Remote post-conditioning and allopurinol reduce ischemia-reperfusion injury in an infra-renal ischemia model

Background: The aim of this study was to evaluate the effects of the antioxidant allopurinol and ischemic post-conditioning on the deleterious effects of ischemia followed by reperfusion (I/R) in a standardized model of ischemia involving infra-renal aortic occlusion in rats. Methods: The animals were randomly divided into five groups: (A) animals not subjected to ischemia; (B) animals subjected to 2 h of ischemia and reperfusion only once; (C) animals given an allopurinol dose by gavage, then subjected to 2 h of ischemia and reperfusion only once; (D) animals subjected to 2 h of ischemia and post-conditioning and (E) animals that received allopurinol, then subjected to 2 h of ischemia and post-conditioning. The blood samples and small intestine segments were harvested for analysis after 3 days. Results: The protective effects of the use of allopurinol and ischemic post-conditioning were observed by measuring aspartate aminotransferase, alanine aminotransferase and lactate levels. The benefits of post-conditioning were evident from the total antioxidant capacity and creatinine levels, but these could not ascertain any positive effects of allopurinol. The histological analysis of mesentery revealed that both methods were effective in minimizing the harmful effects of the ischemia and reperfusion process. Conclusion: Individual protocols significantly reduced I/R systemic injuries, but no additional protection was observed when the two strategies were combined.

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Protective Effects of Hypericum perforatum and Quercetin in a Rat Model of Ischemia/Reperfusion Injury of Testes

European Journal of Pediatric Surgery ◽

10.1055/s-0037-1604397 ◽

2017 ◽

Vol 28 (01) ◽

pp. 096-100

Author(s):

Leyla Tekin ◽

Mehmet Erdemli ◽

Nazile Erturk ◽

Zeynep Aksungur ◽

Serdar Aktas ◽

...

Keyword(s):

Antioxidant Status ◽

Hypericum Perforatum ◽

Ischemia Reperfusion Injury ◽

Histopathological Examination ◽

Ischemia Reperfusion ◽

Total Antioxidant Status ◽

Albino Rats ◽

Protective Effects ◽

Total Antioxidant ◽

Markers Of Oxidative Stress

Purpose This study aimed to compare the protective effects of Hypericum perforatum (Hp) and quercetin, a flavonoid, against ischemia/reperfusion (I/R) injury in rat testes. Materials and Methods This study included 28 male Wistar albino rats that were divided into four groups. Except for the sham group, torsion was created by rotating both testes at an angle of 720 degrees clockwise for 2 hours. The Hp and quercetin groups received 25 mg/kg Hp and quercetin intraperitoneally 30 minutes before detorsion, respectively. Orchiectomy was performed for the measurement of markers of oxidative stress and histopathological examination. Results In the Hp and quercetin groups, malondialdehyde (MDA) and nitric oxide (NO) levels and total oxidant capacity were significantly lower, the glutathione level and total antioxidant status were significantly higher, and Johnsen's testis biopsy scores were significantly higher than in the torsion/detorsion group (p ˂ 0.001). The markers of oxidative injury were significantly lower (p ˂ 0.001) and total antioxidant status was significantly higher (p ˂ 0.001), except for glutathione (p = 0.62) in the Hp group than in the quercetin group. Johnsen's score between Hp and quercetin groups was not significantly different (p = 0.80). Conclusion Both Hp and quercetin have protective effects against I/R injury of the testes, but the protective effect of Hp was found to be stronger than that of quercetin.

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Protective effects of berberine on intestinal ischemia and reperfusion injury in rats

Archives of Biological Sciences ◽

10.2298/abs160114065c ◽

2017 ◽

Vol 69 (1) ◽

pp. 45-51 ◽

Cited By ~ 2

Author(s):

Tanzhou Chen ◽

Bin Lv

Keyword(s):

Reperfusion Injury ◽

Intestinal Ischemia ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Immunoglobulin A ◽

Male Rats ◽

Ischemia And Reperfusion ◽

Protective Effects ◽

Ischemia And Reperfusion Injury ◽

Intestinal Ischemia Reperfusion

This study aims to investigate the potential protective effects of berberine on ischemia and reperfusion (IR) injury in rats. Thirty male rats were randomly divided into three experimental groups as follows: the sham group, the IR group and the berberine+IR group. Intestinal ischemia-reperfusion was performed by occlusion of the superior mesenteric artery for 30 min, followed by 2-h reperfusion. The berberine+IR group of rats were administered 200 mg/kg of berberine once a day for 7 days before laparotomy. Compared with the IR group, rats pretreated with berberine prior to IR had significantly reduced intestinal ischemia/reperfusion injury and a significant reduction in Chiu?s score (p<0.05). The level of malondialdehyde and myeloperoxidase in the berberine+IR group was significantly decreased compared with the IR group (p<0.001). Superoxide dismutase activity in the berberine+IR group was significantly higher than in the IR group (p<0.001). Compared with the IR group, diamine oxidase was markedly decreased in the berberine+IR group (p<0.01). The level of secretory immunoglobulin A in the berberine+IR group was significantly increased when compared to the IR group (p<0.001). Our results suggest that berberine can protect from intestinal IR injury and that it can be beneficial in treating conditions associated with intestinal IR injury.

