Mogroside Ⅴ Inhibits M1 Polarization and Inflammation of Diabetic Mouse Macrophages via p38 MAPK/NF-Κb Signaling Pathway

Dong, Xiaoyi; Ye, Zhimao; Li, Cuiping; Li, Kongmei; Zhong, Xiaoxia; Li, Hao

doi:10.1080/08820139.2024.2321353

Cited by 1 publication

(2 citation statements)

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“…Additionally, recent studies have reported that specific components from M2 macrophage-derived exosomes can improve diabetic fracture healing [ 76 ]. Furthermore, compounds like mogroside V (MV) and 4-octyl itaconate (OI), the cell-permeable itaconate derivate, exhibit anti-inflammatory effects [ 77 , 78 ]. Treatment with MV can mitigate the production of pro-inflammatory cytokines in bone marrow-derived macrophages (BMDM), reducing inflammation [ 77 ].…”

Section: Macrophage Activation In Diabetes and Its Regulatorsmentioning

confidence: 99%

“…Furthermore, compounds like mogroside V (MV) and 4-octyl itaconate (OI), the cell-permeable itaconate derivate, exhibit anti-inflammatory effects [ 77 , 78 ]. Treatment with MV can mitigate the production of pro-inflammatory cytokines in bone marrow-derived macrophages (BMDM), reducing inflammation [ 77 ]. The administration of OI in the mouse models of streptozotocin (STZ)-induced type 1 diabetes (T1D) and spontaneous autoimmune diabetes reduce M1 polarization, alleviating β cell dysfunction and further improving glucose metabolism [ 78 ].…”

Section: Macrophage Activation In Diabetes and Its Regulatorsmentioning

confidence: 99%

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The Pivotal Role of Macrophages in the Pathogenesis of Pancreatic Diseases

Ryu,

Lee

2024

IJMS

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The pancreas is an organ with both exocrine and endocrine functions, comprising a highly organized and complex tissue microenvironment composed of diverse cellular and non-cellular components. The impairment of microenvironmental homeostasis, mediated by the dysregulation of cell-to-cell crosstalk, can lead to pancreatic diseases such as pancreatitis, diabetes, and pancreatic cancer. Macrophages, key immune effector cells, can dynamically modulate their polarization status between pro-inflammatory (M1) and anti-inflammatory (M2) modes, critically influencing the homeostasis of the pancreatic microenvironment and thus playing a pivotal role in the pathogenesis of the pancreatic disease. This review aims to summarize current findings and provide detailed mechanistic insights into how alterations mediated by macrophage polarization contribute to the pathogenesis of pancreatic disorders. By analyzing current research comprehensively, this article endeavors to deepen our mechanistic understanding of regulatory molecules that affect macrophage polarity and the intricate crosstalk that regulates pancreatic function within the microenvironment, thereby facilitating the development of innovative therapeutic strategies that target perturbations in the pancreatic microenvironment.

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