Down regulation of COX-2 is involved in hyperbaric oxygen treatment in a rat transient focal cerebral ischemia model

Yin, Wei; Badr, Ahmed; Mychaskiw, George; Zhang, Junyi

doi:10.1016/s0006-8993(01)03304-2

Cited by 105 publications

(83 citation statements)

References 20 publications

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“…2,3,7-Triphenyltetrazolium chloride (TTC) staining was performed at 7 days after reperfusion as described previously (Badr et al, 2001b;Yin et al, 2002). Coronal sections of the brain (2 mm thick) were cut and immersed in a 2% solution of TTC for 30 minutes at 37°C.…”

Section: Ttc Stainingmentioning

confidence: 99%

Inhibition of Apoptosis by Hyperbaric Oxygen in a Rat Focal Cerebral Ischemic Model

Yin

Zhou

Kusaka

et al. 2003

J Cereb Blood Flow Metab

142

109

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Summary: The hypothesis was tested that hyperbaric oxygen therapy (HBO) reduced brain infarction by preventing apoptotic death in ischemic cortex in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) and subsequently were exposed to HBO (2.5 atmospheres absolute) for 2 h, at 6 h after reperfusion. Rats were killed and brain samples were collected at 24, 48, 72 h, and 7 days after reperfusion. Neurologic deficits, infarction area, and apoptotic changes were evaluated by clinical scores, 2,3,7-triphenyltetrazolium chloride staining, caspase-3 expression, DNA fragmentation assay, and terminal deoxynucleotidyl transferase-mediated 2Ј-deoxyuridine 5Ј-triphosphate-biotin nick end labeling (TUNEL)-hematoxylin and eosin (H&E) costaining. In MCAO/R without HBO treatment animals, DNA fragmentation was observed in injured cortex at 24, 48, and 72 h but not in samples at 7 days after reperfusion. Double labeling of brain slides with NeuN and caspase-3 demonstrated neurons in the injured cortex labeled with caspase-3. TUNEL+H&E costaining revealed morphologic apoptotic changes at 24, 48, and 72 h after reperfusion. Hyperbaric oxygen therapy abolished DNA fragmentation and reduced the number of TUNEL-positive cells. Hyperbaric oxygen therapy reduced infarct area and improved neurologic scores at 7 days after reperfusion. One of the molecular mechanisms of HBO-induced brain protection is to prevent apoptosis, and this effect of HBO might preserve more brain tissues and promote neurologic functional recovery. Key Words: Cerebral ischemia-HBO-Apoptosis-Infarction.Cell death, either necrosis or apoptosis, occurred in the brain tissues during the first few days after cerebral ischemia (Johnson et al., 1995;Rink et al., 1995). Necrotic cell death is characterized by cellular swelling, nuclear pyknosis with karyorrhexis, and cytoplasmic eosinophilia (Searle et al., 1982;Dure et al., 1995). Apoptosis is characterized by morphologic and biochemical features, including cell shrinkage, formation of apoptotic bodies, and extensive internucleosomal fragmentation (Johnson Jr et al., 1995, 1996. Cerebral hypoxia/ischemia produces a cascade of interconnected pathologic processes, including changes in intracellular Ca 2+ , excitatory amino acid, oxidative stress, and inflammatory response, and leads to apoptosis in the ischemic penumbra (Okamoto et al., 1993;Johnson Jr et al., 1995;Rink et al., 1995;Leker et al., 1999). Prevention of apoptosis becomes a therapeutic strategy to preserve brain tissues and promote functional recovery (Graham and Chen, 2001).Hyperbaric oxygen therapy (HBO) is a potent mean to increase the amount of oxygen dissolved in blood plasma and thereby delivered to the ischemic brain. However, HBO is not currently used in acute stroke management, partially due to the insufficient information of its molecular mechanisms (Kawamura et al., 1990;Anderson et al., 1991;Mink and Dutka, 1995;Nighoghossian and Trouillas, 1997;Chuba et al., 1997;Ro...

