Pre-Treatment with Laminarin Protects Hippocampal CA1 Pyramidal Neurons and Attenuates Reactive Gliosis Following Transient Forebrain Ischemia in Gerbils
"> Figure 1
<p>Cresyl Violet (CV) staining in the hippocampus (<b>A</b>–<b>H</b>) and its Cornu Ammonis 1 (CA1) field (<b>a</b>–<b>h</b>) of the vehicle/sham (<b>A</b>,<b>a</b>), 10, 50 and 100 mg/kg laminarin (LA)/sham (<b>C</b>,<b>c</b>,<b>E</b>,<b>e</b>,<b>G</b>,<b>g</b>), vehicle/ischemia (<b>B</b>,<b>b</b>) and 10, 50 and 100 mg/kg LA/ischemia (<b>D</b>,<b>d</b>,<b>F</b>,<b>f</b>,<b>H</b>,<b>h</b>) groups at 5 days after sham or transient forebrain ischemia (TFI) operation. In the vehicle/ischemia group, CV dyeability is remarkably reduced in the stratum pyramidale (SP, arrows) of the CA1 field (asterisks). In the 10 mg/kg LA/ischemia group, the distribution pattern of CV stained cells is similar to that in the vehicle/ischemia group. However, in the 50 mg/kg and 100 mg/kg LA/ischemia groups, CV stainability is conserved. DG, dentate gyrus; SO, stratum oriens; SR stratum radiatum. Scale bars = 400 μm (<b>A</b>–<b>H</b>) and 100 μm (<b>a</b>–<b>h</b>).</p> "> Figure 2
<p>NeuN immunohistochemistry in the CA1 field of the vehicle/sham (<b>A</b>), 10, 50 and 100 mg/kg LA/sham (<b>C</b>,<b>E</b>,<b>G</b>), vehicle/ischemia (<b>B</b>) and 10, 50 and 100 mg/kg LA/ischemia (<b>D</b>,<b>F</b>,<b>H</b>) groups at 5 days after sham or TFI operation. Numerous NeuN immunoreactive CA1 pyramidal neurons can be observed in the vehicle/sham group. In the vehicle/ischemia and 10 mg/kg LA/ischemia groups, significant decreases in NeuN immunoreactive CA1 pyramidal neurons were detected. In the 50 mg/kg and 100 mg/kg LA/ischemia groups, CA1 pyramidal neurons show strong NeuN immunoreactivity. Scale bar = 100 μm. (<b>I</b>) Mean number of NeuN immunoreactive pyramidal cells in the CA1 field at 5 days after TFI (<span class="html-italic">n</span> = 7 in each group, * <span class="html-italic">p</span> < 0.05 versus vehicle/sham group, † <span class="html-italic">p</span> < 0.05 versus vehicle/ischemia group). The bars indicate the means ± SEM.</p> "> Figure 3
<p>F-J B histofluorescence staining in the CA1 field of the vehicle/sham (<b>A</b>), 10, 50 and 100 mg/kg LA/sham (<b>C</b>,<b>E</b>,<b>G</b>), vehicle-ischemia (<b>B</b>) and 10, 50 and 100 mg/kg LA/ischemia (<b>D</b>,<b>F</b>,<b>H</b>) groups at 5 days after sham or TFI operation. In all the sham groups, no F-J B positive cells are found in the CA1 field; numerous F-J B positive cells are shown in the SP (asterisks) in the vehicle/ and 10 mg/kg LA/ischemia groups. However, in the 50 mg/kg and 100 mg/kg LA/ischemia groups, F-J B positive cells (arrows) are significantly decreased. Scale bar = 100 μm. (<b>I</b>) Mean number of F-J B positive pyramidal cells in the CA1 field at 5 days after TFI (<span class="html-italic">n</span> = 7 in each group, * <span class="html-italic">p</span> < 0.05 versus vehicle/sham group, † <span class="html-italic">p</span> < 0.05 versus vehicle/ischemia group). The bars indicate the means ± SEM.</p> "> Figure 4
<p>Glial fibrillary acidic protein (GFAP) immunohistochemistry in the CA1 field of the vehicle/sham (<b>A</b>), 10, 50 and 100 mg/kg LA/sham (<b>C</b>,<b>E</b>,<b>G</b>), vehicle/ischemia (<b>B</b>) and 10, 50 and 100 mg/kg LA/ischemia (<b>D</b>,<b>F</b>,<b>H</b>) groups at 5 days after sham or TFI operation. In all the sham groups, typical GFAP immunoreactive astrocytes are generally distributed in the stratum oriens (SO) and radiatum (SR). In the vehicle/ischemia group, GFAP immunoreactive astrocytes are hypertrophied. In the 10 mg/kg LA/ischemia group, GFAP immunoreactive astrocytes are similar to those in the vehicle/ischemia group. In the 50 mg/kg and 100 mg/kg LA/ischemia groups, hypertrophy of GFAP immunoreactive astrocytes is apparently attenuated. Scale bar = 100 μm. (<b>I</b>) ROD (percentage) of GFAP immunoreactive structures in the CA1 field at 5 days after TFI (<span class="html-italic">n</span> = 7 in each group, * <span class="html-italic">p</span> < 0.05 versus vehicle/sham group, † <span class="html-italic">p</span> < 0.05 versus vehicle/ischemia group). The bars indicate the means ± SEM.</p> "> Figure 5
