PPAR-γ Promotes Hematoma Clearance through Haptoglobin-Hemoglobin-CD163 in a Rat Model of Intracerebral Hemorrhage

Abstract EN

Background and Purpose.

PPAR-γ is a transcriptional factor which is associated with promoting hematoma clearance and reducing neurological dysfunction after intracerebral hemorrhage (ICH).

Haptoglobin- (Hp-) hemoglobin- (Hb-) CD163 acts as a main pathway to Hb scavenging after ICH.

The effect of PPAR-γ on the Hp-Hb-CD163 signaling pathway has not been reported.

We hypothesized that PPAR-γ might protect against ICH-induced neuronal injury via activating the Hp-Hb-CD163 pathway in a rat ICH model.

Methods.

107 Sprague-Dawley rats were used in this research.

They were randomly allocated to 4 groups as follows: sham group, vehicle group, monascin-treated group, and Glivec-treated group.

Animals were euthanized at 3 days after the model was established successfully.

We observed the effects of PPAR-γ on the brain water content, hemoglobin levels, and the expressions of CD163 and Hp in Western blot and real-ime PCR; meanwhile, we measured hematoma volumes and edema areas by MRI scanning.

Result.

The results showed that PPAR-γ agonist significantly reduced hematoma volume, brain edema, and hemoglobin after ICH.

It also enhanced CD163 and Hp expression while PPAR-γ antagonist had the opposite effects.

Conclusions.

PPAR-γ promotes hematoma clearance and plays a protective role through the Hp-Hb-CD163 pathway in a rat collagenase infusion ICH model.