Department of Gastrointestinal Surgery, Ping Yang Hospital Affiliated to Wenzhou Medical University, 325400 Wenzhou, Zhejiang, China.
Department of Interventional Oncology, Ping Yang Hospital Affiliated to Wenzhou Medical University, 325400 Wenzhou, Zhejiang, China.
Discov Med. 2024 Jul;36(186):1408-1419. doi: 10.24976/Discov.Med.202436186.131.
Obesity is linked to impaired intestinal barrier function and inflammation. Saikosaponin A (SSA), a triterpene saponin from , has shown beneficial effects on intestinal colitis in mice. However, the mechanisms underlying SSA's protective effects against obesity are not fully understood.
To investigate the effects of SSA on body weight, metabolic disturbances, and intestinal health in diet-induced obese (DIO) mice, and to elucidate the potential mechanisms involved.
In the study, DIO mice were supplemented with SSA. Body weight, fasting blood glucose, and metabolic parameters were measured. Intestinal barrier function and inflammation were assessed. In the study, intestinal epithelial cells were treated with palmitic acid and lipopolysaccharide to induce inflammation. SSA was then administered to evaluate its effects on cell barrier integrity and inflammatory responses. The role of the nuclear factor-E2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway was investigated by silencing Nrf2.
SSA supplementation significantly ( < 0.05) decreased body weight and fasting blood glucose levels in DIO mice, and markedly improved metabolic disturbances. This treatment also enhanced intestinal barrier function and reduced metabolic inflammation, likely through increased antioxidant capacity of intestinal epithelial cells via activation of the Nrf2/ARE signaling pathway. , SSA maintained cell barrier integrity and reduced inflammatory responses by activating the Nrf2/ARE signaling pathway, decreasing intracellular reactive oxygen species content, and increasing transepithelial electrical resistance. However, silencing Nrf2 abolished SSA's protective effects.
SSA enhances the antioxidant capacity of intestinal epithelial cells, maintains intestinal barrier integrity, and reduces intestinal inflammation in DIO mice through the activation of the Nrf2/ARE signaling pathway. These findings offer new insights into the protective role of SSA in obesity and metabolic diseases.
肥胖与肠道屏障功能障碍和炎症有关。柴胡皂苷 A（SSA）是一种来自 的三萜皂苷，已显示出对小鼠结肠炎的有益作用。然而，SSA 对肥胖的保护作用的机制尚不完全清楚。
研究 SSA 对饮食诱导肥胖（DIO）小鼠体重、代谢紊乱和肠道健康的影响，并阐明其潜在的作用机制。
在这项研究中，DIO 小鼠用 SSA 补充。测量体重、空腹血糖和代谢参数。评估肠道屏障功能和炎症。在这项研究中，用棕榈酸和脂多糖处理肠上皮细胞以诱导炎症。然后给予 SSA 以评估其对细胞屏障完整性和炎症反应的影响。通过沉默 Nrf2 研究核因子-E2 相关因子 2（Nrf2）/抗氧化反应元件（ARE）信号通路的作用。
SSA 补充显著（ < 0.05）降低了 DIO 小鼠的体重和空腹血糖水平，并显著改善了代谢紊乱。这种治疗还增强了肠道屏障功能，减少了代谢炎症，可能是通过激活 Nrf2/ARE 信号通路增加了肠上皮细胞的抗氧化能力。SSA 通过激活 Nrf2/ARE 信号通路，维持细胞屏障完整性并减少炎症反应，降低细胞内活性氧物质含量并增加跨上皮电阻。然而，沉默 Nrf2 消除了 SSA 的保护作用。
SSA 通过激活 Nrf2/ARE 信号通路，增强肠上皮细胞的抗氧化能力，维持肠道屏障完整性，减少 DIO 小鼠的肠道炎症。这些发现为 SSA 在肥胖和代谢性疾病中的保护作用提供了新的见解。
