Hot water extract of turmeric (Curcuma longa) prevents non-alcoholic steatohepatitis in mice by inhibiting hepatic oxidative stress and inflammation

Ryusei Uchio; Shinji Murosaki; Hiroshi Ichikawa

doi:10.1017/jns.2018.27

Hot water extract of turmeric (Curcuma longa) prevents non-alcoholic steatohepatitis in mice by inhibiting hepatic oxidative stress and inflammation

J Nutr Sci. 2018 Dec 27:7:e36. doi: 10.1017/jns.2018.27. eCollection 2018.

Authors

Ryusei Uchio¹, Shinji Murosaki², Hiroshi Ichikawa¹

Affiliations

¹ Department of Medical Life Systems, Faculty of Life and Medical Sciences, Doshisha University, 1-3 Tatara Miyakodani, Kyotanabe City, Kyoto 610-0321, Japan.
² Nihon Pharmaceutical University, Komuro 10281, Ina-machi, Kitaadachi-gun, Saitama 362-0806, Japan.

Abstract

Curcuma longa, also known as turmeric, has long been used as a medicinal herb with various biological effects. A hot water extract of C. longa (WEC) has been reported to show antioxidant and anti-inflammatory activity, but its effect on hepatic inflammation is poorly understood. In the present study, to investigate the effect of WEC on non-alcoholic steatohepatitis, C57BL/6J mice were fed a low-methionine, choline-deficient diet with 0·175 % WEC (WEC group) or without WEC (control group) for 6 or 12 weeks. Although hepatic steatosis was similar in the WEC group and the control group, WEC suppressed the elevation of plasma aspartate aminotransferase and alanine aminotransferase, which are markers of hepatocellular damage. Compared with the control group, the WEC group had higher hepatic levels of reduced glutathione and superoxide dismutase, as well as a lower hepatic level of thiobarbituric acid-reactive substances. WEC also reduced hepatic expression of mRNA for inflammatory factors, including TNF-α, IL-1β, IL-6, monocyte chemoattractant protein-1, vascular cell adhesion molecule-1, F4/80 and CC motif chemokine receptor 2. Histological examination revealed that WEC suppressed hepatic recruitment of F4/80⁺ monocytes/macrophages and inhibited hepatic fibrosis. Furthermore, WEC inhibited hepatic expression of mRNA for molecules related to fibrosis, such as transforming growth factor-β, α-smooth muscle actin, type I collagen (α1-chain) and tissue inhibitor of matrix metalloproteinase-1. These findings suggest that dietary intake of WEC prevents the progression of non-alcoholic steatohepatitis by alleviating hepatic oxidative stress and inflammation.

Keywords: ALT, alanine aminotransferase; AST, aspartate aminotransferase; CCR2, CC motif chemokine receptor 2; COL1A1, α1-chain of type I collagen; Fibrosis; GSH, reduced glutathione; GSSG, oxidised glutathione; HSC, hepatic stellate cells; Inflammation; KC, Kupffer cells; LMCD, low-methionine, choline-deficient; MCP-1, monocyte chemoattractant protein-1; NASH, non-alcoholic steatohepatitis; Non-alcoholic steatohepatitis; Oxidative stress; ROS, reactive oxygen species; SOD, superoxide dismutase; TBARS, thiobarbituric acid-reactive substances; TGF-β, transforming growth factor-β; TIMP-1, tissue inhibitor of metalloproteinases-1; Turmeric (Curcuma longa); VCAM-1, vascular cell adhesion molecule-1; WEC, hot water extract of Curcuma longa; α-SMA, α-smooth muscle actin.