Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, College of Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang 150030, People's Republic of China.
College of Veterinary Medicine, South China Agricultural University, Guangzhou, Guangdong 510642, People's Republic of China.
J Agric Food Chem. 2022 Aug 31;70(34):10532-10542. doi: 10.1021/acs.jafc.2c04593. Epub 2022 Aug 17.
Chronic stress can cause chronic inflammatory injury to the liver. Chlorogenic acid (CGA) is known to have a wide range of biological activities and anti-inflammatory effects. Resolvin D1 (RvD1) is a polyunsaturated fatty acid derivative that has inhibitory effects on a variety of inflammatory diseases. However, whether CGA can inhibit liver inflammation in chronic stress through RvD1 remains unclear. In this work, male rats were subjected to restraint stress for 6 h every day and built a chronic stress model for 21 days. CGA (100 mg/kg) was administered intragastrically 1 h before restraint, with intraperitoneal injection of RvD1 inhibitor WRW4 (antagonist of FPR2, 0.1 mg/kg) or WRW4 solution every 2 days for 30 min before CGA administration. CGA reduced hepatic hemorrhage and inflammatory cell infiltration, alleviated hepatic injury, decreased the activation of the NF-κB pathway and the expression of interleukin 1β, interleukin 6, and tumor necrosis factor α in the liver, and increased RvD1 in the serum and liver. The therapeutic effect of CGA was blocked after WRW4 intervention. These results suggest that the protective effects of CGA mediate the NF-κB pathway by upregulating the generation of RvD1. Above all, this research demonstrates the liver protective effect of CGA and provides a potential treatment strategy for chronic inflammatory disease.
慢性应激可导致肝脏发生慢性炎症损伤。绿原酸(CGA)具有广泛的生物学活性和抗炎作用。解析素 D1(RvD1)是一种多不饱和脂肪酸衍生物,对多种炎症性疾病具有抑制作用。然而,CGA 是否可以通过 RvD1 抑制慢性应激引起的肝炎症尚不清楚。在这项工作中,雄性大鼠每天接受 6 小时的束缚应激,并建立了 21 天的慢性应激模型。CGA(100mg/kg)在束缚前 1 小时经胃内给药,束缚前 2 天每隔 2 天腹腔注射 RvD1 抑制剂 WRW4(FPR2 的拮抗剂,0.1mg/kg)或 WRW4 溶液 30 分钟,然后给予 CGA。CGA 减少了肝出血和炎症细胞浸润,缓解了肝损伤,降低了 NF-κB 通路的激活和肝内白细胞介素 1β、白细胞介素 6 和肿瘤坏死因子 α 的表达,并增加了血清和肝脏中的 RvD1。WRW4 干预后阻断了 CGA 的治疗效果。这些结果表明,CGA 的保护作用通过上调 RvD1 的产生来介导 NF-κB 通路。综上所述,本研究证明了 CGA 的肝脏保护作用,并为慢性炎症性疾病提供了一种潜在的治疗策略。