Korean J Neurotrauma.  2017 Oct;13(2):76-84. 10.13004/kjnt.2017.13.2.76.

Ganoderma Lucidum Protects Rat Brain Tissue Against Trauma-Induced Oxidative Stress

Affiliations
  • 1Department of Neurosurgery, Faculty of Medicine, Dicle University, Diyarbakır, Turkey.
  • 2Department of Medical Biology, Faculty of Medicine, Dicle University, Diyarbakır, Turkey.
  • 3Department of Histology and Embryology, Faculty of Medicine, Dicle University, Diyarbakır, Turkey. firatasir@gmail.com
  • 4Ataturk Health Hıgh School, Dicle University, Diyarbakır, Turkey.

Abstract


OBJECTIVE
Traumatic brain injury causes tissue damage, breakdown of cerebral blood flow and metabolic regulation. This study aims to investigate the protective influence of antioxidant Ganoderma lucidum (G. lucidum) polysaccharides (GLPs) on brain injury in brain-traumatized rats.
METHODS
Sprague-Dawley conducted a head-traumatized method on rats by dropping off 300 g weight from 1 m height. Groups were categorized as control, G. lucidum, trauma, trauma+ G. lucidum (20 mL/kg per day via gastric gavage). Brain tissues were dissected from anesthetized rats 7 days after injury. For biochemical analysis, malondialdehyde, glutathione and myeloperoxidase values were measured.
RESULTS
In histopathological examination, neuronal damage in brain cortex and changes in blood brain barrier were observed. In the analysis of immunohistochemical and western blot, p38 mitogen-activated protein kinase, vascular endothelial growth factor and cluster of differentiation 68 expression levels were shown. These analyzes demonstrated the beneficial effects of GLPs on brain injury.
CONCLUSION
We propose that GLPs treatment after brain injury could be an alternative treatment to decraseing inflammation and edema, preventing neuronal and glial cells degeneration if given in appropriate dosage and in particular time intervals.

Keyword

Brain; Ganoderma lucidum; Oxidative stress; Rat; Trauma

MeSH Terms

Animals
Blood-Brain Barrier
Blotting, Western
Brain Injuries
Brain*
Cerebrovascular Circulation
Edema
Ganoderma*
Glutathione
Inflammation
Malondialdehyde
Methods
Neuroglia
Neurons
Oxidative Stress*
Peroxidase
Polysaccharides
Protein Kinases
Rats*
Rats, Sprague-Dawley
Reishi*
Vascular Endothelial Growth Factor A
Glutathione
Malondialdehyde
Peroxidase
Polysaccharides
Protein Kinases
Vascular Endothelial Growth Factor A

Figure

  • FIGURE 1 (A) Normal appearance of regular cells and vascular structures in brain cortex, hematoxylin and eosin (H & E) staining bar 50 µm (control group). (B) Dilation in blood vessels and hemorrhage (arrowhead), degeneration in some neuron (arrow) H & E staining bar 50 µm (trauma group). (C) Reduction in vascular dilatation, regular structure of the nucleus and cytoplasm in neurons and glial cells, H & E staining bar 50 µm (trauma + Ganoderma group). (D) Expression of phosphorylated p38 mitogen activated protein kinase (MAPK) in neuron nucleus (arrow), phosphorylated p38 immunohistochemistry (IHC) staining bar 50 µm (control group). (E) Positive expression of phosphorylated p38 MAPK in nucleus of neuron and glia cells (arrows), phosphorylated p38 IHC staining bar 50 µm (trauma group). (F) Increased p38 expression in neuronal membranes (yellow arrow) and nucleus of glial cells phosphorylated p38 (red arrow) IHC staining bar 50 µm (trauma+Ganoderma group).

  • FIGURE 2 (A) Vascular endothelial growth factor (VEGF) expression of vascular endothelial cells in the cortex (arrow) VEGF immunohistochemistry staining bar 50 µm (control group). (B) Positive VEGF expression in endothelial cells and inflammatory cells (arrows) VEGF immunohistochemistry staining bar 50 µm (trauma group). (C) Increased VEGF expression in endothelial cells (arrow), VEGF immunohistochemistry staining bar 50 µm (trauma+Ganoderma group). (D) Positive cluster of differentiation 68 (CD68) expression in glial cells surrounding of the blood vessels, CD68 immunohistochemistry staining bar 50 µm (control group). (E) Weak CD68 expression in glial cells (arrow) CD68 immunohistochemistry staining bar 50 µm (trauma group). (F) Positive CD68 expression in glia cells around blood vessels (CD68 immunohistochemistry staining bar 50 µm) (trauma+Ganoderma group).

  • FIGURE 3 Ganoderma treatment did not affect trauma-induced phosphorylation of p38 in brain tissue. Equal amounts of total proteins were run on the gel and analyzed by Western blot analysis for VEGE and β-actin. The β-actin was used as loading control.

  • FIGURE 4 Western blot analysis for vascular endothelial growth factor (VEGF) and β-actin. Ganoderma treatment did not affect trauma-induced expression of VEGF in brain tissue. Equal amounts of total proteins were run on the gel and analyzed by Western blotting using anti-VEGF and anti-β-actin antibodies. The β-actin was used as loading control.

  • FIGURE 5 Trauma-induced reduced cluster of differentiation 68 (CD68) expression in brain tissue was dramatically increased by ganoderma treatment. Equal amounts of total proteins were run on the gel and analyzed by Western blot analysis for CD68 and β-actin. The β-actin was used as loading control.


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