Inhibition by Aminosalicylates of Lipid Peroxidation in Large Intestinal Mucosa after Mesenteric Ischemia/Reperfusion in the Rat.

Apoptosis was demonstrated to be a major mode of intestinal epithelial cell death caused by intestinal ischemia/reperfusion ( II / R ). Ceramide has been proposed as a messenger for apoptosis. The present study was aimed to investigate the effect of Ginkgo biloba extract 761 (EGb 761) pretreatment on II / R -induced intestinal mucosal epithelial apoptosis in rats and the mechanism related to ceramide. The rat model of II / R injury was produced by clamping superior mesenteric artery for 60 min followed by reperfusion for 180 min. Twenty four rats were randomly allocated into Sham, II / R and EGb + II / R groups. In EGb + II / R group, EGb 761 (100 mg/kg per day) was administered intragastrically for 7 days before the surgery. Animals in II / R and sham groups were treated with equal volume of normal saline solution. Intestinal mucosal epithelial apoptosis was detected via electron microscopy and TUNEL method. Lipid peroxidation in intestinal mucosa was determined by detecting the malondialdehyde level and the activities of superoxide dismutase and peroxidase glutathione. The ceramide generation and sphingomyelinase (SMase) mRNA expression in intestinal mucosa were determined by high performance, thin layer chromatography, and RT-PCR, respectively. II / R caused intestinal mucosal epithelial apoptosis and over-production of the ceramide accompanied by up-regulation of SMase mRNA expression and increases of lipid peroxidation. EGb 761 pretreatment significantly decreased apoptosis index, and concurrently reduced the ceramide generation accompanied by down-regulation of SMase expression and inhibition of lipid peroxidation. The findings indicate that EGb 761 pretreatment attenuates II / R -induced intestinal epithelial apoptosis, which might be attributable to its antioxidant action of mediating ceramide pathway.

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The ischemic preconditioning and postconditioning effect on the intestinal mucosa of rats undergoing mesenteric ischemia/reperfusion procedure

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502008000100005 ◽

2008 ◽

Vol 23 (1) ◽

pp. 22-28 ◽

Cited By ~ 31

Author(s):

Carlos Henrique Marques dos Santos ◽

Otoni Moreira Gomes ◽

José Carlos Dorsa Vieira Pontes ◽

Luciana Nakao Odashiro Miiji ◽

Marco Aurélio Feltrin Bispo

Keyword(s):

Intestinal Mucosa ◽

Ischemic Preconditioning ◽

Mesenteric Ischemia ◽

Tissue Injury ◽

Ischemia Reperfusion ◽

Ischemic Postconditioning ◽

Ischemia And Reperfusion ◽

Mean Values ◽

Group A ◽

Group B

PURPOSE: To evaluate the effect of the ischemic preconditioning and the ischemic postconditioning over the tissue injury in the intestinal mucosa of rats undergoing the procedure of mesenteric ischemia and reperfusion. METHODS: Thirty Wistar rats were studied, divided in three groups: group A, undergoing mesenteric ischemia (30 minutes) and reperfusion (60 minutes); group B, mesenteric ischemia and reperfusion preceded by ischemic preconditioning; group C, mesenteric ischemia and reperfusion and, before the beginning of reperfusion, the ischemic postconditioning was performed. At the end, a segment of the small intestine was dissected for histological analysis. The results were evaluated using the CHIU et al.6 classification followed by the statistic treatment. RESULTS: The mean values of the tissue injury levels were: group A, 3.5; group B, 1.2; and group C, 1. The difference between the result of group A with the results of groups B and C was considered statistically significant (p < 0,05). CONCLUSION: The ischemic preconditioning and postconditioning are able to minimize the tissue injury in the intestines of rats that underwent the procedure of mesenteric ischemia and reperfusion.

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Captopril increases endothelin serum concentrations and preserves intestinal mucosa after mesenteric ischemia-reperfusion injury

Research in Experimental Medicine ◽

10.1007/bf02576396 ◽

1994 ◽

Vol 194 (1) ◽

pp. 339-348 ◽

Cited By ~ 17

Author(s):

Oĝuzhan Büyükgebiz ◽

A. Özdemir Aktan ◽

Cumhur Yeĝen ◽

A. Süha Yalçin ◽

Gonca Haklar ◽

...

Keyword(s):

Reperfusion Injury ◽

Intestinal Mucosa ◽

Mesenteric Ischemia ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Serum Concentrations

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Mibefradil, a T-Type Ca2+ Channel Blocker, Protects Against Mesenteric Ischemia-Reperfusion-Induced Oxidative Injury and Histologic Alterations in Intestinal Mucosa in Rats

Digestive Diseases and Sciences ◽

10.1007/s10620-005-9060-6 ◽

2006 ◽

Vol 51 (8) ◽

pp. 1454-1460 ◽

Cited By ~ 5

Author(s):

Hayrettin Ozturk ◽

Hulya Ozturk ◽

Hatun Duran ◽

Ali Kemal Uzunlar

Keyword(s):

