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

• Published in: Journal of functional foods Vol. 116; p. 106142
• Main Authors: Yang, Hua-Yu, Li, Yi-Jun, Chen, Xuan-Ying, Yang, Song-Yu, Chen, Sheng-Bin, Li, Wen-Juan
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.05.2024
• Subjects: antioxidant enzymes; apoptosis; calcium; cell lines; cell viability; Chimonanthus; Chimonanthus salicifolius essential oil; essential oils; free radicals; Intestinal protection; intestines; membrane potential; mitochondria; Mitochondria-associated membranes; Mitochondria-endoplasmic reticulum crosstalk; Mitochondrial fusion protein; reactive oxygen species; reticulum; DPPH; EI; CSEO; DCF; EM; SOD; Mitochondria-associated membranes; Mitochondrial fusion protein; MDA; ER; AsA; IEC-6 cells; BHT; Intestinal protection; BSA; Chimonanthus salicifolius essential oil; FBS; Rho-123; MAMs; Mfn2; ABTS; Mitochondria-endoplasmic reticulum crosstalk
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2024.106142

[Display omitted] •41 compounds in Chimonanthus salicifolius essential oil (CSEO) identified by GC–MS.•CSEO protected intestinal epithelial cells from H2O2-induced oxidative stress.•Mfn2-tethered MAMs was implicated in the intestinal protection of CSEO.•Beneficial effects of CSEO linked to mitochondria-endoplasmic reticulum crosstalk. 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.