Ropivacaine Prevents the Activation of the NLRP3 Inflammasome Caused by High Glucose in HUVECs

Huang, Xin; Jiang, Jingyan; Huang, Lijun; Ren, Qiusheng; Gao, Xiang; Yu, Shenghui

doi:10.1021/acsomega.0c03143

Cited by 2 publications

(3 citation statements)

References 34 publications

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“…HMGB1 has also been associated with high glucose levels. Huang et al showed that culturing human umbilical vein endothelial cells (HUVECs) under high glucose conditions led to increased secretion of HMGB1 96 . Since diabetes is associated with an increased risk of malignancies, HMGB1 may play a role in driving tumor growth and metastasis due to its effects on Erk1/2 activation and DRP‐1 phosphorylation.…”

Section: Pathobiological Implications Of the Imbalance In Mitochondrial Fusion And Fissionmentioning

confidence: 99%

“…Huang et al showed that culturing human umbilical vein endothelial cells (HUVECs) under high glucose conditions led to increased secretion of HMGB1. 96 Since diabetes is associated with an increased risk of malignancies, HMGB1 may play a role in driving tumor growth and metastasis due to its effects on Erk1/2 activation and DRP-1 phosphorylation. More studies are required to investigate the link between hyperglycemia and imbalance in mitochondrial dynamics as a contributor to tumor growth.…”

Section: Carcinogenesismentioning

confidence: 99%

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Mitochondrial fusion and fission: The fine‐tune balance for cellular homeostasis

et al. 2021

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Mitochondria are highly dynamic, maternally inherited cytoplasmic organelles, which fulfill cellular energy demand through the oxidative phosphorylation system. Besides, they play an active role in calcium and damage‐associated molecular patterns signaling, amino acid, and lipid metabolism, and apoptosis. Thus, the maintenance of mitochondrial integrity and homeostasis is extremely critical, which is achieved through continual fusion and fission. Mitochondrial fusion allows the transfer of gene products between mitochondria for optimal functioning, especially under metabolic and environmental stress. On the other hand, fission is crucial for mitochondrial division and quality control. The imbalance between these two processes is associated with various ailments such as cancer, neurodegenerative and cardiovascular diseases. This review discusses the molecular mechanisms that control mitochondrial fusion and fission and how the disruption of mitochondrial dynamics manifests into various disease conditions.

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Section: Pathobiological Implications Of the Imbalance In Mitochondrial Fusion And Fissionmentioning

confidence: 99%

Section: Carcinogenesismentioning

confidence: 99%

Mitochondrial fusion and fission: The fine‐tune balance for cellular homeostasis

et al. 2021

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“…A previous study reported that PM2.5 triggered the immune response in the lung by activating NLRP3/Caspase-1 signaling ( 17 ), whereas ropivacaine prevented the activation of NLRP3( 18 ). Thus, in the present study, it was hypothesized that ropivacaine exerted effects on ALI via NLRP3/Caspase-1 signaling.…”

Section: Resultsmentioning

confidence: 99%

Ropivacaine has the potential to relieve PM2.5‑induced acute lung injury

Zuo

2022

Exp Ther Med

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Ropivacaine is a commonly used local anesthetic in the clinic due to its low toxicity to the cardiovascular system or central nervous system, good tolerance and high clearance rate. The present study intended to investigate the effect of ropivacaine on PM2.5-induced acute lung injury (ALI) and reveal the underlying mechanism. After ropivacaine exposure, cell viability, oxidative stress and inflammation in PM2.5-induced BEAS-2B cells were assessed by Cell Counting Kit-8 and DCFH-DA staining, corresponding commercial kits and ELISA, respectively. The effects of ropivacaine on the expression of MMP9 and MMP12 and the proteins related to NLRP3/Caspase-1 signaling were then determined by western blot and reverse transcription-quantitative PCR analyses. In addition, NLR family pyrin domain containing 3 (NLRP3) agonist monosodium urate (MSU) was used to treat BEAS-2B cells followed by ropivacaine treatment and the effects on the above-mentioned cellular behaviors were determined again. The results indicated that the viability of BEAS-2B cells was decreased after PM2.5 induction, accompanied by aggravated oxidative stress and inflammation. However, ropivacaine alleviated oxidative stress and inflammation in PM2.5-induced BEAS-2B cells in a dose-dependent manner. Ropivacaine was also indicated to decrease the expression levels of NLRP3/Caspase-1 signaling-related proteins in PM2.5-induced BEAS-2B cells. Furthermore, cell viability was decreased, while oxidative stress and inflammatory response were aggravated, in PM2.5-induced BEAS-2B cells treated with MSU. In summary, the present results implied that ropivacaine exerted protective effects on PM2.5-induced ALI, and this effect may be related to NLRP3/Caspase-1 signaling.

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Ropivacaine Prevents the Activation of the NLRP3 Inflammasome Caused by High Glucose in HUVECs

Cited by 2 publications

References 34 publications

Mitochondrial fusion and fission: The fine‐tune balance for cellular homeostasis

Mitochondrial fusion and fission: The fine‐tune balance for cellular homeostasis

Ropivacaine has the potential to relieve PM2.5‑induced acute lung injury

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