Protective Mechanisms of Avocado Oil Extract Against Ototoxicity
| Autor: | Se-Young Choung, Seo Yeon Jeong, Tong Ho Kang, Thu Nguyen Minh Pham, Kwang Won Jeong, Seung Hyun Kim, Yu Hwa Park, Do Hoon Kim, Kye Wan Lee, In Seok Moon, Jung Suk Lee |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Chemokine Antioxidant medicine.medical_treatment Gene Expression lcsh:TX341-641 avocado oil Pharmacology Article GSTA4 03 medical and health sciences 0302 clinical medicine Ototoxicity Gene expression medicine Autophagy Humans Plant Oils Cells Cultured hearing loss ear hair cell Nutrition and Dietetics Hair Cells Auditory Inner biology Chemistry Persea Tumor Necrosis Factor-alpha Interleukin Neomycin medicine.disease Glutathione Anti-Bacterial Agents Oxidative Stress 030104 developmental biology Aminoglycosides Apoptosis biology.protein aminoglycoside Cytokines Metabolic Detoxication Phase I Inflammation Mediators lcsh:Nutrition. Foods and food supply 030217 neurology & neurosurgery Food Science medicine.drug |
| Zdroj: | Nutrients Volume 12 Issue 4 Nutrients, Vol 12, Iss 947, p 947 (2020) |
| ISSN: | 2072-6643 |
| Popis: | Despite the excellent antimicrobial activity of aminoglycoside antibiotics, permanent inner ear damage associated with the use of these drugs has resulted in the need to develop strategies to address the ototoxic risk given their widespread use. In a previous study, we showed that avocado oil protects ear hair cells from damage caused by neomycin. However, the detailed mechanism by which this protection occurs is still unclear. Here, we investigated the auditory cell-protective mechanism of enhanced functional avocado oil extract (DKB122). RNA sequencing followed by pathway analysis revealed that DKB122 has the potential to enhance the expression of detoxification and antioxidant genes associated with glutathione metabolism (Hmox4, Gsta4, Mgst1, and Abcc3) in HEI-OC1 cells. Additionally, DKB122 effectively decreased ROS levels, resulting in the inhibition of apoptosis in HEI-OC1 cells. The expression of the inflammatory genes that encode chemokines and interleukins was also downregulated by DKB122 treatment. Consistent with these results, DKB122 significantly inhibited p65 nuclear migration induced by TNF-&alpha or LPS in HEI-OC1 cells and THP-1 cells and the expression of inflammatory chemokine and interleukin genes induced by TNF-&alpha was significantly reduced. Moreover, DKB122 treatment increased LC3-II and decreased p62 in HEI-OC1 cells, suggesting that DKB122 increases autophagic flux. These results suggest that DKB122 has otoprotective effects attributable to its antioxidant activity, induction of antioxidant gene expression, anti-inflammatory activity, and autophagy activation. |
| Databáze: | OpenAIRE |
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