Sodium butyrate attenuate hyperglycemia-induced inflammatory response and renal injury in diabetic mice

The activation of the monocyte-macrophage system and the damage to the renal and pancreatic tissue are common complications in patients with diabetes induced by hyper-glycemia. This study aimed to evaluate the effect and mechanism of butyrate (NaB), a metabolite of intestinal flora, on inhibiting th...

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Main Authors: Yan Man, Zhang Yan-Yan, Xi Yue, Ding Long-Kun, Sun Chang, Qu Li-Juan, Qian Xin, Xu Jing-Wen, Sun Wen, Wu Liang
Format: Article
Language:English
Published: Sciendo 2023-03-01
Series:Acta Pharmaceutica
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Online Access:https://doi.org/10.2478/acph-2023-0008
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author Yan Man
Zhang Yan-Yan
Xi Yue
Ding Long-Kun
Sun Chang
Qu Li-Juan
Qian Xin
Xu Jing-Wen
Sun Wen
Wu Liang
author_facet Yan Man
Zhang Yan-Yan
Xi Yue
Ding Long-Kun
Sun Chang
Qu Li-Juan
Qian Xin
Xu Jing-Wen
Sun Wen
Wu Liang
author_sort Yan Man
collection DOAJ
description The activation of the monocyte-macrophage system and the damage to the renal and pancreatic tissue are common complications in patients with diabetes induced by hyper-glycemia. This study aimed to evaluate the effect and mechanism of butyrate (NaB), a metabolite of intestinal flora, on inhibiting the inflammatory response of human monocyte-macrophages (THP-1 cells) induced by high glucose and the damage of pancreatic and renal tissue in diabetic mice. The results showed that high concentration glucose significantly up-regulated the expressions of IL-1β, TNF-α, and NLRP3 in THP-1 cells and mouse spleen, and that NaB could inhibit the overexpression of those genes. The abundance of Beclin-1, LC3B and reactive oxygen species (ROS) in THP-1 cells is increased due to the high glucose concentration, and NaB can inhibit the genes responsible for upregulating the expression. In diabetic mice, vacuolar degeneration of renal tubules was observed. Then we observed that some of the epithelial cells of the renal tubules were exfoliated and some formed tubules. NaB could alleviate these pathological lesions, but NaB cannot alleviate pancreatic injury. Our results indicated that NaB could be used for the prevention and adjuvant treatment of diabetic kidney injury.
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institution Kabale University
issn 1846-9558
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series Acta Pharmaceutica
spelling doaj-art-107fe43babc34de692921dbad2c6d02f2025-02-03T07:26:16ZengSciendoActa Pharmaceutica1846-95582023-03-0173112113210.2478/acph-2023-0008Sodium butyrate attenuate hyperglycemia-induced inflammatory response and renal injury in diabetic miceYan Man0Zhang Yan-Yan1Xi Yue2Ding Long-Kun3Sun Chang4Qu Li-Juan5Qian Xin6Xu Jing-Wen7Sun Wen8Wu Liang9School of Medicine, Jiangsu University Zhenjiang, Jiangsu, 212013, ChinaTesting Center, Yangzhou University Yangzhou, Jiangsu, 225009, ChinaSchool of Medicine, Jiangsu University Zhenjiang, Jiangsu, 212013, ChinaSchool of Medicine, Jiangsu University Zhenjiang, Jiangsu, 212013, ChinaSchool of Medicine, Jiangsu University Zhenjiang, Jiangsu, 212013, ChinaDental Treatment Center, Shanghai Ninth People’s Hospital, Shanghai Shanghai, 200000, ChinaSchool of Medicine, Jiangsu University Zhenjiang, Jiangsu, 212013, ChinaDepartment of Critical Care MedicineJurong Hospital Affiliated to Jiangsu University, Zhenjiang212444, ChinaDepartment of Critical Care MedicineJurong Hospital Affiliated to Jiangsu University, Zhenjiang212444, ChinaSchool of Medicine, Jiangsu University Zhenjiang, Jiangsu, 212013, ChinaThe activation of the monocyte-macrophage system and the damage to the renal and pancreatic tissue are common complications in patients with diabetes induced by hyper-glycemia. This study aimed to evaluate the effect and mechanism of butyrate (NaB), a metabolite of intestinal flora, on inhibiting the inflammatory response of human monocyte-macrophages (THP-1 cells) induced by high glucose and the damage of pancreatic and renal tissue in diabetic mice. The results showed that high concentration glucose significantly up-regulated the expressions of IL-1β, TNF-α, and NLRP3 in THP-1 cells and mouse spleen, and that NaB could inhibit the overexpression of those genes. The abundance of Beclin-1, LC3B and reactive oxygen species (ROS) in THP-1 cells is increased due to the high glucose concentration, and NaB can inhibit the genes responsible for upregulating the expression. In diabetic mice, vacuolar degeneration of renal tubules was observed. Then we observed that some of the epithelial cells of the renal tubules were exfoliated and some formed tubules. NaB could alleviate these pathological lesions, but NaB cannot alleviate pancreatic injury. Our results indicated that NaB could be used for the prevention and adjuvant treatment of diabetic kidney injury.https://doi.org/10.2478/acph-2023-0008high concentration glucosediabetic nephropathybutyrateinflammation
spellingShingle Yan Man
Zhang Yan-Yan
Xi Yue
Ding Long-Kun
Sun Chang
Qu Li-Juan
Qian Xin
Xu Jing-Wen
Sun Wen
Wu Liang
Sodium butyrate attenuate hyperglycemia-induced inflammatory response and renal injury in diabetic mice
Acta Pharmaceutica
high concentration glucose
diabetic nephropathy
butyrate
inflammation
title Sodium butyrate attenuate hyperglycemia-induced inflammatory response and renal injury in diabetic mice
title_full Sodium butyrate attenuate hyperglycemia-induced inflammatory response and renal injury in diabetic mice
title_fullStr Sodium butyrate attenuate hyperglycemia-induced inflammatory response and renal injury in diabetic mice
title_full_unstemmed Sodium butyrate attenuate hyperglycemia-induced inflammatory response and renal injury in diabetic mice
title_short Sodium butyrate attenuate hyperglycemia-induced inflammatory response and renal injury in diabetic mice
title_sort sodium butyrate attenuate hyperglycemia induced inflammatory response and renal injury in diabetic mice
topic high concentration glucose
diabetic nephropathy
butyrate
inflammation
url https://doi.org/10.2478/acph-2023-0008
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