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Carnosine Attenuates Early Brain Injury Through Its Antioxidative and Anti-apoptotic Effects in a Rat Experimental Subarachnoid Hemorrhage Model

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Abstract

Carnosine (β-alanyl-l-histidine) has been demonstrated to provide antioxidative and anti-apoptotic roles in the animal of ischemic brain injuries and neurodegenerative diseases. The aim of this study was to examine whether carnosine prevents subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) in rats. We found that intraperitoneal administration of carnosine improved neurobehavioral deficits, attenuated brain edema and blood–brain barrier permeability, and decreased reactive oxygen species level at 48 h following SAH in rat models. Carnosine treatment increased tissue copper/zinc superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px) enzymatic activities, and reduced post-SAH elevated lactate dehydrogenase (LDH) activity, the concentration of malondialdehyde (MDA), 3-nitrotyrosine (3-NT), 8-hydroxydeoxyguanosine (8-OHDG), interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) in rats. Furthermore, carnosine treatment attenuated SAH-induced microglia activation and cortical neuron apoptosis. These results indicated that administration of carnosine may provide neuroprotection in EBI following SAH in rat models.

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Acknowledgments

This work was partially supported by the National Natural Science Foundation of China (NSFC) (No. 81301018 for Z.Z. and No. 81271275 for B.S.).

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The authors have declared that no conflict of interest exists.

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Correspondence to Zong-yong Zhang or Bao-liang Sun.

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Zhang, Zy., Sun, Bl., Yang, Mf. et al. Carnosine Attenuates Early Brain Injury Through Its Antioxidative and Anti-apoptotic Effects in a Rat Experimental Subarachnoid Hemorrhage Model. Cell Mol Neurobiol 35, 147–157 (2015). https://doi.org/10.1007/s10571-014-0106-1

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  • DOI: https://doi.org/10.1007/s10571-014-0106-1

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