Wu You, Wang Minghui, Yang Tao, Qin Lingling, Hu Yaomu, Zhao Dan, Wu Lili, Liu Tonghua
Key Laboratory of Health Cultivation of the Ministry of Education, Beijing University of Chinese Medicine, Beijing 100029, China.
Key Laboratory of Health Cultivation of Beijing, Beijing University of Chinese Medicine, Beijing 100029, China.
Evid Based Complement Alternat Med. 2021 Sep 2;2021:9561613. doi: 10.1155/2021/9561613. eCollection 2021.
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.
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.
CA treatment reduced the lipid accumulation in HepG2 cells and in db/db mouse livers. ACLY, ACC, FAS, SCD1, PPAR, and CD36 were significantly downregulated, while CPT1A, PGC1, and PPAR were significantly upregulated.
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.
肉桂酸（CA）已被证明具有多种有益作用，包括调节脂质代谢和减轻肥胖。然而，其对非酒精性脂肪性肝病（NAFDL）的影响尚未得到详细研究。因此，我们进行了这项研究，以探讨CA对肝脏脂质代谢的影响及其潜在机制。
使用油酸（OA）诱导HepG2细胞中的脂质积累。与CA共同孵育后，用油红O对细胞进行染色，并评估甘油三酯（TG）含量。检测脂肪生成和脂肪酸氧化途径中的关键基因。此外，将db/db和wt/wt小鼠分为三组，wt/wt小鼠代表正常组，db/db小鼠分为非酒精性脂肪性肝病组和CA组。经过4周的口服治疗后，处死所有小鼠并评估血脂谱和肝脏组织。
CA治疗减少了HepG2细胞和db/db小鼠肝脏中的脂质积累。ACLY、ACC、FAS、SCD1、PPAR和CD36显著下调，而CPT1A、PGC1和PPAR显著上调。
CA对非酒精性脂肪性肝病的治疗作用可能归因于其降低肝脏脂质积累的能力，这是通过抑制肝脏脂肪生成和脂肪酸摄取以及增加脂肪酸氧化来介导的。
