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. 2015 Apr;10(4):540-1.
doi: 10.4103/1673-5374.155414.

Oleanolic acid: a promising neuroprotective agent for cerebral ischemia

Laura Caltana  1 , María Luisa Nieto  2 , Alicia Brusco  1
Affiliations

Oleanolic acid: a promising neuroprotective agent for cerebral ischemia

Laura Caltana et al. Neural Regen Res. 2015 Apr.
No abstract available

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Figures

Figure 1
Figure 1
Photomicrographs showing neurons (A, D, G), astrocytes (B, E, H) and microglial cells (C, F, I) in different experimental conditions. Hypoxia induces neuronal degeneration with loss of dendritic trees (D) and glial reaction – astrocytosis (E) and microglial activation (F). The pretreatment with oleanolic acid (OA) decreases neuronal damage (G), astrocytic reaction (H) and microglial activation (I). (A–C) Normoxic conditions. (D–F) Hypoxic coditions. (G–I) Pretreatment with OA and hypoxic conditions. Immunofluorescence for 200 kDa neurofilaments in A, D, and G, and for gliofribrillary acidic protein in B, E and H. Histochemical staining for microglial cells (C, F and I) was made with tomato lectin. Scale bar: 15 μm.
Figure 2
Figure 2
Schematic representation of cellular processes occurring in the hypoxic brain and the effects of oleanolic acid (OA) pretreatment. Hypoxia induces the activation of microglial cells, which suffer morphological transformations and become ameboid-shaped. The activated microglial cells release proinflammatory cytokines and reactive oxygen species (ROS) such as nitric oxide, which induce astroglial reaction and neuronal damage. OA reduces microglial reaction and then decreases astroglial reaction, thus protecting neuron morphology and function. Gray arrows indicate the effects of hypoxia on neurons, astrocytes and microglial cells. Orange arrows indicate inflammatory effects on nervous tissue cells. Yellow arrows indicate OA preventive effects.
See this image and copyright information in PMC

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