Curcumin, a CBP HAT activity inhibitor, reduces histone acetylation and attenuates ischemic preconditioning in primary cortical cultures.

<p><b>A</b>, Representative result of Western blotting analyses of neuronal cultures following treatment with indicated concentrations of Curcumin for 24 h using antibodies against ac-histone H4, ac-histone H4 and actin. <b>B</b>, Quantification of the Western blotting images was performed using ImageJ program and one-way ANOVA followed by Tukey test was conducted for statistical analyses. Bar graphs represent the mean values from 4 experiments ± SEM. *<i>p</i><0.05. <b>C</b>, Experimental design. Rat cortical neurons were exposed to 30 min non-injurious preconditioning oxygen-glucose deprivation (OGD) on DIV 9 (<i>in vitro</i> day 9), and treated with 1 µM curcumin for the 24 h interval between the preconditioning and injurious OGDs. Damaging OGD of 150 min was conducted on DIV 10, and neuronal cell death was monitored by lactate dehydrogenase analysis (LDH) further 24 h later. <b>D</b>, Neuronal death was assessed 24 h after the injurious OGD exploiting the increase in LDH in the culture medium. Curcumin per se had no significant impact on the release of LDH in controls or OGD treated cultures which were not exposed to preceding preconditioning OGD. *p<0.05, unpaired t-test. The graph shows LDH release in preconditioned cultures relative to non-preconditioned cultures for vehicle and curcumin treatment conditions. N = 2 experiments. Data is shown as scattered dot blots representing cell culture wells with mean relative protection ± SEM.