Dataset Information

Edaravone Suppresses Reperfusion Injury following Leg Ischemia in Rats: A Transmission Electron Microscopic Study.

ABSTRACT: It is well known that free radicals cause reperfusion injury following leg ischemia. We showed that the free radical scavenger, edaravone (Radicut, Mitsubishi Tanabe Pharma Co., Osaka, Japan), might suppress reperfusion injury in rat. In this study, we used transmission electron microscope (TEM) to investigate how edaravone suppresses reperfusion injury by focusing on glycogen granules in the lower extremity muscles. Male Lewis rats (582 ± 35 g) were intraperitoneally injected with edaravone (3.0 mg/kg, edaravone group, n = 5) or the same dose of saline (control group, n = 5). The rat reperfusion injury models were induced by clamping the bilateral common femoral arteries for 5 hours and then declamping. The muscles were harvested at 5 hours after the start of reperfusion. Under a TEM (JEM-1220, Nippon Denshi Co., Tokyo, Japan), we counted the number of glycogen granules at ×50,000 magnification on each five different fields. The TEM sections from the control group showed a marked loss of glycogen granules and swollen mitochondria. In contrast, the TEM sections from the edaravone group showed numerous glycogen granules and normal mitochondria. The mean density of glycogen granules in the edaravone group was significantly higher than that in the control group (88.5 ± 5.3 vs. 16.4 ± 3.1 particles/µm(2), p < 0.001). Our TEM results confirmed that edaravone suppresses reperfusion injury following leg ischemia by maintaining the glycogen granules in muscles.

SUBMITTER: Yamamura M

PROVIDER: S-EPMC3830573 | biostudies-other | 2013 Dec

REPOSITORIES: biostudies-other

ACCESS DATA

Similar Datasets

Project description:BackgroundMany retinal diseases are associated with vascular dysfunction accompanied by neuroinflammation. We examined the ability of minocycline (Mino), a tetracycline derivative with anti-inflammatory and neuroprotective properties, to prevent vascular permeability and inflammation following retinal ischemia-reperfusion (IR) injury, a model of retinal neurodegeneration with breakdown of the blood-retinal barrier (BRB).MethodsMale Sprague-Dawley rats were subjected to 45 min of pressure-induced retinal ischemia, with the contralateral eye serving as control. Rats were treated with Mino prior to and following IR. At 48 h after reperfusion, retinal gene expression, cellular inflammation, Evan's blue dye leakage, tight junction protein organization, caspase-3 activation, and DNA fragmentation were measured. Cellular inflammation was quantified by flow-cytometric evaluation of retinal tissue using the myeloid marker CD11b and leukocyte common antigen CD45 to differentiate and quantify CD11b+/CD45low microglia, CD11b+/CD45hi myeloid leukocytes and CD11bneg/CD45hi lymphocytes. Major histocompatibility complex class II (MHCII) immunoreactivity was used to determine the inflammatory state of these cells.ResultsMino treatment significantly inhibited IR-induced retinal vascular permeability and disruption of tight junction organization. Retinal IR injury significantly altered mRNA expression for 21 of 25 inflammation- and gliosis-related genes examined. Of these, Mino treatment effectively attenuated IR-induced expression of lipocalin 2 (LCN2), serpin peptidase inhibitor clade A member 3 N (SERPINA3N), TNF receptor superfamily member 12A (TNFRSF12A), monocyte chemoattractant-1 (MCP-1, CCL2) and intercellular adhesion molecule-1 (ICAM-1). A marked increase in leukostasis of both myeloid leukocytes and lymphocytes was observed following IR. Mino treatment significantly reduced retinal leukocyte numbers following IR and was particularly effective in decreasing the appearance of MHCII+ inflammatory leukocytes. Surprisingly, Mino did not significantly inhibit retinal cell death in this model.ConclusionsIR induces a retinal neuroinflammation within hours of reperfusion characterized by inflammatory gene expression, leukocyte adhesion and invasion, and vascular permeability. Despite Mino significantly inhibiting these responses, it failed to block neurodegeneration.

Dataset Information

Edaravone Suppresses Reperfusion Injury following Leg Ischemia in Rats: A Transmission Electron Microscopic Study.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets