<i>Gryllus bimaculatus</i> Extract Protects against Lipopolysaccharide-Derived Inflammatory Response in Human Colon Epithelial Caco-2 Cells
Increased tight junction permeability and overproduction of proinflammatory cytokines are crucial pathophysiological mechanisms in inflammatory bowel disease (IBD). This study evaluated anti-inflammatory effects of aqueous ethanolic <i>Gryllus bimaculatus</i> extract (AE-GBE) against int...
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MDPI AG
2021-09-01
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| Series: | Insects |
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| Online Access: | https://www.mdpi.com/2075-4450/12/10/873 |
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| author | Kyong Kim Eun-Young Park Dong-Jae Baek Se-Eun Jang Yoon-Sin Oh |
| author_facet | Kyong Kim Eun-Young Park Dong-Jae Baek Se-Eun Jang Yoon-Sin Oh |
| author_sort | Kyong Kim |
| collection | DOAJ |
| description | Increased tight junction permeability and overproduction of proinflammatory cytokines are crucial pathophysiological mechanisms in inflammatory bowel disease (IBD). This study evaluated anti-inflammatory effects of aqueous ethanolic <i>Gryllus bimaculatus</i> extract (AE-GBE) against intestinal permeability on lipopolysaccharide (LPS)-treated Caco-2 cells. Treatment with AE-GBE increased cell viability and significantly reduced inflammatory mediators such as nitric oxide and LPS-induced reactive oxidative stress. LPS increased the expression levels of iNOS, Cox-2, and 4-hydroxylnonenal; however, these levels were attenuated by AE-GBE treatment. Moreover, the mRNA and protein expression levels of the inflammatory cytokines TNFα, IL-6, IL-1β, and IFNγ were increased by LPS, but were significantly reduced by AE-GBE treatment. Intestinal epithelial permeability and the related expression of the proteins Zoula ocludence-1, occludin, and claudin-1 was increased by LPS treatment, and this effect was significantly reduced by AE-GBE treatment. The reduction in AMPK phosphorylation in LPS-treated Caco-2 cells was reversed in activation by co-treatment with AE-GBE. In conclusion, AE-GBE can protect epithelial cells from LPS-induced impaired barrier integrity by increasing tight junction proteins and preventing various inflammatory mediators. Thus, AE-GBE has the potential to improve inflammation-related diseases, including IBD, by inhibiting excessive production of inflammation-inducing mediators. |
| first_indexed | 2024-03-10T06:29:26Z |
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| issn | 2075-4450 |
| language | English |
| last_indexed | 2024-03-10T06:29:26Z |
| publishDate | 2021-09-01 |
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| spelling | doaj.art-05c01451a5e149c3a44f142cfc17223e2023-11-22T18:38:51ZengMDPI AGInsects2075-44502021-09-01121087310.3390/insects12100873<i>Gryllus bimaculatus</i> Extract Protects against Lipopolysaccharide-Derived Inflammatory Response in Human Colon Epithelial Caco-2 CellsKyong Kim0Eun-Young Park1Dong-Jae Baek2Se-Eun Jang3Yoon-Sin Oh4Department of Food and Nutrition, Eulji University, Seongnam 13135, KoreaCollege of Pharmacy and Natural Medicine Research Institute, Mokpo National University, Mokpo 58554, KoreaCollege of Pharmacy and Natural Medicine Research Institute, Mokpo National University, Mokpo 58554, KoreaDepartment of Food and Nutrition, Eulji University, Seongnam 13135, KoreaDepartment of Food and Nutrition, Eulji University, Seongnam 13135, KoreaIncreased tight junction permeability and overproduction of proinflammatory cytokines are crucial pathophysiological mechanisms in inflammatory bowel disease (IBD). This study evaluated anti-inflammatory effects of aqueous ethanolic <i>Gryllus bimaculatus</i> extract (AE-GBE) against intestinal permeability on lipopolysaccharide (LPS)-treated Caco-2 cells. Treatment with AE-GBE increased cell viability and significantly reduced inflammatory mediators such as nitric oxide and LPS-induced reactive oxidative stress. LPS increased the expression levels of iNOS, Cox-2, and 4-hydroxylnonenal; however, these levels were attenuated by AE-GBE treatment. Moreover, the mRNA and protein expression levels of the inflammatory cytokines TNFα, IL-6, IL-1β, and IFNγ were increased by LPS, but were significantly reduced by AE-GBE treatment. Intestinal epithelial permeability and the related expression of the proteins Zoula ocludence-1, occludin, and claudin-1 was increased by LPS treatment, and this effect was significantly reduced by AE-GBE treatment. The reduction in AMPK phosphorylation in LPS-treated Caco-2 cells was reversed in activation by co-treatment with AE-GBE. In conclusion, AE-GBE can protect epithelial cells from LPS-induced impaired barrier integrity by increasing tight junction proteins and preventing various inflammatory mediators. Thus, AE-GBE has the potential to improve inflammation-related diseases, including IBD, by inhibiting excessive production of inflammation-inducing mediators.https://www.mdpi.com/2075-4450/12/10/873<i>Gryllus bimaculatus</i>Caco-2lipopolysaccharidesinflammatory mediatorstight junction |
| spellingShingle | Kyong Kim Eun-Young Park Dong-Jae Baek Se-Eun Jang Yoon-Sin Oh <i>Gryllus bimaculatus</i> Extract Protects against Lipopolysaccharide-Derived Inflammatory Response in Human Colon Epithelial Caco-2 Cells Insects <i>Gryllus bimaculatus</i> Caco-2 lipopolysaccharides inflammatory mediators tight junction |
| title | <i>Gryllus bimaculatus</i> Extract Protects against Lipopolysaccharide-Derived Inflammatory Response in Human Colon Epithelial Caco-2 Cells |
| title_full | <i>Gryllus bimaculatus</i> Extract Protects against Lipopolysaccharide-Derived Inflammatory Response in Human Colon Epithelial Caco-2 Cells |
| title_fullStr | <i>Gryllus bimaculatus</i> Extract Protects against Lipopolysaccharide-Derived Inflammatory Response in Human Colon Epithelial Caco-2 Cells |
| title_full_unstemmed | <i>Gryllus bimaculatus</i> Extract Protects against Lipopolysaccharide-Derived Inflammatory Response in Human Colon Epithelial Caco-2 Cells |
| title_short | <i>Gryllus bimaculatus</i> Extract Protects against Lipopolysaccharide-Derived Inflammatory Response in Human Colon Epithelial Caco-2 Cells |
| title_sort | i gryllus bimaculatus i extract protects against lipopolysaccharide derived inflammatory response in human colon epithelial caco 2 cells |
| topic | <i>Gryllus bimaculatus</i> Caco-2 lipopolysaccharides inflammatory mediators tight junction |
| url | https://www.mdpi.com/2075-4450/12/10/873 |
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