Melatonin prevents focal rat cerebellum injury as assessed by induction of heat shock protein (HO-1) following subarachnoid injections of lysed blood

Martinez-Cruz, Francisco; Espinar, Auxiliadora; Pozo, David; Osuna, Carmen; Guerrero, Juan M.

doi:10.1016/s0304-3940(02)00884-4

Cited by 25 publications

(24 citation statements)

References 13 publications

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“…There have been many studies focusing on the neurovascular protective effects of melatonin in SAH models [5–7, 16]. Most of these previous studies used the one-hemorrhage SAH model; however in the current research, we used the two-hemorrhage model that was more suitable for SAH-cerebral vasospasm research than one-hemorrhage model because the time course of vasospasm accurately correlates with that observed in humans, which peaked on day 5 after SAH [17].…”

Section: Discussionmentioning

confidence: 99%

Influence of Melatonin on Cerebrovascular Proinflammatory Mediators Expression and Oxidative Stress Following Subarachnoid Hemorrhage in Rabbits

Fang

Chen

Zhu

et al. 2009

Mediators of Inflammation

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The aim of this study is to analyze whether melatonin administration influenced the nuclear factor-kappa B (NF-κB) activity, proinflammatory cytokines expression, and oxidative response in the basilar artery after SAH. A total of 48 rabbits were randomly divided into four groups: control group, SAH group, SAH + vehicle group, and SAH + melatonin group. All SAH animals were subjected to injection of autologous blood into cisterna magna twice on day 0 and day 2. The melatonin was administered intraperitoneally at a dose of 5 mg/kg/12 h simultaneously with SAH from day 0 to day 5. The basilar arteries were extracted on day 5 after SAH. As a result, we found that vascular inflammation and oxidative stress were induced in all SAH animals. In animals given melatonin, basilar arterial NF-κB and pro-inflammatory cytokines were decreased in comparison to vehicle-treated animals. Measures of oxidative stress also showed significant downregulation after melatonin treatment. Furthermore, administration of melatonin prevented vasospasm on day 5 following SAH. In conclusion, post-SAH melatonin administration may attenuate inflammatory response and oxidative stress in the spasmodic artery, and this may be one mechanism involved in the therapeutic effect of melatonin on the subsequent vasospasm after SAH.

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Section: Discussionmentioning

confidence: 99%

Influence of Melatonin on Cerebrovascular Proinflammatory Mediators Expression and Oxidative Stress Following Subarachnoid Hemorrhage in Rabbits

Fang

Chen

Zhu

et al. 2009

Mediators of Inflammation

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“…This experiment is only one of a few to test the effects of melatonin ( N ‐acetyl‐5‐methoxytryptamine) in experimental models of SAH, and it is the first to test the efficacy of melatonin in treating acute brain injury after SAH [40, 41]. Aydin et al.…”

Section: Discussionmentioning

confidence: 99%

“…Martinez‐Cruz et al. [41] evaluated the antioxidant effects of melatonin in an injection model of SAH in rats, and found that melatonin reduced the oxidative stress as measured by the induction of heat shock proteins. Our experiment is the first to evaluate melatonin in the endovascular filament model of SAH, which more closely represents the pathophysiology of human SAH [36].…”

Section: Discussionmentioning

confidence: 99%

“…Severe SAH created a significant increase in brain water content (*P < 0.05 versus SHAM, ANOVA). models of SAH, and it is the first to test the efficacy of melatonin in treating acute brain injury after SAH [40,41]. Aydin et al [40] found that melatonin reduced cerebral vasospasm and cerebrovascular endothelial apoptosis following experimental SAH in rabbits, but there were no reports on mortality or neurologic outcome.…”

Section: Discussionmentioning

confidence: 99%

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Melatonin decreases mortality following severe subarachnoid hemorrhage

