Effect of hyperbaric oxygen therapy on the intestinal ischemia reperfusion injury

Daniel, Rosemary Aparecida Furlan; Cardoso, V.K.; Gois, Emanuel; Parra, Rogério Serafim; Garcia, Sérgio Britto; Rocha, José Joaquim Ribeiro da; Féres, Omar

doi:10.1590/s0102-86502011000600010

Cited by 21 publications

(14 citation statements)

References 30 publications

(24 reference statements)

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“…In the present study, the histological features occurring in the I/R group were characterized by the shortening of the villi, loss of villous epithelium, multiple erosions, inflammatory cell infiltration, necrosis and hemorrhage into the intestinal wall. Our findings were consistent with those in previous studies on intestinal I/R in animals [22]–[23]. Our results indicated that the mucosal lesions (grade 4, 5) were more severe at 6 h after intestinal I/R and KGF significantly decreased the mucosal lesions (grade 2, 3), which suggested that KGF could improve the mucosal morphology in a mouse model of acute intestinal I/R.…”

Section: Discussionsupporting

confidence: 92%

Keratinocyte Growth Factor Improves Epithelial Structure and Function in a Mouse Model of Intestinal Ischemia/Reperfusion

et al. 2012

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BackgroundIntestinal ischemia/reperfusion (I/R) induces the desquamation of the intestinal epithelium, increases the intestinal permeability, and in patients often causes fatal conditions including sepsis and multiple organ failure. Keratinocyte growth factor (KGF) increases intestinal growth, although little is known about KGF activity on intestinal function after intestinal I/R. We hypothesized that KGF administration would improve the intestinal function in a mouse model of intestinal I/R.MethodsAdult C57BL/6J mice were randomized to three groups: Sham, I/R group and I/R+KGF group. Mice were killed on day 5, and the small bowel was harvested for histology, wet weight, RNA and protein content analysis. Epithelial cell (EC) proliferation was detected by immunohistochemistry for PCNA, and apoptosis was determined by TUNEL staining. The expressions of Claudin-1 and ZO-1 were detected by immunohistochemistry. Epithelial barrier function was assessed with transepithelial resistance (TER).ResultsKGF significantly increased the intestinal wet weight, contents of intestinal protein and RNA, villus height, crypt depth and crypt cell proliferation, while KGF resulted in the decrease of epithelial apoptosis. KGF also stimulated the recovery of mucosal structures and attenuated the disrupted distribution of TJ proteins. Moreover, KGF attenuated the intestinal I/R-induced decrease in TER and maintained the intestinal barrier function.ConclusionKGF administration improves the epithelial structure and barrier function in a mouse model of intestinal I/R. This suggests that KGF may have clinical applicability.

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Section: Discussionsupporting

confidence: 92%

Keratinocyte Growth Factor Improves Epithelial Structure and Function in a Mouse Model of Intestinal Ischemia/Reperfusion

et al. 2012

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“…In our study, we believe that hyperbaric oxygenation preserved the collagen fibers in the regions investigated due to inhibition of the inflammatory process. Numerous studies report that the improvement patchwork undergoing HBO is due to the significant increase in vascular angiogenesis, since it enhances the production of vascular endothelial growth factor (VEGF), which helps to provide nutrients to the cells, blockage of enzyme activation and the decrease in the collagen metabolism 4,18 .…”

Section: Microscopic Evaluationmentioning

confidence: 99%

Action of hyperbaric oxygenation in the rat skin flap

et al. 2015

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PURPOSE:To evaluate the morphology, necrotic area and collagen content in skin flaps of rats subjected to hyperbaric oxygenation (HBO). METHODS:Forty adult rats were divided into four groups: GEC -epilated; GE/HBO -epilated subjected to HBO; GER -epilated submitted to skin flap (2 cm in width /8 cm length in the dorsal area) and GER/HBO -epilated, subjected to skin flap and HBO. HBO (2.4 ATA) was performed for two hours during seven consecutive days. In the eighth day, the rats were anesthetized and the skin flaps were removed and separated into three portions, relative to pedicle fixation. The material fixed in 10% formalin was processed for paraffin embedding; sections were stained by H.E and subjected to picrosirius-red method. The slides examined under light microscopy for evaluation of the collagen content in polarized light microscope and ImageLab ® software (Bio-Rad). RESULTS:The data showed larger area of necrosis and lower levels of collagen in the three regions of the GER group, whereas in the GER/HBO group the collagen content was similar to the GEC and GE/HBO groups. CONCLUSION:Hyperbaric oxygenation reduced the area of necrosis and preserved the morphology and collagen content in skin flaps of rats.

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“…HBOT can attenuate inflammatory responses by altering cytokine production and signaling (Alex et al 2005;Daniel et al 2011;Lin et al 2012). The anti-inflammatory action of HBOT may arise in part from its ability to increase the expression of antioxidant genes and other cellular defense genes through the induction of a noncytotoxic oxidative stimulus (Matsunami et al 2009(Matsunami et al , 2011Simsek et al 2011;Godman et al 2010a, b;He et al 2011).…”

mentioning

confidence: 99%

Hyperbaric oxygen therapy (HBOT) suppresses biomarkers of cell stress and kidney injury in diabetic mice

Verma

Chopra

Giardina

et al. 2015

Cell Stress and Chaperones

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The disease burden from diabetic kidney disease is large and growing. Effective therapies are lacking, despite an urgent need. Hyperbaric oxygen therapy (HBOT) activates Nrf2 and cellular antioxidant defenses; therefore, it may be generally useful for treating conditions that feature chronic oxidative tissue damage. Herein, we determined how periodic exposure to oxygen at elevated pressure affected type 2 diabetes mellitus-related changes in the kidneys of db/db mice. Two groups of db/db mice, designated 2.4 ATA and 1.5 ATA, were treated four times per week with 100 % oxygen at either 1.5 or 2.4 ATA (atmospheres absolute) followed by tests to assess kidney damage and function. The sham group of db/db mice and the Hets group of db/+ mice were handled but did not receive HBOT. Several markers of kidney damage were reduced significantly in the HBOT groups including urinary biomarkers neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C (CyC) along with significantly lower levels of caspase-3 activity in kidney tissue extracts. Other stress biomarkers also showed trends to improvement in the HBOT groups, including urinary albumin levels. Expressions of the stress response genes NRF2, HMOX1, MT1, and HSPA1A were reduced in the HBOT groups at the end of the experiment, consistent with reduced kidney damage in treated mice. Urinary albumin/creatinine ratio (ACR), a measure of albuminuria, was significantly reduced in the db/db mice receiving HBOT. All of the db/db mouse groups had qualitatively similar changes in renal histopathology. Glycogenated nuclei, not previously reported in db/db mice, were observed in these three experimental groups but not in the control group of nondiabetic mice. Overall, our findings are consistent with therapeutic HBOT alleviating stress and damage in the diabetic kidney through cytoprotective responses. These findings support an emerging paradigm in which tissue oxygenation and cellular defenses effectively limit damage from chronic oxidative stress more effectively than chemical antioxidants.

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Effect of hyperbaric oxygen therapy on the intestinal ischemia reperfusion injury

Cited by 21 publications

References 30 publications

Keratinocyte Growth Factor Improves Epithelial Structure and Function in a Mouse Model of Intestinal Ischemia/Reperfusion

Keratinocyte Growth Factor Improves Epithelial Structure and Function in a Mouse Model of Intestinal Ischemia/Reperfusion

Action of hyperbaric oxygenation in the rat skin flap

Hyperbaric oxygen therapy (HBOT) suppresses biomarkers of cell stress and kidney injury in diabetic mice

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