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Section: Ttc Stainingmentioning

confidence: 99%

Inhibition of Apoptosis by Hyperbaric Oxygen in a Rat Focal Cerebral Ischemic Model

Yin

Zhou

Kusaka

et al. 2003

J Cereb Blood Flow Metab

142

109

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“…In general, the effects of HBO are similar to those accomplished with immunosuppressant drugs, leading to a decrease in inflammatory response in the body [4,35], which is achieved by reducing the synthesis of inflammatory mediators such as nitric oxide (NO) [36,37], prostaglandin E2 (PGE2) [38,39], tumour necrosis factor α (TNF-α), interleukin 1β and 12 (IL-1β, IL-12) and interferon γ (IFN-γ) [9,16,18,23,38,40,41], as well as a reduced expression of cyclooxygenase-type 2 mRNA (COX-2), an enzyme involved in inflammation [42]. In addition to the inhibitory effect on the synthesis of proinflammatory cytokines, the consequence of hyperbaric oxygen therapy is an increased release of antiinflammatory cytokines such as interleukin 10 (IL-10) [9,43].…”

Section: Research Results and Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Therapy (HBOT) as a Therapeutic Option for Patients with Atopic Dermatitis (AD) – Own Experiences and Literature Review

Olszański¹,

Konarski

Siermontowski³

2017

Polish Hyperbaric Research

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The paper discusses the treatment results of ten patients with severe atopic dermatitis (AD) who did not respond to standard pharmacotherapy and underwent hyperbaric oxygen therapy (HBOT). Each patient was subject to 10 oxygen exposures at pO2 2.5 ATA (~ 250 kPa) with the duration time of 60 minutes. In the period of implementation of the hyperbaric procedures the general treatment plan was suspended for all patients while maintaining typical local treatment. Clinical evaluation was performed in the study group as well as determination of levels of immunoglobulins: IgA, IgG, IgM and IgE and C3 and C4 complement. All patients indicated clinical improvement and a decreased IgE immunoglobulin and complement C3 level upon the completion of the exposure cycle. Taking into account the authors' own observations and data from literature, an overall improvement in the clinical status and a decrease in the level of immunoglobulin E and C3 complement following a cycle of exposures may be indicative of an immunomodulating HBOT effect on AD, whereas hyperbaric oxygenation may constitute a therapeutic option for some patients with AD, especially those exhibiting a poor response to standard treatment.

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“…Improved survival, function and behavior in HBO treated animals were also reported (2,3,5,6,9,10,11,13,14,15,16,17,18,19). Several of the studies used a model involving the nearly immediate institution of HBO, starting treatment immediately (2,9,13,20) or within minutes (8,11,12,14) of ischemia. In models more consistent with conditions in a clinical setting, however, HBO delayed until several hours after the beginning of ischemia was also been shown to be effective.…”

Section: Hyperbaric Oxygen For Stroke Protocol Backgroundmentioning

confidence: 88%

“…HBO therapy of cerebral ischemia has been shown to be effective in numerous animal models of AIS (1). Animals treated with HBO after either temporary (2,3,4,5,6,7,8,9,10) or permanent (9, 10) cerebral arterial occlusion showed decreased infarct size versus controls. Improved survival, function and behavior in HBO treated animals were also reported (2,3,5,6,9,10,11,13,14,15,16,17,18,19).…”

Section: Hyperbaric Oxygen For Stroke Protocol Backgroundmentioning

confidence: 99%

“…In models more consistent with conditions in a clinical setting, however, HBO delayed until several hours after the beginning of ischemia was also been shown to be effective. (3,4,7,8,10,15) There may, though, be an early window of opportunity after ischemia for HBO to be effective. One study found that treatment after 1 or 3 hours of ischemia decreased infarct size and improved outcome behaviorally, whereas, treatment after 4 hours had no effect on infarct size.…”

Section: Hyperbaric Oxygen For Stroke Protocol Backgroundmentioning

confidence: 99%

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Hyperbaric Oxygen for Stroke

Helms¹,

Whelan²

2012

Acute Ischemic Stroke

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Down regulation of COX-2 is involved in hyperbaric oxygen treatment in a rat transient focal cerebral ischemia model

Cited by 105 publications

References 20 publications

Inhibition of Apoptosis by Hyperbaric Oxygen in a Rat Focal Cerebral Ischemic Model

Inhibition of Apoptosis by Hyperbaric Oxygen in a Rat Focal Cerebral Ischemic Model

Hyperbaric Oxygen Therapy (HBOT) as a Therapeutic Option for Patients with Atopic Dermatitis (AD) – Own Experiences and Literature Review

Hyperbaric Oxygen for Stroke

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