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Anti-Inflammatory Effect of Onion Peel Extract in the Intestine /

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Anti-Inflammatory Effect of Onion Peel Extract in the Intestine // Olugbenga Balogun.
作者:	Balogun, Olugbenga,
面頁冊數:	1 electronic resource (259 pages)
附註:	Source: Dissertations Abstracts International, Volume: 86-11, Section: B.
Contained By:	Dissertations Abstracts International86-11B.
標題:	Biology. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31934959
ISBN:	9798315776871

Anti-Inflammatory Effect of Onion Peel Extract in the Intestine /
Balogun, Olugbenga,

Anti-Inflammatory Effect of Onion Peel Extract in the Intestine /Olugbenga Balogun. - 1 electronic resource (259 pages)

Source: Dissertations Abstracts International, Volume: 86-11, Section: B.

The global obesity epidemic is significantly influenced by high-fat diets (HFDs), particularly those rich in saturated fats, which contribute to chronic low-grade inflammation and metabolic disorders including diabetes and cardiovascular diseases. The intestine, comprising a mucus layer, epithelial cells, tight junctions (TJs), immune cells, and gut microbiota, serves as the primary site for nutrient absorption and host-microbiome interaction. HFDs disrupt gut microbiota composition, causing dysbiosis and increased intestinal permeability that allows bacterial endotoxins such as lipopolysaccharides (LPS) to enter circulation, triggering systemic inflammation and related disorders. This study investigated the anti-inflammatory effects of onion peel extract (OPE) and its major bioactive compound quercetin (Q) in vivo and in vitro. OPE was prepared using 70% ethanol (v/v) by liquid-liquid extraction, and then OPE and Q were digested using gastrointestinal digestive enzymes in vitro. The effects of OPE, digested OPE (DOPE), Q, and digested Q (DQ) on carbohydrate digestion were examined by measuring intestinal carbohydrate-hydrolyzing enzyme activities, with acarbose serving as a positive control. Glucose uptake was measured using fluorescent glucose in Caco-2/HT-29 cells, and paracellular permeability was measured in LPS-stimulated Caco-2/HT-29 cells using fluorescein isothiocyanate (FITC) and lucifer yellow. For in vivo studies, C57BL/6 male mice were fed either a low-fat diet (LFD) or HFD with or without 1% quercetin for 12 weeks. Intestinal permeability was measured using FITC. Expression of genes and proteins related to glucose uptake, tight junctions, inflammation, and antioxidants were analyzed using qPCR and Western blot. Results showed that OPE and Q, with or without digestion, inhibited α-glucosidase and α-amylase, with DOPE demonstrating more effect at concentrations above 2.5 µg/mL. DOPE and Q exhibited the strongest inhibition with IC50 values of 5.506 and 5.83 µg/mL for α-glucosidase and 4.879 and 5.847 µg/mL for α-amylase, respectively. At 20 µg/mL, these samples inhibited maltase, sucrase, and glucoamylase similarly to 1 mg/ml acarbose. All samples reduced glucose uptake by decreasing SGLT1 and GLUT2 expression through AMP-activated protein kinase activation and hepatocyte nuclear factor 1α reduction. OPE and DOPE showed greater protective effects against LPS-induced tight junction disruption and inflammation than Q and DQ in Caco-2/HT-29 cells. DOPE had a better effect than OPE, but digestion did not change the effect on Q. The anti-inflammatory effects were mediated through inhibition of nuclear factor kappa B (NFκB) via AMP-activated protein kinase (AMPK)-activated silent mating-type information regulation 2 homolog 1 (SIRT1). In HFD-fed mice, quercetin reduced inflammation markers (cyclooxygenase 2, tumor necrosis factor-α, monocyte chemoattractant protein-1, interleukins) and increased antioxidant enzymes (superoxide dismutase 2/3, glutathione peroxidase 1, catalase) by modulating NFκB and nuclear factor erythroid 2-related factor 2 (NRF2). Quercetin improved intestinal permeability by increasing tight junction proteins (zonula occludens, occludin, claudin1) and mucin production receptors and genes (free fatty acid receptor 2/3, mucin 2). These effects were also observed in LFD-fed mice. Quercetin decreased blood levels of LPS, cluster of differentiation 14, and LPS-binding protein, and reduced myeloperoxidase activity in HFD-fed mice. Its anti-inflammatory action in the intestine was attributed to AMPK-SIRT1-NFκB or NRF2-NFκB signaling pathways, enhanced by increased miRNA-16-5p and miRNA-200b-3p expression, which suppress inflammation and promote tight junction integrity. In conclusion, quercetin shows potential for enhancing intestinal function by alleviating inflammation and oxidative stress, suggesting its value as a therapeutic agent for diet-induced intestinal dysfunction.

