Engineering Research Center of Chestnut Industry Technology of Ministry of Education, Hebei Key Laboratory of Active Components and Functions in Natural Products, College of Food Science & Technology, Hebei Normal University of Science and Technology, Qinhuangdao, Hebei 066004, China.
Hebei Yanshan Special Industrial Technology Research Institute, Qinhuangdao, Hebei 066004, China.
Food Funct. 2023 May 22;14(10):4807-4823. doi: 10.1039/d3fo00604b.
Chinese chestnut shell is a by-product of chestnut food processing and is rich in polyphenols. This study sought to investigate the effect of chestnut shell polyphenol extract (CSP) on weight loss and lipid reduction in a 12-week high-fat diet (HFD)-induced murine obesity model. CSP (300 mg per kg body weight) was administered intragastrically daily. AG490, a JAK2 protein tyrosine kinase inhibitor, was also intraperitoneally injected. The results showed that an HFD induced leptin resistance (LR). Compared to corresponding values in the HFD group, CSP treatment improved blood lipid levels, weight, and leptin levels in obese mice ( < 0.01). Additionally, CSP treatment enhanced enzyme activity by improving total antioxidant capacity, attenuating oxidative stress, and reducing fat droplet accumulation and inflammation in the liver, epididymal, and retroperitoneal adipose tissue. CSP also activated the LEPR-JAK2/STAT3-PTP1B-SOCS-3 signal transduction pathway in hypothalamus tissue and improved LR while regulating the expression of proteins related to lipid metabolism (PPARγ, FAS, and LPL) in white adipose tissue in the retroperitoneal cavity. However, the amelioration of lipid metabolism by CSP was dependent on JAK2. Molecular docking simulation further demonstrated the strong binding affinity of procyanidin C1 (-10.3983297 kcal mol) and procyanidin B1 (-9.12686729 kcal mol) to the crystal structure of JAK2. These results suggest that CSP may be used to reduce HFD-induced obesity with potential application as a functional food additive.
板栗壳是板栗食品加工的副产物，富含多酚。本研究旨在探讨板栗壳多酚提取物（CSP）对 12 周高脂饮食（HFD）诱导的肥胖小鼠模型中体重减轻和脂质减少的影响。CSP（300mg/kg 体重）每天灌胃给药。还通过腹腔内注射 JAK2 蛋白酪氨酸激酶抑制剂 AG490。结果表明，HFD 诱导瘦素抵抗（LR）。与 HFD 组相应值相比，CSP 治疗可改善肥胖小鼠的血脂水平、体重和瘦素水平（<0.01）。此外，CSP 治疗通过提高总抗氧化能力、减轻氧化应激、减少肝、附睾和腹膜后脂肪组织中脂肪滴积累和炎症来增强酶活性。CSP 还通过激活下丘脑组织中的 LEPR-JAK2/STAT3-PTP1B-SOCS-3 信号转导通路来改善 LR，同时调节腹膜后腔白色脂肪组织中与脂质代谢相关的蛋白（PPARγ、FAS 和 LPL）的表达。然而，CSP 改善脂质代谢依赖于 JAK2。分子对接模拟进一步证明了原花青素 C1（-10.3983297kcal/mol）和原花青素 B1（-9.12686729kcal/mol）与 JAK2 晶体结构的强结合亲和力。这些结果表明，CSP 可能用于减轻 HFD 诱导的肥胖，具有作为功能性食品添加剂的潜在应用。
