Carnosine Attenuates Brain Oxidative Stress and Apoptosis After Intracerebral Hemorrhage in Rats
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Carnosine, an endogenous dipeptide (β-alanyl-l-histidine), exerts multiple neuroprotective properties, but its role in intracerebral hemorrhage (ICH) remains unclear. This study investigates the effect of Carnosine on brain injury using the rat ICH model, which is established by type IV collagenase caudatum infusion. The results indicate that intraperitoneal administration of Carnosine (1000 mg/kg) significantly attenuates brain edema, blood–brain barrier (BBB) disruption, oxidative stress, microglia activation and neuronal apoptosis of perihematoma at 72 h following ICH in rats models, as convinced by preventing the disruption of tight junction protein ZO-1, occludin and claudin-5, followed by the decrease of ROS, MDA, 3-NT, 8-OHDG level and the increase of GSH-Px and SOD activity, then followed by the decline of Iba-1, ED-1, active caspase-3 and TUNEL positive cells and the decrease of IL-1β, IL-6, TNF-α, active caspase-3 and cytochrome c level. Our results suggest that Carnosine may provide neuroprotective effect after experimental ICH in rat models.
KeywordsIntracerebral hemorrhage Carnosine Blood–brain barrier Oxidative stress Microglia activation Neuronal apoptosis
The national natural science foundation of China (NSFC) (Grant Numbers 81301018, 81471212 and 81671141) supported this work.
ZZ, BS and XY conceived the project and designed experiments. RX, DL, XL, MY, JF, and XY performed the experiments; ZZ and XY analyzed the results and wrote the manuscript. XY revised the manuscript. All authors read and approved the final manuscript.
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Conflict of interest
All authors declare that they have no conflict of interest.
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