Curcumin attenuation of lipopolysaccharide induced cardiac hypertrophy in rodents.

ISRN inflammation Pub Date : 2013-10-21 eCollection Date: 2013-01-01 DOI:10.1155/2013/539305
Rupak Chowdhury, Ramadevi Nimmanapalli, Thomas Graham, Gopal Reddy
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引用次数: 25

Abstract

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  μ g/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.

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Abstract Image

姜黄素对脂多糖的抑制作用诱导啮齿动物心肌肥厚。
为了研究姜黄素对脂多糖(LPS)诱导的心肌肥厚的改善作用,将小鼠分为4组(每组3公3母):(A)对照组,(B)姜黄素:100 μ g/kg体重腹腔注射(IP), (C) LPS: 60 mg/kg (IP), (D) LPS +姜黄素:均为预先设定的浓度(IP)。LPS注射后12 h和24 h分别处死小鼠。采集心脏,拍照检查有无心脏肿大,称重比较心重/脑重(HW/BW),单位为mg/mg。免疫组化,组织切片暴露于组蛋白H3, H4和乙酰化组蛋白H3, H4抗体。强染色显示LPS诱导组蛋白乙酰化显著增加。姜黄素+ LPS处理小鼠的细胞核染色与对照组相似,表明姜黄素穿越了LPS的组蛋白乙酰化活性。为了进一步研究姜黄素的作用机制,我们分析了p300蛋白乙酰化水平。本研究提示姜黄素的作用机制可能是通过降低p300 HAT活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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