Prostaglandin E1 analog increases spinal cord blood flow at the point of compression during and after experimental spinal cord injury

Hamamoto, Yuichiro; Ogata, Tadanori; Morino, Tadao; Hino, Masayuki; Yamamoto, Haruyasu

doi:10.1038/sc.2009.99

Cited by 7 publications

(3 citation statements)

References 17 publications

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“…bFGF stimulated the migration of cultured keratinocytes (27) and accelerated wound healing in a diabetic mouse model (9) and in pressure ulcers (10). PGE1 increased the intracellular cyclic AMP and reduced platelet aggregation (28,29) and was also found to increase tissue blood flow in an animal model (30). Furthermore, intravenous administration of PGE1 was effective in treating venous ulcers (31), diabetic skin ulcers (32) and skin ulcers stemming from collagen diseases (33).…”

Section: Discussionmentioning

confidence: 99%

Influence of various treatments including povidone‐iodine and healing stimulatory reagents in a rabbit ear wound model

Arai

Yamazaki

Maeda

et al. 2012

International Wound Journal

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Selecting an appropriate treatment for a given case of skin wound is crucial for inducing optimal healing. We used an animal model developed from normal rabbit ears in order to assess the efficacy of treatments for skin wounds with or without a wet dressing, anti microbial reagent or topical wound-stimulatory reagents. The degree of healing in each group was evaluated and compared using four histological parameters: (i) degree of reepithelialisation, (ii) amount of granulation tissue formation, and (iii) the number of capillary lumens and (iv) fibroblasts in the granulation tissue. Treatment using wet dressings resulted in an increase in capillary number compared with the open dry wound. Although the retention of povidone-iodine (PI) in wound tissue after application significantly inhibited reepithelialisation (P < 0.05), rinsing PI off with saline was comparable in effect to using only a wet dressing. The three topical reagents, namely, basic fibroblast growth factor, prostaglandin E1 and dibutyryl cyclic adenosine monophosphate, significantly improved reepithelialisation (P < 0.05). In conclusion, wounds should be kept hydrated by applying topical reagents. If there are any signs of bacterial infection, PI can be applied and rinsed later with saline in order to minimise its cytotoxic effects.

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Section: Discussionmentioning

confidence: 99%

Influence of various treatments including povidone‐iodine and healing stimulatory reagents in a rabbit ear wound model

Arai

Yamazaki

Maeda

et al. 2012

International Wound Journal

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“…The exact mechanism underlying PGE1's beneficial effect on ICH remains elusive. PGE1 may increase c-Fos and Myc proteins' expression and protect rat hippocampal cells from hypoxic injury (15,16), and prevent neuronal apoptosis in the rat spinal cord induced by sciatic nerve constriction (17,18). PGE1 may also effectively protect cortical neurons from glutamate cytotoxicity (19).…”

Section: Introductionmentioning

confidence: 99%

PGE1 triggers Nrf2/HO-1 signal pathway to resist hemin-induced toxicity in mouse cortical neurons

Shen¹,

Cao²,

Zhou³

et al. 2021

Ann Transl Med

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Background: Prostaglandin E1 (PGE1) exerts various pharmacological effects such as membrane stabilization, anti-inflammatory functions, vasodilation, and platelet aggregation inhibition. We have previously demonstrated that PGE1 has a beneficial impact on patients suffering from intracerebral hemorrhage (ICH). The related mechanism underlying PGE1's beneficial effect on ICH treatment needs further exploration.Methods: The present study elucidates the mechanism of PGE1 on ICH treatment using a neuronal apoptosis model in vitro. The mouse primary cortical neurons were pretreated with different concentrations of PGE1, followed by the treatment with hemin, the main catabolite in whole blood, to mimic the clinical ICH.Results: Comparing with the vehicle-treated group, PGE1 prevented cultured cortical neurons from the accumulation of inhibited intracellular levels of reactive oxygen species (ROS), amelioration of mitochondrial membrane potential, and hemin-induced apoptosis. The reduction of ROS and apoptosis were associated with the up-regulation of Heme oxygenase-1 (HO-1) expression. Knockdown of nuclear transcription factor erythroid 2-related factor (Nrf2) by siRNA attenuated the upregulation of HO-1 as well as the protective effect of PGE1.Conclusions: Our work suggests that the Nrf2/HO-1 molecular pathway may play a crucial role in treating ICH patients with PGE1 and may represent novel molecular targets, resulting in discovering new drugs for ICH treatment.

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“…Prostaglandin E1 (PGE1)—a hormone-like substance, with antiischemic, antiinflammatory, 7 – 9 antiplatelet, and fibrinolytic properties 10 and tissue-protective effects (originates in the vascular endothelium)— 11 has been shown to increase perfusion in a rat model of cerebral ischemia 12 and in experimental studies of animals subjected to traumatic compression/decompression damage of the spine. 13 In a study on random pattern flaps in rabbits, increased distal perfusion was found up to 60 minutes after injection of PGE1. 14 …”

mentioning

confidence: 98%

Prostaglandin E1 Increases Microcirculation in Random Pattern Flaps on Rats Measured with Laser Doppler Perfusion Imaging

Tønseth

Sneistrup

Berg

2017

Plastic and Reconstructive Surgery - Global Open

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Background:Reconstructive procedures with pedicled and free flaps are associated with a risk of ischemia. Prostaglandin E1 (PGE1) is a hormone-like substance with known antiischemic and tissue-protective effects. The aim of this study was to evaluate the effect of PGE1 on the microcirculation in random pattern skin flaps on rats.Methods:Twenty-four rats were divided into 2 groups: an intervention group given PGE1 for 6 hours and a control group given saline. The flap (2 × 10 cm) was created on the back of the rats, and the microcirculation was monitored with laser Doppler perfusion imaging in 5 different zones (1, proximal; 5, distal) before surgery and after 60, 180, and 360 minutes postoperatively.Results:Before surgery, there was no difference in the perfusion in any zones between the intervention group and the control group. The mean perfusion values in zone 1 in the intervention group were significantly higher than those in the control group at 60, 180, and 360 minutes postoperatively (P = 0.02, P = 0.05, and P = 0.04, respectively). At 360 minutes, we also found significantly higher levels of perfusion in the intervention group in zones 4 and 5 (P = 0.05 and P = 0.03, respectively) compared with the controls. Comparing the perfusion at 360 to 60 minutes in the intervention group, we found a significant increase in microcirculation in all zones, which were not seen in the control group.Conclusion:PGE1 increased perfusion in the dermal random pattern flaps on rats.

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Prostaglandin E1 analog increases spinal cord blood flow at the point of compression during and after experimental spinal cord injury

Cited by 7 publications

References 17 publications

Influence of various treatments including povidone‐iodine and healing stimulatory reagents in a rabbit ear wound model

Influence of various treatments including povidone‐iodine and healing stimulatory reagents in a rabbit ear wound model

PGE1 triggers Nrf2/HO-1 signal pathway to resist hemin-induced toxicity in mouse cortical neurons

Prostaglandin E1 Increases Microcirculation in Random Pattern Flaps on Rats Measured with Laser Doppler Perfusion Imaging

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