Sukjamnong Suporn, Chen Hui, Saad Sonia, Santiyanont Rachana
Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, 154 Soi Chula 12, Rama 1 Road, Wangmai, Pathum Wan, Bangkok, 10330 Thailand.
Systems Neuroscience of Autism and Psychiatric Disorders (SYNAPS) Research Unit, Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand.
Toxicol Res. 2022 Jan 30;38(3):331-343. doi: 10.1007/s43188-021-00114-0. eCollection 2022 Jul.
Advanced glycation end products (AGEs) can induce inflammatory signaling pathways through the receptor for AGEs (RAGE). Targeting RAGE could be a therapeutic strategy for treating chronic inflammation mediated by the AGE-RAGE axis. This study aimed to investigate the effects of and extracts on AGE-RAGE signaling and AGE-mediated oxidative stress and inflammation in THP-1 cells. and were extracted by a Soxhlet extraction, and antioxidant capacity was evaluated using DPPH and ABTS assays. The human monocytic cell line THP-1 was treated with AGE (600 µg/ml) with and without and extracts (100 µg/ml). The mitochondria-targeting antioxidant MitoQ (2 μg/ml) was used as a positive control. Cell viability, ROS generation, RAGE, AGE-RAGE signaling pathway components, and inflammatory cytokine levels were analyzed. and extracts showed antioxidative effects in non-cell-based assays. Treatment of THP-1 cells with AGE significantly increased the protein levels of RAGE and significantly increased the mRNA expression of cytokines, including TNF-α, IL-1β, and IL-6. AGEs induced the generation of ROS and levels of signaling molecules downstream of RAGE, including phosphorylated and total Erk1/2, JNK, and p38 MAPK, although not significantly. and extracts significantly decreased the protein levels of RAGE and significantly decreased the mRNA levels of cytokines. In conclusion, this study revealed that and extracts exert anti-inflammatory effects through the AGE-RAGE axis. However, details on this anti-inflammatory effect through AGE-RAGE signaling should be further investigated.
The online version contains supplementary material available at 10.1007/s43188-021-00114-0.
晚期糖基化终产物（AGEs）可通过晚期糖基化终产物受体（RAGE）诱导炎症信号通路。靶向RAGE可能是治疗由AGE-RAGE轴介导的慢性炎症的一种治疗策略。本研究旨在探讨[具体提取物名称1]和[具体提取物名称2]提取物对THP-1细胞中AGE-RAGE信号传导以及AGE介导的氧化应激和炎症的影响。[具体提取物名称1]和[具体提取物名称2]通过索氏提取法提取，并使用DPPH和ABTS测定法评估抗氧化能力。人单核细胞系THP-1用AGE（600μg/ml）处理，同时添加或不添加[具体提取物名称1]和[具体提取物名称2]提取物（100μg/ml）。将线粒体靶向抗氧化剂MitoQ（2μg/ml）用作阳性对照。分析细胞活力、活性氧生成、RAGE、AGE-RAGE信号通路成分和炎性细胞因子水平。[具体提取物名称1]和[具体提取物名称2]提取物在非细胞实验中显示出抗氧化作用。用AGE处理THP-1细胞显著增加了RAGE的蛋白质水平，并显著增加了包括TNF-α、IL-1β和IL-6在内的细胞因子的mRNA表达。AGEs诱导了活性氧的生成以及RAGE下游信号分子的水平，包括磷酸化和总Erk1/2、JNK和p38 MAPK，尽管增幅不显著。[具体提取物名称1]和[具体提取物名称2]提取物显著降低了RAGE的蛋白质水平，并显著降低了细胞因子的mRNA水平。总之，本研究表明[具体提取物名称1]和[具体提取物名称2]提取物通过AGE-RAGE轴发挥抗炎作用。然而，关于通过AGE-RAGE信号传导产生的这种抗炎作用的详细情况应进一步研究。
在线版本包含可在10.1007/s43188-021-00114-0获取的补充材料。
