Protective effect of erythropoietin on myocardial apoptosis in rats exposed to carbon monoxide

Rezaee, Mitra Asgharian; Mohammadpour, Amir Hooshang; Imenshahidi, Mohsen; Mahmoudi, Mahmoud; Sankian, Mojtaba; Tsarouhas, Konstantinos; Tsakalof, Andreas; Tsatsakis, Aristidis; Moallem, Seyed Adel

doi:10.1016/j.lfs.2016.02.007

Cited by 23 publications

(16 citation statements)

References 34 publications

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“…As shown by recent literature, the Bax/Bcl2 ratio alone stands as an index of cell apoptosis or survival (25–28). In addition, in our previous studies using a model of CO poisoning, a clear connection between apoptosis and the Bax/Bcl2 ratio was proven by TUNEL assay and caspase activity measurements (29). Moreover, Akt is regarded as a pro-survival factor (30,31), whose activation induces phosphorylation at different sites.…”

Section: Introductionmentioning

confidence: 81%

Magnesium sulfate ameliorates carbon monoxide‑induced cerebral injury in male rats

et al. 2018

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Carbon monoxide (CO) has been shown to induce several cardiovascular abnormalities, as well as necrosis, apoptosis and oxidative stress in the brain. Magnesium sulfate (MS) has been shown to have beneficial activities against hypoxia in the brain. In the present study, the possible protective effects of MS against CO-induced cerebral ischemia were investigated. For this purpose, 25 male Wistar rats were exposed to 3,000 ppm CO for 1 h. The animals were divided into 5 groups (n=5 in each group) as follows: The negative control group (not exposed to CO), the positive control group (CO exposed and treated with normal saline), and 3 groups of CO-exposed rats treated with MS (75, 150 and 300 mg/kg/day) administered intraperitoneally for 5 consecutive days. On the 5th day, the animals were sacrificed and the brains were harvested for the evaluation of necrosis, apoptosis and oxidative stress. Histopathological evaluation revealed that MS reduced the number and intensity of necrotic insults. The Bax/Bcl2 ratio and malondialdehyde (MDA) levels were significantly decreased in a dose-dependent manner in the MS-treated rats compared to the positive control group, while a significant dose-dependent increase in Akt expression, a pro-survival protein, was observed. In addition, MS administration reduced pro-apoptotic indice levels, ameliorated histological insults, favorably modulated oxidative status and increased Akt expression levels, indicating a possible neuroprotective effect in the case of CO poisoning. On the whole, the findings of this study indicate that MS may prove to be useful in protecting against CO-induced cerebral injury.

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Section: Introductionmentioning

confidence: 81%

Magnesium sulfate ameliorates carbon monoxide‑induced cerebral injury in male rats

et al. 2018

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“…Puchulu et al suggested 3 days of EPO treatment (1,000 IU/kg) decreased oxidative damage and improved heart function in a rat hypovolemic model. Single-dose EPO (5,000 IU/kg) protected myocardial apoptosis in rats following carbon monoxide exposure [103]. Overexpressed EPO improved rat heart fibrosis through the PI3K/Akt/TLR4 pathway to suppress the release of mediators such as TGF-β1, proinflammatory cytokines, and matrix metalloproteinase [58].…”

Section: Discussionmentioning

confidence: 99%

Erythropoietin Alleviates Burn-induced Muscle Wasting

Tai

et al. 2020

Int. J. Med. Sci.

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Background: Burn injury induces long-term skeletal muscle pathology. We hypothesized EPO could attenuate burn-induced muscle fiber atrophy. Methods: Rats were allocated into four groups: a sham burn group, an untreated burn group subjected to third degree hind paw burn, and two burn groups treated with weekly or daily EPO for four weeks. Gastrocnemius muscle was analyzed at four weeks post-burn. Results: EPO attenuated the reduction of mean myofiber cross-sectional area post-burn and the level of the protective effect was no significant difference between two EPO-treated groups (p=0.784). Furthermore, EPO decreased the expression of atrophy-related ubiquitin ligase, atrogin-1, which was up-regulated in response to burn. Compared to untreated burn rats, those receiving weekly or daily EPO groups had less cell apoptosis by TUNEL assay. EPO decreased the expression of cleaved caspase 3 (key factor in the caspase-dependent pathway) and apoptosis-inducing factor (implicated in the caspase-independent pathway) after burn. Furthermore, EPO alleviated connective tissue overproduction following burn via transforming growth factor beta 1-Smad2/3 pathway. Daily EPO group caused significant erythrocytosis compared with untreated burn group but not weekly EPO group. Conclusion: EPO therapy attenuated skeletal muscle apoptosis and fibrosis at four weeks post-burn. Weekly EPO may be a safe and effective option in muscle wasting post-burn.

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“…Myocardial infarction leads to myocardial ischemia and even irreversible myocardial necrosis if blood supply is not timely restored [11,12]. It has been reported that myocardial ischemia results from the imbalance between the supply of oxygen to the heart and oxygen demand by the heart [13,14].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of total saponins from Ilex pubescens Hook against hydrogen peroxide-induced cardiomyocyte apoptosis

Ying¹,

Wu²,

Yin³

et al. 2018

Trop. J. Pharm Res

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Protective effect of erythropoietin on myocardial apoptosis in rats exposed to carbon monoxide

Cited by 23 publications

References 34 publications

Magnesium sulfate ameliorates carbon monoxide‑induced cerebral injury in male rats

Magnesium sulfate ameliorates carbon monoxide‑induced cerebral injury in male rats

Erythropoietin Alleviates Burn-induced Muscle Wasting

Inhibitory effects of total saponins from Ilex pubescens Hook against hydrogen peroxide-induced cardiomyocyte apoptosis

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