in control rats. However, cerebral iNOS immunoreactivity and NO levels were all greater after the onset of heat stroke. The serum levels of interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha were all increased after the onset of heat stroke. Shengmai San (1.2 g/ml per rat) or aminoguanidine (30 micromol/ml per rat) was administered orally, daily, and consecutively for 7 days before the initiation of heat stress; and this significantly attenuated the heat stress-induced arterial hypotension, cerebral ischemia, and increased levels of brain iNOS-dependent NO production and serum cytokines formation. Shengmai San shared with the aminoguanidine almost the same efficacy in reducing iNOS-dependent NO and cytokines overproduction during heat stroke. These results suggest that Shengmai San or aminoguanidine protects against heat stroke-induced arterial hypotension and cerebral ischemia by inhibition of iNOS-dependent NO overproduction in the brain and excessive accumulation of several inflammatory cytokines in the peripheral blood stream.
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PMID:Shengmai San, a Chinese herbal medicine protects against rat heat stroke by reducing inflammatory cytokines and nitric oxide formation. 1587 82


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