To understand the mechanisms involved in the anti-obesity effects Centella asiatica (CA), we examined body weight, serum levels, white adipose tissue (WAT) weight, histological analysis, and the expression of cholesterol homeostasis- and lipid metabolism-related genes in mice with high-fat, high-sugar diet (HFHSD)-induced obesity that were orally treated with CA for 12 weeks. Eight-week-old, male C57BL/6J mice were assigned to the following four groups (8 mice/group): NOR, normal diet; HFHSD (Control), HFHSD; CA-L, HFHSD + CA 300 mg/kg; CA-H, HFHSD+CA 600 mg/kg. The suspension of powdered CA leaf was fed using oral gavage. CA treatment significantly attenuated HFHSD-induced increase in body weight gain, serum glucose, triacylglycerol, and WAT weight (p < 0.05). Compared to that in HFHSD, adipocyte diameter and macrovesicular area of epididymal WAT significantly decreased with CA treatment (p < 0.05). The mRNA expression levels of peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid synthase (FAS), cluster of differentiation 36 (CD36), 3- hydroxyl-3-methylglutaryl CoA reductase (HMGCR), and stearoyl CoA desaturase 1 (SCD 1) were significantly downregulated in the CA-H compared to the HFHSD (p < 0.05). CA exerts anti-obesity effects by lowering body fat accumulation via regulating gene expression and thus, is a potential lipid-lowering agent.

中文翻译：

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积雪草通过调节高脂高糖饮食诱导肥胖小鼠的胆固醇稳态和脂质代谢相关基因来降低体内脂肪积累

为了了解积雪草 (CA) 的抗肥胖作用机制，我们检查了积雪草 (CA) 的体重、血清水平、白色脂肪组织 (WAT) 重量、组织学分析以及胆固醇稳态和脂质代谢相关基因的表达。患有高脂肪、高糖饮食 (HFHSD) 诱导的肥胖小鼠，口服 CA 治疗 12 周。八周大的雄性 C57BL/6J 小鼠被分配到以下四组（8 只小鼠/组）：NOR，正常饮食；HFHSD（控制），HFHSD；CA-L、HFHSD + CA 300 毫克/千克；CA-H、HFHSD+CA 600 毫克/千克。使用口服强饲法饲喂粉状CA叶的悬浮液。CA治疗显着减弱了HFHSD引起的体重增加、血糖、三酰甘油和WAT重量的增加（p < 0.05）。与 HFHSD 相比，CA 治疗后附睾 WAT 的脂肪细胞直径和大泡面积显着减小（p < 0.05）。过氧化物酶体增殖物激活受体 γ (PPARγ)、脂肪酸合酶 (FAS)、分化簇 36 (CD36)、3-羟基-3-甲基戊二酰辅酶 A 还原酶 (HMGCR) 和硬脂酰辅酶 A 去饱和酶 1 (SCD) 的 mRNA 表达水平1) 与 HFHSD 相比，CA-H 中的表达显着下调 (p < 0.05)。CA通过调节基因表达降低体内脂肪积累来发挥抗肥胖作用，因此是一种潜在的降脂剂。