Department of Pharmacology, School of Life Dentistry at Tokyo, The Nippon Dental University, 1-9-20 Fujimi, Chiyoda-ku, Tokyo, 102-8159, Japan.
Department of Life Science Dentistry, School of Life Dentistry at Tokyo, The Nippon Dental University, 1-9-20 Fujimi, Chiyoda-ku, Tokyo, 102-8159, Japan.
Hum Cell. 2022 May;35(3):885-895. doi: 10.1007/s13577-022-00694-5. Epub 2022 Apr 1.
Gut microbial lipopolysaccharides (LPS)-induced inflammatory responses in adipose tissue are associated with the dysfunction of adipocytes, insulin resistance and the development of metabolic syndrome. The aim of this study is to investigate (1) the effects of LPS on the differentiation and inflammatory responses of THP-1 monocytes and OP9 preadipocytes under serum free conditions and (2) the repressive effects of enzyme-digested Colla Corii Asini (CCAD) and fish gelatin (FGD) on LPS-induced inflammatory responses in THP-1 macrophages and OP9 adipocytes. Immunofluorescence and oil red O staining showed that a serum free medium supplied with phorbol 12-myristate 13-acetate (PMA) could induce differentiation and lipid accumulation in THP-1 cells as well as OP9 cells. ELISA showed that LPS significantly increased interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) secretions in PMA-differentiated THP-1 macrophages in a dose-dependent manner. LPS significantly suppressed lipid accumulation and adiponectin secretions, and enhanced IL-6 secretions in OP9 adipocytes. Both CCAD and FGD significantly reduced the levels of both macrophages- and adipocytes-derived inflammatory cytokines and increased the level of OP9-secreted adiponectin. In conclusion, LPS could induce inflammatory responses in both THP-1 and OP9 cells and cause dysfunction of OP9 adipocytes under the serum free conditions. CCAD and FGD can repress LPS-induced inflammatory responses in both THP-1 macrophages and OP9 adipocytes, and increase the secretion of adiponectin in OP9 adipocytes. They could be used as health care supplements for improving metabolic syndrome.
肠道微生物脂多糖（LPS）诱导的脂肪组织炎症反应与脂肪细胞功能障碍、胰岛素抵抗和代谢综合征的发展有关。本研究旨在探讨：（1）LPS 在无血清条件下对 THP-1 单核细胞和 OP9 前脂肪细胞分化和炎症反应的影响；（2）酶解的阿胶（CCAD）和鱼明胶（FGD）对 LPS 诱导的 THP-1 巨噬细胞和 OP9 脂肪细胞炎症反应的抑制作用。免疫荧光和油红 O 染色显示，无血清培养基中添加佛波醇 12-肉豆蔻酸 13-乙酸酯（PMA）可诱导 THP-1 细胞和 OP9 细胞分化和脂质积累。ELISA 结果显示，LPS 以剂量依赖性方式显著增加 PMA 分化的 THP-1 巨噬细胞中白细胞介素 6（IL-6）和肿瘤坏死因子-α（TNF-α）的分泌。LPS 显著抑制 OP9 脂肪细胞的脂质积累和脂联素分泌，并增强 IL-6 的分泌。CCAD 和 FGD 均显著降低巨噬细胞和脂肪细胞来源的炎症细胞因子水平，增加 OP9 分泌的脂联素水平。综上所述，LPS 可在无血清条件下诱导 THP-1 和 OP9 细胞的炎症反应，并导致 OP9 脂肪细胞功能障碍。CCAD 和 FGD 可抑制 LPS 诱导的 THP-1 巨噬细胞和 OP9 脂肪细胞的炎症反应，并增加 OP9 脂肪细胞分泌脂联素。它们可用作改善代谢综合征的保健品。
