Experimental neurology · 2026
Oleic acid ameliorates the disrupted blood-brain barrier and neuroinflammation following intracerebral hemorrhage in mice by regulating PPARγ.
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Li Jingjing, Guo Pingping, Liu Yang, Qian Juanfeng, Wang Qingli, Xia Bin, Yong V Wee, Xue Mengzhou
Аннотация
BACKGROUND: Oleic acid (OA) is demonstrated to have neuroprotective effects and may improve the therapy of neurological disorders. However, the mechanism of OA impact on blood-brain barrier (BBB) and neuroinflammation following intracerebral hemorrhage (ICH) remains indistinct. Here, we aimed to affirm the neuroprotective influence of OA in ICH and to explore the latent molecular mechanism.
METHODS: The male C57BL/6 mice (n = 124) was used for this study. ICH model was induced by intracerebral injection of collagenase. OA (60 mg/kg) was administrated 2 h after ICH. Neurobehavioral tests were performed to assess the neurofunctional outcome after ICH. The wet-dry method was used for quantifying brain edema at day 3 after ICH injury. The change of tight junctions (TJs) proteins (ZO-1, occludin, claudin5) and Evans Blue (EB) extravasation were used for evaluating BBB integrity. Microglial cell activation and neutrophil infiltration were evaluated by immunofluorescence staining. The levels of apoptosis-related factors and inflammatory cytokines were determined by western blot, and the apoptotic cells were tested by TUNEL assay.
RESULTS: OA treatment visibly decreased hemoglobin content and improved neurological function after ICH. OA also decreased the BBB permeability, as clarified by the declined EB extravasation and brain water content. OA remarkably reduced MMP-9 level and elevated TJs proteins (ZO-1, occludin, claudin5) levels, also reduced brain cell apoptosis. OA could markedly reduce MPO positive neutrophil infiltration and microglia activation of IBA-1+CD16+ cells, and increased microglia activation of Arg-1+IBA-1+ cells. Meanwhile, OA elevated peroxisome proliferator-activated receptor-gamma (PPARγ) level and decreased the levels of inflammatory cytokines. However, GW9662 (PPARγ antagonist) abolished OA protection in brain injury of mouse ICH model.
CONCLUSION: OA could attenuate brain injury in experimental ICH by mitigating BBB disruption and attenuating neuroinflammation associated with PPARγ, thereby, OA might act as a latent neuroprotectant for treating ICH.
METHODS: The male C57BL/6 mice (n = 124) was used for this study. ICH model was induced by intracerebral injection of collagenase. OA (60 mg/kg) was administrated 2 h after ICH. Neurobehavioral tests were performed to assess the neurofunctional outcome after ICH. The wet-dry method was used for quantifying brain edema at day 3 after ICH injury. The change of tight junctions (TJs) proteins (ZO-1, occludin, claudin5) and Evans Blue (EB) extravasation were used for evaluating BBB integrity. Microglial cell activation and neutrophil infiltration were evaluated by immunofluorescence staining. The levels of apoptosis-related factors and inflammatory cytokines were determined by western blot, and the apoptotic cells were tested by TUNEL assay.
RESULTS: OA treatment visibly decreased hemoglobin content and improved neurological function after ICH. OA also decreased the BBB permeability, as clarified by the declined EB extravasation and brain water content. OA remarkably reduced MMP-9 level and elevated TJs proteins (ZO-1, occludin, claudin5) levels, also reduced brain cell apoptosis. OA could markedly reduce MPO positive neutrophil infiltration and microglia activation of IBA-1+CD16+ cells, and increased microglia activation of Arg-1+IBA-1+ cells. Meanwhile, OA elevated peroxisome proliferator-activated receptor-gamma (PPARγ) level and decreased the levels of inflammatory cytokines. However, GW9662 (PPARγ antagonist) abolished OA protection in brain injury of mouse ICH model.
CONCLUSION: OA could attenuate brain injury in experimental ICH by mitigating BBB disruption and attenuating neuroinflammation associated with PPARγ, thereby, OA might act as a latent neuroprotectant for treating ICH.