To study the ameliorating effects of curcumin in lipopolysaccharide (LPS) induced cardiac hypertrophy, mice were assigned to 4 groups (3 males and 3 females in each group): (A) control, (B) curcumin: 100？μg/kg of body weight by intraperitoneal route (IP), (C) LPS: 60？mg/kg (IP), and (D) LPS + curcumin: both at previously stated concentrations by IP route. All mice were sacrificed as 12？hr and 24？hrs groups accordingly after LPS injection. The hearts were collected, photographed for cardiomegaly, and weighed to compare heart weight/brain weight (HW/BW) in mg/mg. For immunohistochemistry, the tissue sections were exposed to histone H3, H4 and acetylated histone H3, H4 antibody. LPS induced a significant increase in histone acetylation as shown by intense staining. In curcumin + LPS treated mice nuclear staining was similar to the control group indicating that curcumin traversed the histone acetylation activity of the LPS. To further check the mechanism of action of curcumin, p300 protein acetylation levels were analyzed. This study suggests that the probable mechanism of action of curcumin is via the reduction of p300 HAT activity. 1. Introduction In the United States, foodborne pathogens cause 76 million illnesses, 325,000 hospitalizations, and 5,000 deaths annually [1]. Some of the main pathogens behind these sicknesses are gram-negative bacteria such as Salmonella, Escherichia, and Campylobacter [2]. Infections with gram-negative bacteria may lead to endotoxemia caused by lipopolysaccharides (LPS) which is a complex of glycolipids made up of two distinct regions. These are hydrophilic polysaccharide region (composed of O antigen and core oligosaccharide) and hydrophobic regions known as lipid A [3]. Lipid A is responsible for most of the LPS induced biological effects. Since lipid A is the innermost component of LPS, it is closely adherent to the inner cell wall of bacteria and is generally not released (and therefore not toxic) until the death of the bacterial cell [4]. LPS is heat stable and not strongly immunogenic, so it cannot be converted to a toxoid [4]. LPS increases histone acetylation in hypertrophic myocardium. Histone modification is the central point for the control of cardiac growth and gene expression in response to acute and chronic stress stimuli [5]. In the prevention and treatment of cardiac disease, histone modification and the signaling pathways manipulation is a major therapeutic step [5]. Histone acetyltransferases (HATs) mediate acetylation of histone tails, loosening the interaction between DNA and histones. Acetylation of
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