Abstract Title:

Evidence for the protective effects of curcumin against oxyhemoglobin-induced injury in rat cortical neurons.

Abstract Source:

Brain Res Bull. 2015 Nov 10 ;120:34-40. Epub 2015 Nov 10. PMID: 26551062

Abstract Author(s):

Xia Li, Lei Zhao, Liang Yue, Haixiao Liu, Xiangmin Yang, Xinchuan Wang, Yan Lin, Yan Qu

Article Affiliation:

Xia Li


Curcumin (CCM) is a natural polyphenolic compound in Curcuma longa that has been reported to exhibit neuroprotective effects. Subarachnoid hemorrhage (SAH) is a severe neurological disorder with an unsatisfactory prognosis. Oxyhemoglobin (OxyHb) plays an important role in mediating the neurological deficits following SAH. The present study, therefore, aimed to investigate the effect of CCM on primary cortical neurons exposed to OxyHb neurotoxicity. Cortical neurons were exposed to OxyHb at a concentration of 10μM in the presence or absence of 5μM (low dose) or 10μM (high dose) CCM for 24h. Morphological changes in the neurons were observed. Cell viability and lactate dehydrogenase (LDH) release were assayed to determine the extent of cell injury. Additionally, levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and reactive oxygen species (ROS) were measured. Neuronal apoptosis was assayed via TUNEL staining and protein levels of cleaved caspase-3, Bax, and Bcl-2 were measured by Western blot. Levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 were measured using ELISA kits. Our results suggested that CCM at both low and high doses markedly improved cell viability and decreased LDH release. CCM treatment decreased neuronal apoptosis. Additionally, oxidative stress and inflammation induced by OxyHb were alleviated by CCMtreatment. In conclusion, CCM inhibits neuronal apoptosis, and alleviates oxidative stress and inflammation in neurons subjected to OxyHb, suggesting that it may be beneficial in the treatment of brain damage following SAH.

Study Type : In Vitro Study

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