Hyperbaric Oxygen Attenuates Apoptosis and Decreases Inflammation in an Ischemic Wound Model

Zhang, Qixu; Chang, Qing; Cox, Robert A.; Gong, Xue-Mei; Gould, Lisa

doi:10.1038/jid.2008.53

Cited by 112 publications

(94 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[39][40][41][42][43] Bcl-2 proteins were previously shown to exert a neuroprotective effect by reducing the release of cytochrome c and blocking caspase activation. 44 Bcl-2 is not only involved in the pathway of apoptosis, but also participates in the regulation of the autophagy signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection of hyperbaric oxygen treatment for traumatic brain injury involving autophagy pathway in rats

Li¹,

Wen²,

Wang³

et al. 2017

View full text Add to dashboard Cite

Abstract:In the present study, we evaluated the changes in autophagy after hyperbaric oxygen (HBO) treatment for traumatic brain injury (TBI) and investigated whether autophagy takes part in the neuroprotection after HBO treatment. Male Sprague Dawley rats were assigned to four groups randomly: sham injury, sham injury and HBO, TBI, and TBI and HBO. The HBO rats received HBO treatment for 100 min immediately after injury. Rats were sacrificed at 24 h after the brain injury and the levels of cleaved caspase-3 and the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cells in the injured cortex were measured to determine cell death. The expression levels of autophagy-associated proteins were measured by immunohistochemistry and Western blotting to assess changes in autophagy. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positive cell density and cleaved caspase-3 expression were increased 24 h after TBI. These increases were suppressed by post-TBI HBO treatment. Immunohistochemistry and Western blotting of autophagy-associated proteins showed that TBI can induce autophagy and that HBO treatment can further upregulate the expression of autophagy makers, as shown by an increase in LC3, ATG-5, and Beclin-1 expression and reduction in P62 expression. In conclusion, HBO treatment can reduce apoptosis and further upregulate autophagy in the injured cortex after brain injury, and the autophagy pathway may take part in the neuroprotection provided by HBO treatment for TBI.

show abstract

Section: Discussionmentioning

confidence: 99%

Neuroprotection of hyperbaric oxygen treatment for traumatic brain injury involving autophagy pathway in rats

Li¹,

Wen²,

Wang³

et al. 2017

View full text Add to dashboard Cite

show abstract

“…A genes have been described and are a basis of its use in treating chronic (diabetic) wounds (31)(32)(33). Genes that were most upregulated by RT included the early response genes Fos, Jun and Egr1.…”

Section: Continued On Next Pagementioning

confidence: 99%

Gene Expression Analysis Reveals Inhibition of Radiation-Induced TGFβ-Signaling by Hyperbaric Oxygen Therapy in Mouse Salivary Glands

Spiegelberg

Swagemakers

IJcken

et al. 2014

Mol Med

View full text Add to dashboard Cite

A side effect of radiation therapy in the head and neck region is injury to surrounding healthy tissues such as irreversible impaired function of the salivary glands. Hyperbaric oxygen therapy (HBOT) is clinically used to treat radiation-induced damage but its mechanism of action is largely unknown. In this study, we investigated the molecular pathways that are affected by HBOT in mouse salivary glands two weeks after radiation therapy by microarray analysis. Interestingly, HBOT led to significant attenuation of the radiation-induced expression of a set of genes and upstream regulators that are involved in processes such as fibrosis and tissue regeneration. Our data suggest that the TGFβ-pathway, which is involved in radiation-induced fibrosis and chronic loss of function after radiation therapy, is affected by HBOT. On the longer term, HBOT reduced the expression of the fibrosis-associated factor α-smooth muscle actin in irradiated salivary glands. This study highlights the potential of HBOT to inhibit the TGFβ-pathway in irradiated salivary glands and to restrain consequential radiation induced tissue injury.

show abstract

“…HBOT'nin yara dokusunda VEGF seviyesini artırdığını gösteren çalışmalar olmakla birlikte, güncel bir çalışma HBOT'nin iskemik yara modelinde VEGF/KDR (Kinase insert domain receptor) sinyal yolunu aşağı regüle ederek VEGF seviyesini ve inflamasyonu azatlığını göstermiştir. 17,18 HBOT korneada hipoksiyi azaltarak VEGF salınımını azaltmış olabilir.…”

Section: Re Si̇munclassified

Utilization of Hyperbaric Oxygen in Treatment of Corneal Neovascularization Due to Herpes Simplex Keratitis: Case Report

Uzun¹,

Ayata²,

Mutluoğlu³

et al. 2012

Turkiye Klinikleri J Med Sci

View full text Add to dashboard Cite

erpes simpleks virüsü (HSV), en yaygın viral enfeksiyon kaynaklarından birisidir. HSV, gelişmiş ülkelerde enfeksiyona bağlı oluşan körlüklerin en sık nedenidir.1 Oküler HSV enfeksiyonu sonrası hastaların büyük çoğunluğunda kalıcı görme kusuru oluşmamakla birlikte, pek çok hastada korneal epitel enfeksiyonuna bağlı olarak korneal ülserasyon, derin stromal skarlaşma ve neovaskülarizasyon gelişir.

show abstract

Hyperbaric Oxygen Attenuates Apoptosis and Decreases Inflammation in an Ischemic Wound Model

Cited by 112 publications

References 52 publications

Neuroprotection of hyperbaric oxygen treatment for traumatic brain injury involving autophagy pathway in rats

Neuroprotection of hyperbaric oxygen treatment for traumatic brain injury involving autophagy pathway in rats

Gene Expression Analysis Reveals Inhibition of Radiation-Induced TGFβ-Signaling by Hyperbaric Oxygen Therapy in Mouse Salivary Glands

Utilization of Hyperbaric Oxygen in Treatment of Corneal Neovascularization Due to Herpes Simplex Keratitis: Case Report

Contact Info

Product

Resources

About