Limits...
Docosahexaenoic Acid therapy of experimental ischemic stroke.

Belayev L, Khoutorova L, Atkins KD, Eady TN, Hong S, Lu Y, Obenaus A, Bazan NG - Transl Stroke Res (2010)

Bottom Line: Treatment with DHA significantly improved behavior and reduced total infarct volume by a mean of 40% when administered at 3 h, by 66% at 4 h, and by 59% at 5 h.Total lesion volumes computed from T2-weighted images were reduced in the DHA group at all time points.Lipidomic analysis showed that DHA treatment potentiates neuroprotectin D1 (NPD1) synthesis in the penumbra 3 days after MCAo.

View Article: PubMed Central - PubMed

ABSTRACT
We examined the neuroprotective efficacy of docosahexaenoic acid (DHA), an omega-3 essential fatty acid family member, in acute ischemic stroke; studied the therapeutic window; and investigated whether DHA administration after an ischemic stroke is able to salvage the penumbra. In each series described below, SD rats underwent 2 h of middle cerebral artery occlusion (MCAo). In series 1, DHA or saline was administered i.v. at 3, 4, 5, or 6 h after stroke. In series 2, MRI was conducted on days 1, 3 and 7. In series 3, DHA or saline was administered at 3 h, and lipidomic analysis was conducted on day 3. Treatment with DHA significantly improved behavior and reduced total infarct volume by a mean of 40% when administered at 3 h, by 66% at 4 h, and by 59% at 5 h. Total lesion volumes computed from T2-weighted images were reduced in the DHA group at all time points. Lipidomic analysis showed that DHA treatment potentiates neuroprotectin D1 (NPD1) synthesis in the penumbra 3 days after MCAo. DHA administration provides neurobehavioral recovery, reduces brain infarction and edema, and activates NPD1 synthesis in the penumbra when administered up to 5 h after focal cerebral ischemia in rats.

No MeSH data available.


Related in: MedlinePlus

a Coronal brain diagram showing locations of regions for cell counts in cortex (1, 2, and 3), and striatum (S). b–d Number of GFAP-positive astrocytes, ED-1 positive microglia cells, and NeuN-positive neurons on day 7 after 2 h of MCAo. DHA or saline was given at 3 h after onset of stroke. DHA treatment decreased ED-1, increased NeuN- and GFAP-positive cell counts. Data are mean ± SEM. Asterisk, significantly different from saline (p < 0.05; repeated-measures ANOVA followed by Bonferroni tests)
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3037476&req=5

Fig2: a Coronal brain diagram showing locations of regions for cell counts in cortex (1, 2, and 3), and striatum (S). b–d Number of GFAP-positive astrocytes, ED-1 positive microglia cells, and NeuN-positive neurons on day 7 after 2 h of MCAo. DHA or saline was given at 3 h after onset of stroke. DHA treatment decreased ED-1, increased NeuN- and GFAP-positive cell counts. Data are mean ± SEM. Asterisk, significantly different from saline (p < 0.05; repeated-measures ANOVA followed by Bonferroni tests)

Mentions: Saline-treated rats showed extensive neuronal loss, GFAP-positive reactive astrocytes outlining the lesion territory, and massive ED-1-positive microglia/macrophage infiltration (Fig. 1f, top). In contrast, DHA-attenuated damage as well as decreased ED-1-positive microglia/macrophages and increased GFAP-positive reactive astrocytes (Fig. 1f, bottom). Figure 2 presents GFAP-, ED-1-, and NeuN-positive cell counts. DHA treatment significantly decreased ED-1 (p < 0.01) and increased NeuN (p < 0.01) and GFAP-positive (p < 0.005) cell counts.Fig. 2


Docosahexaenoic Acid therapy of experimental ischemic stroke.

Belayev L, Khoutorova L, Atkins KD, Eady TN, Hong S, Lu Y, Obenaus A, Bazan NG - Transl Stroke Res (2010)

a Coronal brain diagram showing locations of regions for cell counts in cortex (1, 2, and 3), and striatum (S). b–d Number of GFAP-positive astrocytes, ED-1 positive microglia cells, and NeuN-positive neurons on day 7 after 2 h of MCAo. DHA or saline was given at 3 h after onset of stroke. DHA treatment decreased ED-1, increased NeuN- and GFAP-positive cell counts. Data are mean ± SEM. Asterisk, significantly different from saline (p < 0.05; repeated-measures ANOVA followed by Bonferroni tests)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3037476&req=5

Fig2: a Coronal brain diagram showing locations of regions for cell counts in cortex (1, 2, and 3), and striatum (S). b–d Number of GFAP-positive astrocytes, ED-1 positive microglia cells, and NeuN-positive neurons on day 7 after 2 h of MCAo. DHA or saline was given at 3 h after onset of stroke. DHA treatment decreased ED-1, increased NeuN- and GFAP-positive cell counts. Data are mean ± SEM. Asterisk, significantly different from saline (p < 0.05; repeated-measures ANOVA followed by Bonferroni tests)
Mentions: Saline-treated rats showed extensive neuronal loss, GFAP-positive reactive astrocytes outlining the lesion territory, and massive ED-1-positive microglia/macrophage infiltration (Fig. 1f, top). In contrast, DHA-attenuated damage as well as decreased ED-1-positive microglia/macrophages and increased GFAP-positive reactive astrocytes (Fig. 1f, bottom). Figure 2 presents GFAP-, ED-1-, and NeuN-positive cell counts. DHA treatment significantly decreased ED-1 (p < 0.01) and increased NeuN (p < 0.01) and GFAP-positive (p < 0.005) cell counts.Fig. 2

Bottom Line: Treatment with DHA significantly improved behavior and reduced total infarct volume by a mean of 40% when administered at 3 h, by 66% at 4 h, and by 59% at 5 h.Total lesion volumes computed from T2-weighted images were reduced in the DHA group at all time points.Lipidomic analysis showed that DHA treatment potentiates neuroprotectin D1 (NPD1) synthesis in the penumbra 3 days after MCAo.

View Article: PubMed Central - PubMed

ABSTRACT
We examined the neuroprotective efficacy of docosahexaenoic acid (DHA), an omega-3 essential fatty acid family member, in acute ischemic stroke; studied the therapeutic window; and investigated whether DHA administration after an ischemic stroke is able to salvage the penumbra. In each series described below, SD rats underwent 2 h of middle cerebral artery occlusion (MCAo). In series 1, DHA or saline was administered i.v. at 3, 4, 5, or 6 h after stroke. In series 2, MRI was conducted on days 1, 3 and 7. In series 3, DHA or saline was administered at 3 h, and lipidomic analysis was conducted on day 3. Treatment with DHA significantly improved behavior and reduced total infarct volume by a mean of 40% when administered at 3 h, by 66% at 4 h, and by 59% at 5 h. Total lesion volumes computed from T2-weighted images were reduced in the DHA group at all time points. Lipidomic analysis showed that DHA treatment potentiates neuroprotectin D1 (NPD1) synthesis in the penumbra 3 days after MCAo. DHA administration provides neurobehavioral recovery, reduces brain infarction and edema, and activates NPD1 synthesis in the penumbra when administered up to 5 h after focal cerebral ischemia in rats.

No MeSH data available.


Related in: MedlinePlus