Sulforaphane protects intestinal epithelial cells against lipopolysaccharide-induced injury by activating the AMPK/SIRT1/PGC-1alpha pathway

被引:39
作者
Zhang, Yu-jie [1 ]
Wu, Qian [1 ]
机构
[1] Hubei Univ Arts & Sci, Affiliated Hosp, Xiangyang Cent Hosp, Dept Pharm, 136 Jingzhou Rd, Xiangyang, Peoples R China
基金
英国科研创新办公室;
关键词
Sulforaphane; intestinal epithelial cells; oxidative stress; apoptosis; inflammation; AMPK; SIRT1; PGC-1alpha pathway; INFLAMMATORY-BOWEL-DISEASE; BARRIER FUNCTION; AMPK; APOPTOSIS; PROMOTE; NETWORK; HEALTH; SIRT1; ROS;
D O I
10.1080/21655979.2021.1952368
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The naturally occurring isothiocyanate sulforaphane, found in vegetables, shows promising anti-inflammatory, anti-apoptosis, and anti-oxidative effects. Whether sulforaphane protects against lipopolysaccharide (LPS)-induced injury in intestinal epithelial cells is unclear. The present study examines the ability of sulforaphane to protect Caco-2 cultures from LPS-induced injury, as well as the mechanism involved. Caco-2 cells were incubated for 24 h with 1 mu g/mL LPS and different concentrations of sulforaphane (0.1-10 mu M). Then, various indicators of oxidative stress, inflammation, apoptosis, and intestinal permeability were assayed. Sulforaphane increased cell viability and reduced lactate dehydrogenase activity in LPS-treated Caco-2 cells in a concentration-dependent manner. Sulforaphane weakened LPS-induced increases in intestinal epithelial cell permeability and oxidative stress (based on assays of reactive oxygen species, DMA, and H2O2), and it increased levels of antioxidants (SOD, GPx, CAT and T-AOC). At the same time, sulforaphane weakened the ability of LPS to induce production of inflammatory cytokines (IL-1 beta, IL-6, IL-8 and TNF-alpha) and the pro-apoptotic caspases-3 and -9. Sulforaphane also upregulated p-AMPK, SIRT1, and PGC-1alpha, whose inhibitors antagonized the compound's protective effects. Sulforaphane can protect intestinal epithelial cells against LPS-induced changes in intestinal permeability, oxidative stress, inflammation, and apoptosis. It appears to act by activating the AMPK/SIRT1/PGC-1alpha pathway. The drug therefore shows potential for preventing LPS-induced intestinal injury.
引用
收藏
页码:4349 / 4360
页数:12
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