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Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
Pseudoginsenoside-F11 promotes functional recovery after transient cerebral ischemia by regulating the
Ying Hou1, Depeng Yang1, Xianshi Wang1
1Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, PR China.
Abstract:
The polarization of microglia/macrophages after cerebral ischemia is critical for post-stroke damage/recovery. Previously, we found that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, has neuroprotective effects on permanent and transient cerebral ischemia in rats. This study aimed to investigate the effects and potential mechanisms of PF11 on microglia/macrophage polarization following transient cerebral ischemia in rats. In vivo data showed that oral administration of PF11 (12 mg/kg) significantly attenuated cognitive deficits and sensorimotor dysfunction, infarct volume and brain edema in transient middle cerebral artery occlusion (tMCAO)-treated rats, as well as reduced the loss of neurons and the over-activation of microglia in penumbra of ipsilateral striatum and cortex. Notably, the proportion of M2 microglia/macrophages in the total activated microglia/macrophages peaked on day 14 after tMCAO in rats, while PF11 promoted its peak advancing to day 3 post-tMCAO, which allowing the damaged brain to enter the repair period more quickly. Furthermore, PF11 increased the expression of anti-inflammatory markers and decreased the expression of pro-inflammatory markers in ipsilateral striatum and cortex. In addition, in vitro data showed that PF11 inhibited the induction of M1 microglia by oxygen glucose deprivation/re-oxygenation (OGD/R)-induced neurons, and promoted the polarization of microglia to M2 phenotype in a Jumonji domain-containing protein 3 (Jmjd3)-dependent manner. Moreover, PF11 promoted the protection of M2 microglia and attenuated the exacerbation of M1 microglia on OGD/R-induced neuronal damage. Taken together, these results indicate that PF11 protects ischemic neurons by promoting M2 microglia/macrophage polarization in a Jmjd3-dependent manner, ultimately facilitating the functional recovery following transient cerebral ischemia.
Insights
Pseudoginsenoside-F11 (PF11) promotes M2 microglia polarization after stroke, accelerating brain repair and improving recovery. This natural compound aids in reducing inflammation and protecting neurons from ischemic damage.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Microglia/macrophage polarization is crucial for outcomes after cerebral ischemia.
- Pseudoginsenoside-F11 (PF11) has demonstrated neuroprotective effects in previous ischemia models.
- Understanding PF11's impact on immune cell polarization is key to stroke recovery.
Purpose of the Study:
- To investigate the effects of PF11 on microglia/macrophage polarization following transient cerebral ischemia.
- To elucidate the underlying mechanisms of PF11's action, particularly its role in M1/M2 polarization.
- To assess PF11's therapeutic potential in improving functional recovery post-stroke.
Main Methods:
- In vivo studies using transient middle cerebral artery occlusion (tMCAO) model in rats.
- In vitro experiments involving oxygen-glucose deprivation/re-oxygenation (OGD/R) to mimic ischemic conditions.
- Assessment of cognitive and sensorimotor functions, infarct volume, brain edema, neuronal loss, and microglia activation.
- Analysis of M1/M2 microglia/macrophage polarization markers and inflammatory mediators.
- Investigation of the role of Jumonji domain-containing protein 3 (Jmjd3) in PF11's mechanism.
Main Results:
- PF11 administration significantly improved cognitive and sensorimotor functions, reduced infarct volume and brain edema in tMCAO rats.
- PF11 promoted a shift towards M2 microglia/macrophage polarization, advancing the repair phase post-ischemia.
- PF11 decreased pro-inflammatory markers and increased anti-inflammatory markers in the ischemic brain.
- In vitro, PF11 inhibited M1 microglia polarization and promoted M2 polarization in a Jmjd3-dependent manner.
- PF11 protected neurons from OGD/R-induced damage by modulating microglia polarization.
Conclusions:
- PF11 exhibits significant neuroprotective effects in transient cerebral ischemia.
- PF11 promotes beneficial M2 microglia/macrophage polarization via a Jmjd3-dependent pathway.
- PF11 facilitates functional recovery after ischemic stroke by modulating neuroinflammation and promoting repair.
