Cinnamic Acid Ameliorates Nonalcoholic Fatty Liver Disease by Suppressing Hepatic Lipogenesis and Promoting Fatty Acid Oxidation

You Wu; Minghui Wang; Tao Yang; Lingling Qin; Yaomu Hu; Dan Zhao; Lili Wu; Tonghua Liu

doi:10.1155/2021/9561613

Cinnamic Acid Ameliorates Nonalcoholic Fatty Liver Disease by Suppressing Hepatic Lipogenesis and Promoting Fatty Acid Oxidation

Evid Based Complement Alternat Med. 2021 Sep 2:2021:9561613. doi: 10.1155/2021/9561613. eCollection 2021.

Authors

You Wu^{1

2}, Minghui Wang³, Tao Yang^{1

2}, Lingling Qin⁴, Yaomu Hu^{1

2

5}, Dan Zhao^{1

2

5}, Lili Wu^{1

2}, Tonghua Liu^{1

2}

Affiliations

¹ Key Laboratory of Health Cultivation of the Ministry of Education, Beijing University of Chinese Medicine, Beijing 100029, China.
² Key Laboratory of Health Cultivation of Beijing, Beijing University of Chinese Medicine, Beijing 100029, China.
³ Chengdu Integrated TCM and Western Medicine Hospital, Chengdu 610016, China.
⁴ Department of Science and Technology, Beijing University of Chinese Medicine, Beijing 100029, China.
⁵ First School of Clinical Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.

Abstract

Background: Cinnamic acid (CA) has been shown to have many beneficial effects including regulating lipid metabolism and reducing obesity. However, its effect on nonalcoholic fatty liver disease (NAFDL) has not been investigated in detail. Thus, we performed this study in order to explore CA's effect on hepatic lipid metabolism and the underlying mechanisms.

Method: Oleic acid (OA) was used to induce lipid accumulation in HepG2 cells. After coincubation with CA, the cells were stained with oil red O and the triglyceride (TG) content was assessed. Key genes in lipogenesis and fatty acid oxidation pathways were tested. Additionally, db/db and wt/wt mice were divided into three groups, with the wt/wt mice representing the normal group and the db/db mice being divided into the NAFLD and CA groups. After 4 weeks of oral treatment, all mice were sacrificed and the blood lipid profile and liver tissues were assessed.

Results: CA treatment reduced the lipid accumulation in HepG2 cells and in db/db mouse livers. ACLY, ACC, FAS, SCD1, PPARγ, and CD36 were significantly downregulated, while CPT1A, PGC1α, and PPARα were significantly upregulated.

Conclusion: CA's therapeutic effect on NAFLD may be attributed to its ability to lower hepatic lipid accumulation, which is mediated by suppression of hepatic lipogenesis and fatty acid intake, as well as increased fatty acid oxidation.