Baicalin Inhibits NLRP3 Inflammasome Activity Via the AMPK Signaling Pathway to Alleviate Cerebral Ischemia-Reperfusion Injury

Zheng, Wenxia; He, Weiming; Zhang, Qianrui; Jia, Jin-Xin; Zhao, Sheng; Wu, Fangjian; Cao, Xiaolu

doi:10.1007/s10753-021-01486-z

Cited by 23 publications

(19 citation statements)

References 63 publications

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“… Chrysophanol Rheum Palmatum L. Inhibits M1-type microglia activation and TRAF6-dependent pyroptosis TRAF6/NLRP3 MCAO; OGD/R [ 101 , 106 ] Isoquercetin Styphnolobium japonicum (L.) Schott Anti-inflammatory, antioxidant, and reduces neuronal apoptosis TLR4/NLRP3; Caspase-3; Nrf2 MCAO/R; OGD/R [ 107 , 108 ] Baicalin Scutellaria baicalensis Georgi Protects glutamine synthetase, antioxidant, and anti-inflammatory AMPK/NLRP3; ROS MCAO/R; OGD/R [ 109 , 110 ] Astragaloside IV Astragalus membranaceus (Fisch.) Bunge Inhibition of pyroptosis and regulation of autophagy Nrf2/NLRP3; GSDMD; LC3 MCAO/R; OGD/R [ 111 , 112 ] Resveratrol Polygonum cuspidatum Sieb. et Zucc.…”

Section: Introductionmentioning

confidence: 99%

Targeting pyroptosis as a preventive and therapeutic approach for stroke

Long

Sun

et al. 2023

Cell Death Discov.

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Stroke has caused tremendous social stress worldwide, yet despite decades of research and development of new stroke drugs, most have failed and rt-PA (Recombinant tissue plasminogen activator) is still the accepted treatment for ischemic stroke. the complexity of the stroke mechanism has led to unsatisfactory efficacy of most drugs in clinical trials, indicating that there are still many gaps in our understanding of stroke. Pyroptosis is a programmed cell death (PCD) with inflammatory properties and are thought to be closely associated with stroke. Pyroptosis is regulated by the GSDMD of the gasdermin family, which when cleaved by Caspase-1/Caspase-11 into N-GSDMD with pore-forming activity can bind to the plasma membrane to form small 10–20 nm pores, which would allow the release of inflammatory factors IL-18 and IL-1β before cell rupture, greatly exacerbating the inflammatory response. The pyroptosis occurs mainly in the border zone of cerebral infarction, and glial cells, neuronal cells and brain microvascular endothelial cells (BMECs) all undergo pyroptosis after stroke, which largely exacerbates the breakdown of the blood-brain barrier (BBB) and thus aggravates brain injury. Therefore, pyroptosis may be a good direction for the treatment of stroke. In this review, we focus on the latest mechanisms of action of pyroptosis and the process by which pyroptosis regulates stroke development. We also suggest potential therapeutic stroke drugs that target the pyroptosis pathway, providing additional therapeutic strategies for the clinical management of stroke.

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Section: Introductionmentioning

confidence: 99%

Targeting pyroptosis as a preventive and therapeutic approach for stroke

Long

Sun

et al. 2023

Cell Death Discov.

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“…This may contribute to its protective effects on neonatal hyperoxia-induced alveolar and vascular simplification. Baicalin activates AMPK in adipose tissues and brain [ 53 , 54 ]. AMPK in turn activates Cpt1a by decreasing its allosteric inhibitor malonyl-CoA through phosphorylation and inactivation of acetyl-CoA carboxylase [ 55 ].…”

Section: Discussionmentioning

confidence: 99%

Upregulating carnitine palmitoyltransferase 1 attenuates hyperoxia-induced endothelial cell dysfunction and persistent lung injury

et al. 2022

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Background Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants that may cause long-term lung dysfunction. Accumulating evidence supports the vascular hypothesis of BPD, in which lung endothelial cell dysfunction drives this disease. We recently reported that endothelial carnitine palmitoyltransferase 1a (Cpt1a) is reduced by hyperoxia, and that endothelial cell-specific Cpt1a knockout mice are more susceptible to developing hyperoxia-induced injury than wild type mice. Whether Cpt1a upregulation attenuates hyperoxia-induced endothelial cell dysfunction and lung injury remains unknown. We hypothesized that upregulation of Cpt1a by baicalin or l-carnitine ameliorates hyperoxia-induced endothelial cell dysfunction and persistent lung injury. Methods Lung endothelial cells or newborn mice (< 12 h old) were treated with baicalin or l-carnitine after hyperoxia (50% and 95% O2) followed by air recovery. Results We found that incubation with l-carnitine (40 and 80 mg/L) and baicalin (22.5 and 45 mg/L) reduced hyperoxia-induced apoptosis, impaired cell migration and angiogenesis in cultured lung endothelial cells. This was associated with increased Cpt1a gene expression. In mice, neonatal hyperoxia caused persistent alveolar and vascular simplification in a concentration-dependent manner. Treatment with l-carnitine (150 and 300 mg/kg) and baicalin (50 and 100 mg/kg) attenuated neonatal hyperoxia-induced alveolar and vascular simplification in adult mice. These effects were diminished in endothelial cell-specific Cpt1a knockout mice. Conclusions Upregulating Cpt1a by baicalin or l-carnitine ameliorates hyperoxia-induced lung endothelial cell dysfunction, and persistent alveolar and vascular simplification. These findings provide potential therapeutic avenues for using l-carnitine and baicalin as Cpt1a upregulators to prevent persistent lung injury in premature infants with BPD.

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“…52 CVDs are the cardiometabolic alterations for which more in vivo studies have explored how polyphenols could modulate the NLRP3 inflammasome, with a total of 18 studies on the topic (17 preclinical and 1 clinical), whose main findings are summarized in Table 2. [53][54][55][56][57][58][59][60][61][62][63][64][65][66][67][68][69][70] Regarding the pre-clinical trials, the two most commonly selected animal models corresponded to the middle cerebral artery occlusion/reperfusion model (MCAO/R) in rats 56,59,61,[64][65][66][67] and the myocardial ischemia/reperfusion model (MI/R) in rats or mice. 53,55,58,69,70 Other different…”

Section: Cardiovascular Diseases (Cvds)mentioning

confidence: 99%