Ayer¹,

Sugawara²,

Chen³

et al. 2007

Journal of Pineal Research

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Aneurysmal subarachnoid hemorrhage (SAH) is a devastating disease that is associated with significant morbidity and mortality. There is substantial evidence to suggest that oxidative stress is significant in the development of acute brain injury following SAH. Melatonin is a strong antioxidant that has low toxicity and easily passes through the blood-brain barrier. Previous studies have shown that melatonin provides neuroprotection in animal models of ischemic stroke. This study hypothesizes that melatonin will provide neuroprotection when administered 2 hr after SAH. The filament perforation model of SAH was performed in male Sprague-Dawley rats weighing between 300 and 380 g. Melatonin (15 or 150 mg/kg), or vehicle was given via intraperitoneal injection 2 hr after SAH. Mortality and neurologic deficits were assessed 24 hr after SAH. A significant reduction in 24-hr mortality was seen following treatment with high dose melatonin. There was no improvement in neurologic scores with treatment. Brain water content and lipid peroxidation were measured following the administration of high dose melatonin to identify a mechanism for the increased survival. High dose melatonin tended to reduce brain water content following SAH, but had no effect on the lipid peroxidation of brain samples. Large doses of melatonin significantly reduces mortality and brain water content in rats following SAH through a mechanism unrelated to oxidative stress.

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“…Both caffeic acid and curcumin are plant extracts that exert potent anti-inflammatory effects, which have also been shown to function through upregulation of HO-1 (53) (see Table 1). Oxidative stress FGF (178) Endoplasmic reticulum stress (205) HGF (179) Heavy metals (206) VEGF (180) Oxidized LDL (207,208) NGF (181,182) Hydroperoxide (209) TGF-β (183) Diphenyl-and dithiol-compounds (210) KGF (184) HNE (208, 211) BMP-7 (185) Dieldrin (212) PDGF (186) Cigarette smoke extract (213) Alcohol ( Physiological changes Estrogen (188) Hypertonic saline (osmotic pressure; 230) Prolactin (189) Transient glucose deprivation (231) Adrenocorticotrophin (190,191) Acidosis (232) Atrial natriuretic peptide (192) Nitric oxide (233-242) Melatonin (193) Cytokine (LPS, IFN-γ , TNF-α, IL-1β; 243) Angiotensin II (55,194) Mechanical shear stress (244, 245) Progesterone (195) Glucocorticoid (regulation of HO-2; 196) Chorionic gonadotropin (testis) (197) Abbreviations: FGF, fibroblast growth factor; HGF, hepatocyte growth factor; VEGF, vascular endothelial cell growth factor; NGF, nerve growth factor; TGF, transforming growth factor; KGF, keratinocyte growth factor; BMP, bone morphogenic protein; PDGF, platelet derived growth factor; oxLDL, oxidized low density lipoprotein; HNE, hydroxynonenal; LPS, lipopolysaccharide; IFN, interferon; IL, interleukin; UV, ultraviolet.…”

Section: Synergistic Inductionmentioning

confidence: 99%

Co as a Cellular Signaling Molecule

Kim

Ryter²,

Choi³

2006

Annu. Rev. Pharmacol. Toxicol.

375

361

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Many biological functions of heme oxygenase (HO), such as cytoprotection against oxidative stress, vasodilation, neurotransmission in the central or peripheral nervous systems, and anti-inflammatory, anti-apoptotic, or anti-proliferative potential, have been attributed to its enzymatic byproduct carbon monoxide (CO), although roles for biliverdin/bilirubin and iron have also been proposed. In addition to these well-characterized effects, recent findings reveal that HO-derived CO may act as an oxygen sensor and circadian modulator of heme biosynthesis. In lymphocytes, CO may participate in regulatory T cell function. A number of the known signaling effects of CO depend on stimulation of soluble guanylate cyclase and/or activation of mitogen-activated protein kinases (MAPK). Furthermore, modulation of caveolin-1 status may serve as an essential component of certain aspects of CO action, such as growth control. In this review, we summarize recent findings of the beneficial or detrimental effects of endogenous CO with an emphasis on the signaling pathways and downstream targets that trigger the action of this gas.

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Melatonin prevents focal rat cerebellum injury as assessed by induction of heat shock protein (HO-1) following subarachnoid injections of lysed blood

Cited by 25 publications

References 13 publications

Influence of Melatonin on Cerebrovascular Proinflammatory Mediators Expression and Oxidative Stress Following Subarachnoid Hemorrhage in Rabbits

Influence of Melatonin on Cerebrovascular Proinflammatory Mediators Expression and Oxidative Stress Following Subarachnoid Hemorrhage in Rabbits

Melatonin decreases mortality following severe subarachnoid hemorrhage

Co as a Cellular Signaling Molecule

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