TRPV1 Regulates Proinflammatory Properties of M1 Macrophages in Periodontitis Via NRF2

Li, Yiyang; Guo, Xiaotong; Zhan, Peimeng; Huang, Shuheng; Chen, Jiayao; Zhou, Yujie; Jiang, Wentao; Chen, Lingling; Lin, Zhengmei

doi:10.1007/s10753-024-02024-3

Inflammation

2024

DOI: 10.1007/s10753-024-02024-3

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TRPV1 Regulates Proinflammatory Properties of M1 Macrophages in Periodontitis Via NRF2

Yiyang Li,

Xiaotong Guo,

Peimeng Zhan

et al.

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2024

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Dexmedetomidine ameliorates diabetic intestinal injury by promoting the polarization of M2 macrophages through the MMP23B pathway

Lu,

Guo,

Zhang

et al. 2024

World J Diabetes

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BACKGROUND Diabetes is often associated with gastrointestinal dysfunctions, which can lead to hypoglycemia. Dexmedetomidine (DEX) is a commonly used sedative in perioperative diabetic patients and may affect gastrointestinal function. AIM To investigate whether sedative doses of DEX alleviate diabetes-caused intestinal dysfunction. METHODS Sedation/anesthesia scores and vital signs of streptozotocin (STZ)-induced diabetic mice under DEX sedation were observed. Diabetic mice were divided into saline and DEX groups. After injecting sedatives intraperitoneally, tight junctions (TJs) and apoptotic levels were evaluated 24 hours later to assess the intestinal barrier function. The role of DEX was validated using Villin-MMP23B flox/flox mice with intestinal epithelial deletion. In vitro , high glucose and hyperosmolarity were used to culture Caco-2 monolayer cells with STZ inter-vention. Immunofluorescence techniques were used to monitor the barrier and mitochondrial functions. RESULTS MMP23B protein levels in the intestinal tissue of STZ-induced diabetic mice were significantly higher than those in the intestinal tissue of control mice, with the DEX group displaying decreased MMP23B levels. Diabetes-mediated TJ dis-ruption, increased intestinal mucosal permeability, and systemic inflammation in wild-type mice might be reversed by DEX. In Caco-2 cells, MMP23B was associated with increased reactive oxygen species accumulation, mitochondrial membrane potential depolarization, and TJ disruption. CONCLUSION DEX reduces MMP23B, which may potentially contribute to STZ-induced intestinal barrier dysfunction, affecting TJ modification through mitochondrial dysfunction.

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Dexmedetomidine ameliorates diabetic intestinal injury by promoting the polarization of M2 macrophages through the MMP23B pathway

Lu,

Guo,

Zhang

et al. 2024

World J Diabetes

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TRPV1 Regulates Proinflammatory Properties of M1 Macrophages in Periodontitis Via NRF2

Cited by 1 publication

References 55 publications

Dexmedetomidine ameliorates diabetic intestinal injury by promoting the polarization of M2 macrophages through the MMP23B pathway

Dexmedetomidine ameliorates diabetic intestinal injury by promoting the polarization of M2 macrophages through the MMP23B pathway

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