Effect of <i>Quamoclit angulata</i> Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice

Type 2 diabetes mellitus (T2DM) is caused by abnormalities of controlling blood glucose and insulin homeostasis. Especially, hyperglycemia causes hyper-inflammation through activation of NLRP3 inflammasome, which can lead to cell apoptosis, hypertrophy, and fibrosis. <i>Quamoclit angulata</...

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Main Authors: Ji Eun Park, Heaji Lee, Hyunkyung Rho, Seong Min Hong, Sun Yeou Kim, Yunsook Lim
Format: Article
Language:English
Published: MDPI AG 2020-05-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/9/6/459
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author Ji Eun Park
Heaji Lee
Hyunkyung Rho
Seong Min Hong
Sun Yeou Kim
Yunsook Lim
author_facet Ji Eun Park
Heaji Lee
Hyunkyung Rho
Seong Min Hong
Sun Yeou Kim
Yunsook Lim
author_sort Ji Eun Park
collection DOAJ
description Type 2 diabetes mellitus (T2DM) is caused by abnormalities of controlling blood glucose and insulin homeostasis. Especially, hyperglycemia causes hyper-inflammation through activation of NLRP3 inflammasome, which can lead to cell apoptosis, hypertrophy, and fibrosis. <i>Quamoclit angulata</i> (QA), one of the annual winders, has been shown ameliorative effects on diabetes. The current study investigated whether the QA extract (QAE) attenuated hyperglycemia-induced renal inflammation related to NLRP inflammasome and oxidative stress in high fat diet (HFD)-induced diabetic mice. After T2DM was induced, the mice were treated with QAE (5 or 10 mg/kg/day) by gavage for 12 weeks. The QAE supplementation reduced homeostasis model assessment insulin resistance (HOMA-IR), kidney malfunction, and glomerular hypertrophy in T2DM. Moreover, the QAE treatment significantly attenuated renal NLRP3 inflammasome dependent hyper-inflammation and consequential renal damage caused by oxidative stress, apoptosis, and fibrosis in T2DM. Furthermore, QAE normalized aberrant energy metabolism (downregulation of p-AMPK, sirtuin (SIRT)-1, and PPARγ-coactivator α (PGC-1 α)) in T2DM mice. Taken together, the results suggested that QAE as a natural product has ameliorative effects on renal damage by regulation of oxidative stress and inflammation in T2DM.
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spelling doaj.art-8e76b9dab1c0460084da70888aee077f2023-11-20T01:57:02ZengMDPI AGAntioxidants2076-39212020-05-019645910.3390/antiox9060459Effect of <i>Quamoclit angulata</i> Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic MiceJi Eun Park0Heaji Lee1Hyunkyung Rho2Seong Min Hong3Sun Yeou Kim4Yunsook Lim5Department of Food and Nutrition, Kyung Hee Univerity, 26 Kyung Hee-Daero, Dongdamun-Gu, Seoul 02447, KoreaDepartment of Food and Nutrition, Kyung Hee Univerity, 26 Kyung Hee-Daero, Dongdamun-Gu, Seoul 02447, KoreaDepartment of Food and Nutrition, Kyung Hee Univerity, 26 Kyung Hee-Daero, Dongdamun-Gu, Seoul 02447, KoreaDepartment of Pharmacognosy, College of Pharmacy, Gachon University, Incheon 21936, KoreaDepartment of Pharmacognosy, College of Pharmacy, Gachon University, Incheon 21936, KoreaDepartment of Food and Nutrition, Kyung Hee Univerity, 26 Kyung Hee-Daero, Dongdamun-Gu, Seoul 02447, KoreaType 2 diabetes mellitus (T2DM) is caused by abnormalities of controlling blood glucose and insulin homeostasis. Especially, hyperglycemia causes hyper-inflammation through activation of NLRP3 inflammasome, which can lead to cell apoptosis, hypertrophy, and fibrosis. <i>Quamoclit angulata</i> (QA), one of the annual winders, has been shown ameliorative effects on diabetes. The current study investigated whether the QA extract (QAE) attenuated hyperglycemia-induced renal inflammation related to NLRP inflammasome and oxidative stress in high fat diet (HFD)-induced diabetic mice. After T2DM was induced, the mice were treated with QAE (5 or 10 mg/kg/day) by gavage for 12 weeks. The QAE supplementation reduced homeostasis model assessment insulin resistance (HOMA-IR), kidney malfunction, and glomerular hypertrophy in T2DM. Moreover, the QAE treatment significantly attenuated renal NLRP3 inflammasome dependent hyper-inflammation and consequential renal damage caused by oxidative stress, apoptosis, and fibrosis in T2DM. Furthermore, QAE normalized aberrant energy metabolism (downregulation of p-AMPK, sirtuin (SIRT)-1, and PPARγ-coactivator α (PGC-1 α)) in T2DM mice. Taken together, the results suggested that QAE as a natural product has ameliorative effects on renal damage by regulation of oxidative stress and inflammation in T2DM.https://www.mdpi.com/2076-3921/9/6/459<i>Quamoclit angulata</i>type 2 diabeteskidney damageinflammationoxidative stressapoptosis
spellingShingle Ji Eun Park
Heaji Lee
Hyunkyung Rho
Seong Min Hong
Sun Yeou Kim
Yunsook Lim
Effect of <i>Quamoclit angulata</i> Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice
Antioxidants
<i>Quamoclit angulata</i>
type 2 diabetes
kidney damage
inflammation
oxidative stress
apoptosis
title Effect of <i>Quamoclit angulata</i> Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice
title_full Effect of <i>Quamoclit angulata</i> Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice
title_fullStr Effect of <i>Quamoclit angulata</i> Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice
title_full_unstemmed Effect of <i>Quamoclit angulata</i> Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice
title_short Effect of <i>Quamoclit angulata</i> Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice
title_sort effect of i quamoclit angulata i extract supplementation on oxidative stress and inflammation on hyperglycemia induced renal damage in type 2 diabetic mice
topic <i>Quamoclit angulata</i>
type 2 diabetes
kidney damage
inflammation
oxidative stress
apoptosis
url https://www.mdpi.com/2076-3921/9/6/459
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