Intestinal Mucosa ◽

Mesenteric Ischemia ◽

Channel Blocker ◽

Ischemia Reperfusion ◽

Oxidative Injury

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Lymphatic Diversion Prevents Myocardial Edema Following Mesenteric Ischemia/Reperfusion

Microcirculation ◽

10.1080/10739680490266135 ◽

2004 ◽

Vol 11 (1) ◽

pp. 1-8 ◽

Cited By ~ 11

Author(s):

Charles S. Cox ◽

Uwe M. Fischer ◽

Steven J. Allen ◽

Glen A. Laine

Keyword(s):

Mesenteric Ischemia ◽

Ischemia Reperfusion ◽

Myocardial Edema

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Kaempferol Ameliorates Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Ferroptosis by Activating Nrf2/SLC7A11/GPX4 Axis

Biomolecules ◽

10.3390/biom11070923 ◽

2021 ◽

Vol 11 (7) ◽

pp. 923

Author(s):

Yuan Yuan ◽

Yanyu Zhai ◽

Jingjiong Chen ◽

Xiaofeng Xu ◽

Hongmei Wang

Keyword(s):

Lipid Peroxidation ◽

Cell Death ◽

Antioxidant Capacity ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Glucose Deprivation ◽

Oxygen Glucose Deprivation ◽

Related Factor ◽

Protective Effects

Kaempferol has been shown to protect cells against cerebral ischemia/reperfusion injury through inhibition of apoptosis. In the present study, we sought to investigate whether ferroptosis is involved in the oxygen-glucose deprivation/reperfusion (OGD/R)-induced neuronal injury and the effects of kaempferol on ferroptosis in OGD/R-treated neurons. Western blot, immunofluorescence, and transmission electron microscopy were used to analyze ferroptosis, whereas cell death was detected using lactate dehydrogenase (LDH) release. We found that OGD/R attenuated SLC7A11 and glutathione peroxidase 4 (GPX4) levels as well as decreased endogenous antioxidants including nicotinamide adenine dinucleotide phosphate (NADPH), glutathione (GSH), and superoxide dismutase (SOD) in neurons. Notably, OGD/R enhanced the accumulation of lipid peroxidation, leading to the induction of ferroptosis in neurons. However, kaempferol activated nuclear factor-E2-related factor 2 (Nrf2)/SLC7A11/GPX4 signaling, augmented antioxidant capacity, and suppressed the accumulation of lipid peroxidation in OGD/R-treated neurons. Furthermore, kaempferol significantly reversed OGD/R-induced ferroptosis. Nevertheless, inhibition of Nrf2 by ML385 blocked the protective effects of kaempferol on antioxidant capacity, lipid peroxidation, and ferroptosis in OGD/R-treated neurons. These results suggest that ferroptosis may be a significant cause of cell death associated with OGD/R. Kaempferol provides protection from OGD/R-induced ferroptosis partly by activating Nrf2/SLC7A11/GPX4 signaling pathway.

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Real-time monitoring of endogenous lipid peroxidation by exhaled ethylene in patients undergoing cardiac surgery

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00168.2014 ◽

2014 ◽

Vol 307 (7) ◽

pp. L509-L515 ◽

Cited By ~ 16

Author(s):

Simona M. Cristescu ◽

Rudolf Kiss ◽

Sacco te Lintel Hekkert ◽

Miles Dalby ◽

Frans J. M. Harren ◽

...

Keyword(s):

Lipid Peroxidation ◽

Cardiac Surgery ◽

Real Time ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Artery Bypass ◽

Organ Injury ◽

Real Time Monitoring ◽

Myocardial Ischemia And Reperfusion ◽

Endogenous Lipid

Pulmonary and systemic organ injury produced by oxidative stress including lipid peroxidation is a fundamental tenet of ischemia-reperfusion injury, inflammatory response to cardiac surgery, and cardiopulmonary bypass (CPB) but is not routinely measured in a surgically relevant time frame. To initiate a paradigm shift toward noninvasive and real-time monitoring of endogenous lipid peroxidation, we have explored pulmonary excretion and dynamism of exhaled breath ethylene during cardiac surgery to test the hypothesis that surgical technique and ischemia-reperfusion triggers lipid peroxidation. We have employed laser photoacoustic spectroscopy to measure real-time trace concentrations of ethylene from the patient breath and from the CPB machine. Patients undergoing aortic or mitral valve surgery-requiring CPB ( n = 15) or off-pump coronary artery bypass surgery (OPCAB) ( n = 7) were studied. Skin and tissue incision by diathermy caused striking (>30-fold) increases in exhaled ethylene resulting in elevated levels until CPB. Gaseous ethylene in the CPB circuit was raised upon the establishment of CPB (>10-fold) and decreased over time. Reperfusion of myocardium and lungs did not appear to enhance ethylene levels significantly. During OPCAB surgery, we have observed increased ethylene in 16 of 30 documented reperfusion events associated with coronary and aortic anastomoses. Therefore, novel real-time monitoring of endogenous lipid peroxidation in the intraoperative setting provides unparalleled detail of endogenous and surgery-triggered production of ethylene. Diathermy and unprotected regional myocardial ischemia and reperfusion are the most significant contributors to increased ethylene.

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