<p>Ionized calcium-binding adapter molecule 1 (Iba-1) immunohistochemistry in the CA1 field of the vehicle/sham (<b>A</b>), 10, 50 and 100 mg/kg LA/sham (<b>C</b>,<b>E</b>,<b>G</b>), vehicle/ischemia (<b>B</b>) and 10, 50 and 100 mg/kg LA/ischemia (<b>D</b>,<b>F</b>,<b>H</b>) groups at 5 days after sham or TFI operation. Iba-1 immunoreactive microglia are in a resting state in all the sham groups. In the vehicle/ischemia and 10 mg/kg LA/ischemia groups, Iba-1 immunoreactive microglia are hypertrophied, showing that many activated microglia gather in the SP (arrows). In the 50 mg/kg and 100 mg/kg LA/ischemia groups, activation of Iba-1 immunoreactive microglia is markedly attenuated, showing that they are evenly distributed in the CA1 field. Scale bar = 100 μm. (<b>I</b>) ROD (percentage) of Iba-1 immunoreactive structures in the CA1 field at 5 days after TFI (<span class="html-italic">n</span> = 7 in each group, * <span class="html-italic">p</span> < 0.05 versus vehicle/sham group, † <span class="html-italic">p</span> < 0.05 versus vehicle/ischemia group). The bars indicate the means ± SEM.</p> "> Figure 6
<p>Double immunofluorescence staining for Iba-1 (red), interleukin 2 (IL-2) (green) and merged images in the hippocampal CA1 field of the vehicle/ischemia (<b>A</b>–<b>C</b>) and 50 mg/kg LA/ischemia (<b>D</b>–<b>F</b>) groups at 5 days after TFI. Many IL-2 immunoreactive microglia (arrows) are shown in the vehicle/ischemia group. However, in the 50 mg/kg LA/ischemia group, a few IL-2 immunoreactive microglia are detected. Scale bar = 40 μm (<span class="html-italic">n</span> = 7 in each group).</p> ">
Abstract
:1. Introduction
2. Results
2.1. Neuroprotection by LA
2.1.1. Cresyl Violet (CV) Stained Cells
2.1.2. Neuronal-Specific Nuclear Protein (NeuN) Immunoreactive Neurons
2.1.3. Fluoro-Jade B (F-J B) Positive Cells
2.2. Attenuation of Gliosis by LA
2.2.1. Glial Fibrillary Acidic Protein (GFAP) Immunoreactive Astrocytes
2.2.2. Ionized Calcium-Binding Adapter Molecule 1 (Iba-1) Immunoreactive Microglia
2.2.3. Interleukin 2 (IL-2) Immunoreactive Microglia
3. Discussion
4. Materials and Methods
4.1. Experimental Animals
4.2. Experimental Groups and Administration of LA
4.3. Induction of TFI
4.4. Tissue Preparation for Histological Examination
4.5. CV Staining
4.6. F-J B Histofluorescence Staining
4.7. Immunohistochemistry
4.8. Double Immunofluorescence
4.9. Data Analyses
4.10. Statistical Analysis
Author Contributions
Funding
Conflicts of Interest
References
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Lee, T.-K.; Ahn, J.H.; Park, C.W.; Kim, B.; Park, Y.E.; Lee, J.-C.; Park, J.H.; Yang, G.E.; Shin, M.C.; Cho, J.H.; et al. Pre-Treatment with Laminarin Protects Hippocampal CA1 Pyramidal Neurons and Attenuates Reactive Gliosis Following Transient Forebrain Ischemia in Gerbils. Mar. Drugs 2020, 18, 52. https://doi.org/10.3390/md18010052
Lee T-K, Ahn JH, Park CW, Kim B, Park YE, Lee J-C, Park JH, Yang GE, Shin MC, Cho JH, et al. Pre-Treatment with Laminarin Protects Hippocampal CA1 Pyramidal Neurons and Attenuates Reactive Gliosis Following Transient Forebrain Ischemia in Gerbils. Marine Drugs. 2020; 18(1):52. https://doi.org/10.3390/md18010052
Chicago/Turabian StyleLee, Tae-Kyeong, Ji Hyeon Ahn, Cheol Woo Park, Bora Kim, Young Eun Park, Jae-Chul Lee, Joon Ha Park, Go Eun Yang, Myoung Cheol Shin, Jun Hwi Cho, and et al. 2020. "Pre-Treatment with Laminarin Protects Hippocampal CA1 Pyramidal Neurons and Attenuates Reactive Gliosis Following Transient Forebrain Ischemia in Gerbils" Marine Drugs 18, no. 1: 52. https://doi.org/10.3390/md18010052