Adiponectin peptide alleviates oxidative stress and NLRP3 inflammasome activation after cerebral ischemia-reperfusion injury by regulating AMPK/GSK-3β

Liu, Haixiao; Wu, Xun; Luo, Jianing; Zhao, Lei; Li, Xia; Guo, Hao; Bai, Hao; Cui, Wenxing; W, Guo; Feng, Dayun; Qu, Yan

doi:10.1016/j.expneurol.2020.113302

Cited by 139 publications

(69 citation statements)

References 82 publications

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“…Other authors support the idea that TXNIP silencing alleviates oxidative stress injury by regulating the MAPK-Nrf2 axis in ischemic stroke [61]. In addition to regulating Nrf2 expression with different compounds, a critical mechanism associated with the downregulation of TXNIP is the nuclear translocation of Nrf2 promoted by AMPK and GSK-3β [108]. This signaling pathway is in line with the improvement of the oxidative defense with augmentation of TRX and the diminution of TXNIP expression [225].…”

Section: Txnip As a Marker In Cerebral Ischemiamentioning

confidence: 59%

The Emerging Role of TXNIP in Ischemic and Cardiovascular Diseases; A Novel Marker and Therapeutic Target

Domingues

Jolibois

Rougé

et al. 2021

IJMS

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Thioredoxin interacting protein (TXNIP) is a metabolism- oxidative- and inflammation-related marker induced in cardiovascular diseases and is believed to represent a possible link between metabolism and cellular redox status. TXNIP is a potential biomarker in cardiovascular and ischemic diseases but also a novel identified target for preventive and curative medicine. The goal of this review is to focus on the novelties concerning TXNIP. After an overview in TXNIP involvement in oxidative stress, inflammation and metabolism, the remainder of this review presents the clues used to define TXNIP as a new marker at the genetic, blood, or ischemic site level in the context of cardiovascular and ischemic diseases.

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Section: Txnip As a Marker In Cerebral Ischemiamentioning

confidence: 59%

The Emerging Role of TXNIP in Ischemic and Cardiovascular Diseases; A Novel Marker and Therapeutic Target

Domingues

Jolibois

Rougé

et al. 2021

IJMS

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“…AMPK, a member of the Serine/threonine (Ser/Thr) kinase group, is widely distributed in various cells and organs as one of the central regulators of metabolism in eukaryotic cells and organisms (Jiang et al, 2018). Adiponectin (APN) was found to reduce oxidative stress and NLRP3 inflammasome activation after cerebral ischemia-reperfusion injury by regulating AMPK/GSK-3 (Liu et al, 2020). Additionally, Yu J et al also found that Ezetimibe (Eze) reduces oxidative stress and subsequent neuroinflammatory response by activating AMPK/ Nrf2/TXNIP pathways in MCAO rats (Yu et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

AMPK/SIRT1 Pathway is Involved in Arctigenin-Mediated Protective Effects Against Myocardial Ischemia-Reperfusion Injury

et al. 2021

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Arctigenin, one of the active ingredients extracted from Great Burdock (Arctium lappa) Achene, has been found to relieve myocardial infarction injury. However, the specific mechanism of Arctigenin against myocardial infarction remains largely unknown. Here, both acute myocardial ischemia-reperfusion injury (AMI/R) rat model and oxygen glucose deprivation (OGD)-induced myocardial cell injury model were constructed to explore the underlying role of AMPK/SIRT1 pathway in Arctigenin-mediated effects. The experimental data in our study demonstrated that Arctigenin ameliorated OGD-mediated cardiomyocytes apoptosis, inflammation and oxidative stress in a dose-dependent manner. Besides, Arctigenin activated AMPK/SIRT1 pathway and downregulated NF-κB phosphorylation in OGD-treated cardiomyocytes, while inhibiting AMPK or SIRT1 by the Compound C (an AMPK inhibitor) or SIRT1-IN-1 (a SIRT1 inhibitor) significantly attenuated Arctigenin-exerted protective effects on cardiomyocytes. In the animal experiments, Arctigenin improved the heart functions and decreased infarct size of the AMI/R-rats, accompanied with downregulated oxidative stress, inflammation and apoptotic levels in the heart tissues. What’s more, Arctigenin enhanced the AMPK/SIRT1 pathway and repressed NF-κB pathway activation. Taken together, our data indicated that Arctigenin reduced cardiomyocytes apoptosis against AMI/R-induced oxidative stress and inflammation at least via AMPK/SIRT1 pathway.

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“…According to a recent study, adiponectin upregulation of the phosphorylation of AMPK can reduce inflammation, inhibit the activation of the NLRP3 inflammasome, while also having a beneficial role in cerebral I/R injury [42]. In this study, we examined whether metformin exerts its cardioprotective effect against myocardial I/R injury by activating AMPK and inhibiting NLRP3 inflammasome activation.…”

Section: Metformin Alleviates Nlrp3 Inflammasome Activation In An Ampmentioning

confidence: 99%

Nod-like Receptor Protein 3 (Nlrp3) Inflammasomes Inhibition by Metformin Limits Myocardial Ischemia/reperfusion Injury

Zhang

Liu

Zhang

et al. 2020

Preprint

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Background Ischemia/reperfusion (I/R) injury is a life-threatening vascular emergency following myocardial infarction. Our previous study showed cardioprotective effects of metformin against myocardial I/R injury. In this study, we further examined the involvement of AMPK mediated activation of NLRP3 inflammasome in this cardioprotective effect of metformin. Methods Myocardial I/R injury was simulated in a rat heart Langendorff model and neonatal rat ventricle myocytes (NRVMs) were subjected to hypoxi/reoxygenation (H/R) to establish an in vitro model. Outcome measures included myocardial infarct size, hemodynamic monitoring, myocardial tissue injury, myocardial apoptotic index and the inflammatory response. myocardial infarct size and cardiac enzyme activities. Results First, we found that metformin postconditioning can not only significantly alleviated myocardial infarct size, attenuated cell apoptosis, and inhibited myocardial fibrosis. Furthermore, metformin activated phosphorylated AMPK, decreased pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β, and decreased NLRP3 inflammasome activation. In isolated NRVMs metformin increased cellular viability, decreased LDH activity and inhibited cellular apoptosis and inflammation. Importantly, inhibition of AMPK phosphorylation by Compound C (CC) resulted in decreased survival of cardiomyocytes mainly by inducing the release of inflammatory cytokines and increasing NLRP3 inflammasome activation. Finally, in vitro studies revealed that the NLRP3 activator nigericin abolished the anti-inflammatory effects of metformin in NRVMs, but it had little effect on AMPK phosphorylation. Conclusions Collectively, our study confirmed that metformin exerts cardioprotective effects by regulating myocardial I/R injury-induced inflammatory response, which was largely dependent on the enhancement of the AMPK pathway, thereby suppressing NLRP3 inflammasome activation.

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Adiponectin peptide alleviates oxidative stress and NLRP3 inflammasome activation after cerebral ischemia-reperfusion injury by regulating AMPK/GSK-3β

Cited by 139 publications

References 82 publications

The Emerging Role of TXNIP in Ischemic and Cardiovascular Diseases; A Novel Marker and Therapeutic Target

The Emerging Role of TXNIP in Ischemic and Cardiovascular Diseases; A Novel Marker and Therapeutic Target

AMPK/SIRT1 Pathway is Involved in Arctigenin-Mediated Protective Effects Against Myocardial Ischemia-Reperfusion Injury

Nod-like Receptor Protein 3 (Nlrp3) Inflammasomes Inhibition by Metformin Limits Myocardial Ischemia/reperfusion Injury

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