Curcumin and Curcuma longa L. extract ameliorate lipid accumulation through the regulation of the endoplasmic reticulum redox and ER stress

Hwa Young Lee, Seung Wook Kim, Geum Hwa Lee, Min Kyung Choi, Han Wool Chung, Yong Chul Lee, Hyung Ryong Kim, Ho Jeong Kwon, Han Jung Chae

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34 Citations (Scopus)


For this study, we examined the effects of curcumin against acute and chronic stress, paying specific attention to ROS. We also aimed to clarify the differences between acute and chronic stress conditions. We investigated the effects of curcumin against acute stress (once/1 day CCl4 treatment) and chronic-stress (every other day/4week CCl4 treatment). Compared with acute stress, in which the antioxidant system functioned properly and aspartate transaminase (AST) and ROS production increased, chronic stress increased AST, alanine aminotransferase (ALT), hepatic enzymes, and ROS more significantly, and the antioxidant system became impaired. We also found that ER-originated ROS accumulated in the chronic model, another difference between the two conditions. ER stress was induced consistently, and oxidative intra-ER protein folding status, representatively PDI, was impaired, especially in chronic stress. The PDI-associated client protein hepatic apoB accumulated with the PDI-binding status in chronic stress, and curcumin recovered the altered ER folding status, regulating ER stress and the resultant hepatic dyslipidemia. Throughout this study, curcumin and curcumin-rich Curcuma longa L. extract promoted recovery from CCl4-induced hepatic toxicity in both stress conditions. For both stress-associated hepatic dyslipidemia, curcumin and Curcuma longa L. extract might be recommendable to recover liver activity.

Original languageEnglish
Article number6513
JournalScientific reports
Issue number1
Publication statusPublished - 2017 Dec 1

Bibliographical note

Funding Information:
This work was supported by National Research Foundation (2015R1A2A1A13001849 and 2008-0062279 to H.J.C. and MSIP; 2015K1A1A2028365 and 2015M3A9C4076321 to H.J.K.). This work was partly supported by the Korea Healthcare Technology R&D Project (A121931), Ministry for Health and Welfare, Republic of Korea to H.J.C.

Publisher Copyright:
© 2017 The Author(s).

All Science Journal Classification (ASJC) codes

  • General


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