1. Academic Validation
  2. Apigenin and apigenin-7, 4'-O-dioctanoate protect against acrolein-aggravated inflammation via inhibiting the activation of NLRP3 inflammasome and HMGB1/MYD88/NF-κB signaling pathway in Human umbilical vein endothelial cells (HUVEC)

Apigenin and apigenin-7, 4'-O-dioctanoate protect against acrolein-aggravated inflammation via inhibiting the activation of NLRP3 inflammasome and HMGB1/MYD88/NF-κB signaling pathway in Human umbilical vein endothelial cells (HUVEC)

  • Food Chem Toxicol. 2022 Oct;168:113400. doi: 10.1016/j.fct.2022.113400.
Jiangqiong Yu 1 Qingqing Jiang 1 Ning Liu 1 Daming Fan 2 Mingfu Wang 3 Yueliang Zhao 4
Affiliations

Affiliations

  • 1 College of Food Science and Technology, Shanghai Ocean University, Shanghai, 201306, China; Laboratory of Quality and Safety Risk Assessment for Aquatic Products on Storage and Preservation (Shanghai), Ministry of Agriculture, Shanghai, 201306, China.
  • 2 School of Food Science and Technology, Jiangnan University, Wuxi, China.
  • 3 Institute for Advanced Study, Shenzhen University, Shenzhen, China.
  • 4 College of Food Science and Technology, Shanghai Ocean University, Shanghai, 201306, China; Laboratory of Quality and Safety Risk Assessment for Aquatic Products on Storage and Preservation (Shanghai), Ministry of Agriculture, Shanghai, 201306, China. Electronic address: yueliang2110@163.com.
Abstract

Exposure to acrolein, one environmental and dietary pollutant, has been shown to cause inflammation. Here, we reported for the first time that acrolein aggravated lipopolysaccharide (LPS)-induced inflammation in Human umbilical vein endothelial cells (HUVEC) as evidenced by the further increased mRNA expression of three pro-inflammatory cytokines, including interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Acrolein also further increased the generation of Reactive Oxygen Species (ROS) and decreased the activity of Glutathione Peroxidase (GSH-Px) in LPS-pretreated HUVEC. Moreover, acrolein treatment further increased the nucleotide oligomerization domain-like receptor protein 3 (NLRP3) and apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) expression, Caspase-1 cleavage, and downstream matures interleukin 18 (IL-18) and IL-1β level in LPS-pretreated HUVEC. Acrolein treatment also further increased the expressions of high-mobility group box 1 (HMGB1), Toll-like Receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and phospho-NF-κB P65 (P-P65) in the LPS pre-treated HUVEC. Thus, acrolein aggravated LPS-induced HUVEC inflammation through induction of oxidative stress, and activation of NLRP3 inflammasome and HMGB1/MyD88/NF-κB signaling pathway. In addition, apigenin and apigenin-7, 4'-O-dioctanoate attenuated acrolein-aggravated inflammation by targeting the above signaling pathways. Our findings could help to develop potential therapeutic strategies against acrolein-enhanced inflammation.

Keywords

4′-O-Dioctanoate; Acrolein; Apigenin; Apigenin-7; HUVEC; Inflammation.

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