College of Food Science and Engineering, Shandong Agricultural University, Key Laboratory of Food Processing Technology and Quality Control of Shandong Higher Education Institutes, Taian, 271018, People's Republic of China.
College of Food Science and Engineering, Shandong Agricultural University, Key Laboratory of Food Processing Technology and Quality Control of Shandong Higher Education Institutes, Taian, 271018, People's Republic of China; School of Chemical Sciences, The University of Auckland, Auckland, New Zealand.
Food Chem Toxicol. 2021 Dec;158:112654. doi: 10.1016/j.fct.2021.112654. Epub 2021 Oct 29.
Cadmium (Cd) is a toxic heavy metal pollutant that can be accumulated in organs including the spleen, thereby threatening human health. In this study, the effect of caffeic acid phenethyl ester (CAPE, a bioactive component of honeybee propolis) on CdCl-induced spleen toxicity and underlying mechanisms were examined in mice. Histological examinations revealed that CAPE (10 μmol/kg/day b.w.) could mitigate spleen damage induced by CdCl (1.5 mg/kg/day b.w.) in mice. Compared to the mice treated only by CdCl, CAPE administration increased the body weight while decreasing the spleen weight, spleen Cd content and spleen to body ratio of the CdCl-treated mice. Western blot and ELISA tests revealed that CAPE suppressed CdCl-induced inflammation (indicated by the decreases in the levels of inflammatory indictors). TUNEL and Western blot results showed that CAPE suppressed CdCl-induced apoptosis through reducing the percentage of TUNEL-positive cells and regulating apoptosis factors. The antagonistic effect of CAPE against CdCl-induced spleen toxicity was realized by increasing miR-182-5p expression to regulate the TLR4/NF-κB pathway. Therefore, CAPE could be a food-derived spleen protector to counteract Cd-induced spleen toxicity through alleviating apoptosis and inflammation via the miR-182-5p/TLR4/NF-κB axis.
镉 (Cd) 是一种有毒的重金属污染物，可在包括脾脏在内的器官中积累，从而威胁人类健康。在这项研究中，研究了咖啡酸苯乙酯 (CAPE，蜂胶的一种生物活性成分) 对氯化镉 (CdCl，1.5mg/kg/天 bw) 诱导的脾毒性的影响及其潜在机制。组织学检查表明，CAPE(10 μmol/kg/天 bw) 可以减轻 CdCl(1.5mg/kg/天 bw) 诱导的小鼠脾脏损伤。与仅用 CdCl 处理的小鼠相比，CAPE 给药增加了体重，同时降低了 CdCl 处理小鼠的脾脏重量、脾脏 Cd 含量和脾脏与体重比。Western blot 和 ELISA 检测结果表明，CAPE 抑制了 CdCl 诱导的炎症(表现为炎症指标水平降低)。TUNEL 和 Western blot 结果表明，CAPE 通过降低 TUNEL 阳性细胞的百分比和调节凋亡因子来抑制 CdCl 诱导的细胞凋亡。CAPE 拮抗 CdCl 诱导的脾毒性的作用是通过增加 miR-182-5p 的表达来调节 TLR4/NF-κB 通路来实现的。因此，CAPE 可以作为一种源自食物的脾脏保护剂，通过 miR-182-5p/TLR4/NF-κB 轴来减轻凋亡和炎症，从而对抗 Cd 诱导的脾毒性。
