Panaxynol ameliorates cardiac ischemia/reperfusion injury by suppressing NLRP3-induced pyroptosis and apoptosis via HMGB1/TLR4/NF-κB axis

Ding, Hua‐Sheng; Huang, Yan; Qu, Jifu; Wang, Yongjian; Huang, Zhongyi; Wang, Feng-Yuan; Yi, Wenjuan; Liu, Xiao-Xiong

doi:10.1016/j.intimp.2023.110222

Cited by 12 publications

(2 citation statements)

References 25 publications

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“…In this investigation, HMGB1 was identified as a key inducer of myocardial apoptosis, aligning with previous research highlighting its involvement in autophagy and apoptosis [44]. While HMGB1-mediated autophagy typically serves as a protective mechanism against apoptosis in cancer cells [45], our study reveals a contrasting effect in the myocardium, where HMGB1 activates pathways such as HMGB1/TLR4/NFκB and HMGB1/extracellular signal-regulated kinase/ETS1, ultimately leading to apoptosis [46,47]. Notably, the HMGB1/RAGE pathway induces both apoptosis and autophagy in the myocardium, contributing to cellular damage [48].…”

Section: Discussionsupporting

confidence: 86%

Berberine Improves Cancer-Derived Myocardial Impairment in Experimental Cachexia Models by Targeting High-Mobility Group Box-1

Goto,

Fujiwara-Tani,

Nukaga

et al. 2024

IJMS

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Cardiac disorders in cancer patients pose significant challenges to disease prognosis. While it has been established that these disorders are linked to cancer cells, the precise underlying mechanisms remain elusive. In this study, we investigated the impact of cancerous ascites from the rat colonic carcinoma cell line RCN9 on H9c2 cardiomyoblast cells. We found that the ascites reduced mitochondrial volume, increased oxidative stress, and decreased membrane potential in the cardiomyoblast cells, leading to apoptosis and autophagy. Although the ascites fluid contained a substantial amount of high-mobility group box-1 (HMGB1), we observed that neutralizing HMGB1 with a specific antibody mitigated the damage inflicted on myocardial cells. Our mechanistic investigations revealed that HMGB1 activated both nuclear factor κB and phosphoinositide 3-kinases-AKT signals through HMGB1 receptors, namely the receptor for advanced glycation end products and toll-like receptor-4, thereby promoting apoptosis and autophagy. In contrast, treatment with berberine (BBR) induced the expression of miR-181c-5p and miR-340-5p while suppressing HMGB1 expression in RCN9 cells. Furthermore, BBR reduced HMGB1 receptor expression in cardiomyocytes, consequently mitigating HMGB1-induced damage. We validated the myocardial protective effects of BBR in a cachectic rat model. These findings underscore the strong association between HMGB1 and cancer cachexia, highlighting BBR as a promising therapeutic agent for myocardial protection through HMGB1 suppression and modulation of the signaling system.

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Section: Discussionsupporting

confidence: 86%

Berberine Improves Cancer-Derived Myocardial Impairment in Experimental Cachexia Models by Targeting High-Mobility Group Box-1

Goto,

Fujiwara-Tani,

Nukaga

et al. 2024

IJMS

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“…For instance, miR-27a interacts with 3’ UTR of TLR4 to down-regulate TLR4 expression and inhibits inflammation, cell adhesion and apoptosis in renal IRI ( 28 ). Other antagonists, inhibitors or miRNAs that target upstream or downstream molecules of TLR4, such as panaxynol for TLR4-NF-κB pathway in cardiac IRI, clemastine fumarate for TLR/Akt pathway in pathway in myocardial IRI, miR-143–3p for TLR4-NF-κB pathway in myocardial IRI, can effectively relieve the IRI by inhibiting inflammation and apoptosis ( 29 – 31 ). The development and utilisation of these molecules are the focus of current research.…”

Section: Crosstalk Between Tlr4 Signalling Inflammation Oxidative Str...mentioning

confidence: 99%

TLR4 signalling in ischemia/reperfusion injury: a promising target for linking inflammation, oxidative stress and programmed cell death to improve organ transplantation outcomes

Wang,

Zhang,

Huang

et al. 2024

Front. Immunol.

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Transplantations represent the principal therapeutic interventions for terminal organ failure, a procedure that has salvaged myriad lives annually. Ischemia/reperfusion injury (IRI) is frequently correlated with an unfavourable prognosis and is relevant for early graft dysfunction and graft survival. IRI constitutes a complex pathological state influenced by a series of factors such as oxidative stress, metabolic stress, leukocytic infiltration, programmed cell death pathways, and inflammatory immune responses. Reducing ischemia/reperfusion injury is one of the main directions of transplantation research. Toll-like receptors (TLRs) are important pattern-recognition receptors expressed on various organs that orchestrate the immune responses upon recognising PAMPs and DAMPs. Targeting the TLR4 signalling has recently been suggested as a promising approach for alleviating IRI by affecting inflammation, oxidative stress and programmed cell death (PCD). In this minireview, we summarise the role of TLR4 signalling in regulating inflammation, oxidative stress and PCD in organ transplantation and discuss their interactions during IRI. A detailed understanding of the multiple functions of TLR4 in IRI provides novel insights into developing therapies to improve organ transplantation outcomes.

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IL-1 signaling pathway, an important target for inflammation surrounding in myocardial infarction

Huang,

Kuang,

Zhou

2024

Inflammopharmacol

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Panaxynol ameliorates cardiac ischemia/reperfusion injury by suppressing NLRP3-induced pyroptosis and apoptosis via HMGB1/TLR4/NF-κB axis

Cited by 12 publications

References 25 publications

Berberine Improves Cancer-Derived Myocardial Impairment in Experimental Cachexia Models by Targeting High-Mobility Group Box-1

Berberine Improves Cancer-Derived Myocardial Impairment in Experimental Cachexia Models by Targeting High-Mobility Group Box-1

TLR4 signalling in ischemia/reperfusion injury: a promising target for linking inflammation, oxidative stress and programmed cell death to improve organ transplantation outcomes

IL-1 signaling pathway, an important target for inflammation surrounding in myocardial infarction

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