Intestinal protective effects of essential oil from Chimonanthus salicifolius linked to Mfn2-tethered mitochondria-endoplasmic reticulum connection

被引:0
|
作者
Yang, Hua-Yu [1 ]
Li, Yi-Jun [2 ]
Chen, Xuan-Ying [3 ]
Yang, Song-Yu [4 ]
Chen, Sheng-Bin [1 ,4 ]
机构
[1] Nanchang Univ, State Key Lab Food Sci & Resources, Nanchang 330047, Peoples R China
[2] Nanchang Univ, Jiangxi Med Coll, Sch Pharm, Nanchang 330031, Peoples R China
[3] Nanchang Univ, Affiliated Hosp 1, Jiangxi Med Coll, Dept Ophthalmol, Nanchang 330006, Peoples R China
[4] Nanchang Univ, Jiangxi Med Coll, Sch Clin Med 4, Nanchang 330031, Peoples R China
基金
中国国家自然科学基金;
关键词
Chimonanthus salicifolius essential oil; Intestinal protection; Mitochondrial fusion protein; Mitochondria-associated membranes; Mitochondria-endoplasmic reticulum crosstalk; OXIDATIVE STRESS; APOPTOSIS; INJURY;
D O I
10.1016/j.jff.2024.106142
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Mitochondrial fusion protein 2 (Mfn2), a molecular tether for forming Mitochondria-associated membranes (MAMs), were dynamic platforms implicated in mitochondria-endoplasmic reticulum crosstalk. Here, 41 compounds were identified in Chimonanthus salicifolius essential oil (CSEO) by GC-MS, and its antioxidant capacities were demonstrated by free radical scavenging assays. Subsequently, cell viability results showed that treatment of intestinal epithelium-derived cell line (IEC-6 cells) with CSEO plus H2O2, considerably reduced oxidative damage, enhanced cell viability and antioxidant enzyme activities, when compared with those of treatment with H2O2 alone. Meanwhile, CSEO was demonstrated to reduce H2O2-caused apoptosis in parallel with enhancement of mitochondrial transmembrane potential, reduction of reactive oxygen species and calcium accumulation. Moreover, H2O2 significantly suppressed Mfn2 expression suggesting that intestinal impairment was involved in MAMs dysfunction. However, combination of H2O2 and CSEO significantly up-regulated Mfn2 protein. Together, CSEO exerted beneficial effects against intestinal injury by maintaining mitochondria-endoplasmic reticulum crosstalk through regulation of Mfn2.
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页数:11
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