English

ISBN: 9798315776871Subjects--Topical Terms:

522710
Biology.
Subjects--Index Terms:

High fat diet

Anti-Inflammatory Effect of Onion Peel Extract in the Intestine /
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520 $a The global obesity epidemic is significantly influenced by high-fat diets (HFDs), particularly those rich in saturated fats, which contribute to chronic low-grade inflammation and metabolic disorders including diabetes and cardiovascular diseases. The intestine, comprising a mucus layer, epithelial cells, tight junctions (TJs), immune cells, and gut microbiota, serves as the primary site for nutrient absorption and host-microbiome interaction. HFDs disrupt gut microbiota composition, causing dysbiosis and increased intestinal permeability that allows bacterial endotoxins such as lipopolysaccharides (LPS) to enter circulation, triggering systemic inflammation and related disorders. This study investigated the anti-inflammatory effects of onion peel extract (OPE) and its major bioactive compound quercetin (Q) in vivo and in vitro. OPE was prepared using 70% ethanol (v/v) by liquid-liquid extraction, and then OPE and Q were digested using gastrointestinal digestive enzymes in vitro. The effects of OPE, digested OPE (DOPE), Q, and digested Q (DQ) on carbohydrate digestion were examined by measuring intestinal carbohydrate-hydrolyzing enzyme activities, with acarbose serving as a positive control. Glucose uptake was measured using fluorescent glucose in Caco-2/HT-29 cells, and paracellular permeability was measured in LPS-stimulated Caco-2/HT-29 cells using fluorescein isothiocyanate (FITC) and lucifer yellow. For in vivo studies, C57BL/6 male mice were fed either a low-fat diet (LFD) or HFD with or without 1% quercetin for 12 weeks. Intestinal permeability was measured using FITC. Expression of genes and proteins related to glucose uptake, tight junctions, inflammation, and antioxidants were analyzed using qPCR and Western blot. Results showed that OPE and Q, with or without digestion, inhibited α-glucosidase and α-amylase, with DOPE demonstrating more effect at concentrations above 2.5 µg/mL. DOPE and Q exhibited the strongest inhibition with IC50 values of 5.506 and 5.83 µg/mL for α-glucosidase and 4.879 and 5.847 µg/mL for α-amylase, respectively. At 20 µg/mL, these samples inhibited maltase, sucrase, and glucoamylase similarly to 1 mg/ml acarbose. All samples reduced glucose uptake by decreasing SGLT1 and GLUT2 expression through AMP-activated protein kinase activation and hepatocyte nuclear factor 1α reduction. OPE and DOPE showed greater protective effects against LPS-induced tight junction disruption and inflammation than Q and DQ in Caco-2/HT-29 cells. DOPE had a better effect than OPE, but digestion did not change the effect on Q. The anti-inflammatory effects were mediated through inhibition of nuclear factor kappa B (NFκB) via AMP-activated protein kinase (AMPK)-activated silent mating-type information regulation 2 homolog 1 (SIRT1). In HFD-fed mice, quercetin reduced inflammation markers (cyclooxygenase 2, tumor necrosis factor-α, monocyte chemoattractant protein-1, interleukins) and increased antioxidant enzymes (superoxide dismutase 2/3, glutathione peroxidase 1, catalase) by modulating NFκB and nuclear factor erythroid 2-related factor 2 (NRF2). Quercetin improved intestinal permeability by increasing tight junction proteins (zonula occludens, occludin, claudin1) and mucin production receptors and genes (free fatty acid receptor 2/3, mucin 2). These effects were also observed in LFD-fed mice. Quercetin decreased blood levels of LPS, cluster of differentiation 14, and LPS-binding protein, and reduced myeloperoxidase activity in HFD-fed mice. Its anti-inflammatory action in the intestine was attributed to AMPK-SIRT1-NFκB or NRF2-NFκB signaling pathways, enhanced by increased miRNA-16-5p and miRNA-200b-3p expression, which suppress inflammation and promote tight junction integrity. In conclusion, quercetin shows potential for enhancing intestinal function by alleviating inflammation and oxidative stress, suggesting its value as a therapeutic agent for diet-induced intestinal dysfunction.
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650 4 $a Biochemistry. $3 518028
650 4 $a Nutrition. $3 517777
653 $a High fat diet
653 $a Inflammation
653 $a Intestine
653 $a Onion peel extract
653 $a Quercetin
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710 2 $a North Carolina Agricultural and Technical State University. $b Applied Science and Technology. $e degree granting institution. $3 3821974
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720 1 $a Waterman, Jenora $e degree supervisor.
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