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Effect of aminoguanidine on sciatic functional index, oxidative stress, and rate of apoptosis in an experimental rat model of ischemia–reperfusion injury

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2014-0315 ◽

2014 ◽

Vol 92 (12) ◽

pp. 1013-1019 ◽

Cited By ~ 4

Author(s):

Alipour Mohsen ◽

Ghadiri Soufi Farhad ◽

Jafari Mohammad-Reza

Keyword(s):

Oxidative Stress ◽

Sciatic Nerve ◽

Reperfusion Injury ◽

Rat Model ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Protective Effects ◽

Functional Index ◽

Positive Effects ◽

Sciatic Functional Index

This study was conducted to investigate the potential protective effects of aminoguanidine (AG) on sciatic functional index (SFI), oxidative stress status, and apoptosis index using a rat model of experimental sciatic nerve ischemia–reperfusion injury (I/R). Treatment groups received 150 mg AG/kg body mass, 24 h after the induction of ischemia. After reperfusion for 2, 4, 7, 14, and 28 days, we evaluated measured SFI, plasma antioxidant enzymes, total antioxidant capacity (TAC), malondialdehyde (MDA), and index of apoptosis. SFI was significantly improved on the 7th and 14th day of reperfusion in the AG-treated groups. AG treatment resulted in the significant reduction of MDA levels on the 7th and 14th day of reperfusion. TAC was only increased after 7 days of reperfusion compared with the untreated group. SOD activity was decreased in both the untreated and AG-treated groups by comparison with the control, but did not show a significant change. GPx activity decreased only after 7 days of reperfusion. The maximal rate of apoptosis occurred on the 7th day of reperfusion. Treatment with AG significantly reduced this enhancement. AG exhibits positive effects against sciatic nerve I/R injury, possibly in part because of the protective effects of AG against apoptosis and I/R-induced oxidative stress.

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Protective effects of Chinese herbal medicine Naoshuantong on neurovascular unit in rats with cerebral ischemia/reperfusion injury

Journal of Chinese Integrative Medicine ◽

10.3736/jcim20121010 ◽

2012 ◽

pp. 1135-1139 ◽

Cited By ~ 2

Author(s):

QH Shi

Keyword(s):

Cerebral Ischemia ◽

Herbal Medicine ◽

Chinese Herbal Medicine ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Neurovascular Unit ◽

Protective Effects ◽

Chinese Herbal ◽

Cerebral Ischemia Reperfusion ◽

Cerebral Ischemia Reperfusion Injury

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Acteoside Presents Protective Effects on Cerebral Ischemia/reperfusion Injury Through Targeting CCL2, CXCL10, and ICAM1

Cell Biochemistry and Biophysics ◽

10.1007/s12013-020-00965-8 ◽

2021 ◽

Author(s):

Weijiang Wu ◽

Gang Wu ◽

Deyan Cao

Keyword(s):

Cerebral Ischemia ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Protective Effects ◽

Cerebral Ischemia Reperfusion ◽

Cerebral Ischemia Reperfusion Injury

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Propofol attenuates lung ischemia/reperfusion injury though the involvement of the MALAT1/microRNA-144/GSK3β axis

Molecular Medicine ◽

10.1186/s10020-021-00332-0 ◽

2021 ◽

Vol 27 (1) ◽

Author(s):

Jian-Ping Zhang ◽

Wei-Jing Zhang ◽

Miao Yang ◽

Hua Fang

Keyword(s):

Cell Apoptosis ◽

Ischemia Reperfusion Injury ◽

Glycogen Synthase ◽

Ischemia Reperfusion ◽

Inflammatory Factors ◽

Therapeutic Effects ◽

Protective Effects ◽

Loss Of Function

Abstract Background Propofol, an intravenous anesthetic, was proven to protect against lung ischemia/reperfusion (I/R) injury. However, the detailed mechanism of Propofol in lung I/R injury is still elusive. This study was designed to explore the therapeutic effects of Propofol, both in vivo and in vitro, on lung I/R injury and the underlying mechanisms related to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA-144 (miR-144)/glycogen synthase kinase-3β (GSK3β). Methods C57BL/6 mice were used to establish a lung I/R injury model while pulmonary microvascular endothelial cells (PMVECs) were constructed as hypoxia/reperfusion (H/R) cellular model, both of which were performed with Propofol treatment. Gain- or loss-of-function approaches were subsequently employed, followed by observation of cell apoptosis in lung tissues and evaluation of proliferative and apoptotic capabilities in H/R cells. Meanwhile, the inflammatory factors, autophagosomes, and autophagy-related proteins were measured. Results Our experimental data revealed that Propofol treatment could decrease the elevated expression of MALAT1 following I/R injury or H/R induction, indicating its protection against lung I/R injury. Additionally, overexpressing MALAT1 or GSK3β promoted the activation of autophagosomes, proinflammatory factor release, and cell apoptosis, suggesting that overexpressing MALAT1 or GSK3β may reverse the protective effects of Propofol against lung I/R injury. MALAT1 was identified to negatively regulate miR-144 to upregulate the GSK3β expression. Conclusion Overall, our study demonstrated that Propofol played a protective role in lung I/R injury by suppressing autophagy and decreasing release of inflammatory factors, with the possible involvement of the MALAT1/miR-144/GSK3β axis.

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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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