Gastrodin Alleviates Cerebral Ischaemia/Reperfusion Injury by Inhibiting Pyroptosis by Regulating the lncRNA NEAT1/miR-22-3p Axis

Zhang, Hengsheng; Ouyang, Bo; Ji, Xiong-Ying; Liu, Meifang

doi:10.1007/s11064-021-03285-2

Cited by 34 publications

(29 citation statements)

References 53 publications

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“…Prior works have disclosed that many lncRNAs mediate hypoxic-ischemic brain damage progression, including MALAT1 [ 42 ], KCNQ1OT1 [ 43 ], lncRNA NEAT1 [ 44 ], and lncRNA GAS5 [ 45 ]. MIR497HG is a member of the lncRNA family, but the current studies on it mostly concentrate on tumors [ 46 , 47 ], while its role in neuroinflammation has not been probed.…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic Acid Prevents Microglia-Induced Neuronal Apoptosis and Oxidative Stress under Hypoxia-Ischemia Environment by Regulating the MIR497HG/miR-29b-3p/SIRT1 Axis

et al. 2022

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Background. Chlorogenic acid (CGA) is a polyphenolic compound with antioxidant and anti-inflammatory properties. CGA has been shown to improve neuroinflammation. This study is aimed at elucidating the exact mechanism by which CGA reduces neuroinflammation. Methods. Oxygen and glucose deprivation (OGD) was utilized to treat BV2 microglia and HT-22 hippocampal neurons to engineer an in vitro model of hypoxic ischemia reperfusion. The levels of inflammatory factors (IL-1β, IL-6, TNF-α, IL-4, and IL-10) and oxidative stress factors (MDA, SOD, and GSH-PX) in microglia were determined by ELISA kits. The neuron proliferation was assessed by CCK-8 assay, and LDH kit was used to determine LDH release in neurons. The fluorescent dye DCF-DA was employed to measure ROS levels in neurons. Correlation of MIR497HG, miR-29b-3p, and SIRT1/NF-κB in neurons and microglia was determined by qRT-PCR. Expressions of inflammatory proteins (COX2, iNOS), oxidative stress pathways (Nrf2, HO-1), and apoptosis-related proteins (Bcl-2, Bax, caspase3, caspase8, and caspase9) in microglia or neurons were determined by western blot. The interactions between MIR497HG and miR-29b-3p, as well as between miR-29b-3p and SIRT1, were determined by dual luciferase assay and RIP assay. Results. CGA attenuated OGD-mediated inflammation and oxidative stress in microglia and inhibited microglia-mediated neuronal apoptosis. CGA increased the levels of MIR497HG and SIRT1 and suppressed the levels of miR-29b-3p in BV2 and HT-22 cells. MIR497HG knockdown, miR-29b-3p upregulation, and SIRT1 inhibition inhibited CGA-mediated anti-inflammatory and neuronal protective functions. There is a targeting correlation between MIR497HG, miR-29b-3p, and Sirt1. MIR497HG sponges miR-29b-3p to regulate SIRT1 expression in an indirect manner. Conclusion. CGA upregulates MIR497HG to curb miR-29b-3p expression, hence initiating the SIRT1/NF-κB signaling pathway and repressing OGD-elicited inflammation, oxidative stress, and neuron apoptosis.

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Section: Discussionmentioning

confidence: 99%

Chlorogenic Acid Prevents Microglia-Induced Neuronal Apoptosis and Oxidative Stress under Hypoxia-Ischemia Environment by Regulating the MIR497HG/miR-29b-3p/SIRT1 Axis

et al. 2022

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“…In this process, several miRNAs have been profiled to be activated and possible therapeutical targets for pyroptosis inhibition (Wang et al, 2020a). Gastrodin regulated the miR-22/NEAT1 axis and reduced the pro-inflammatory cytokines, reducing pyroptosis and attenuating the I/R injuries both in vivo and in vitro (Zhang et al, 2021a). MiR-124, which was previously discussed for apoptosis and was described as a marker of I/R injury, inhibits STAT3 expression and thereby reduces pyroptosis and improves the neurological outcome (Sun et al, 2020a).…”

Section: Pyroptosismentioning

confidence: 99%

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

et al. 2022

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Cerebral ischemia reperfusion injury is a debilitating medical condition, currently with only a limited amount of therapies aimed at protecting the cerebral parenchyma. Micro RNAs (miRNAs) are small, non-coding RNA molecules that via the RNA-induced silencing complex either degrade or prevent target messenger RNAs from being translated and thus, can modulate the synthesis of target proteins. In the neurological field, miRNAs have been evaluated as potential regulators in brain development processes and pathological events. Following ischemic hypoxic stress, the cellular and molecular events initiated dysregulate different miRNAs, responsible for long-terming progression and extension of neuronal damage. Because of their ability to regulate the synthesis of target proteins, miRNAs emerge as a possible therapeutic strategy in limiting the neuronal damage following a cerebral ischemic event. This review aims to summarize the recent literature evidence of the miRNAs involved in signaling and modulating cerebral ischemia-reperfusion injuries, thus pointing their potential in limiting neuronal damage and repair mechanisms. An in-depth overview of the molecular pathways involved in ischemia reperfusion injury and the involvement of specific miRNAs, could provide future perspectives in the development of neuroprotective agents targeting these specific miRNAs.

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“…The process was iterated until no more publications would be obtained. A total of 15 publications were identified in this section, [50][51][52][53][54][55][56][57][58][59][60][61][62][63][64] which were performed between 2017 and 2021. The most widely used species and related inflammatory models are mice and middle cerebral artery occlusion (MCAO), respectively.…”

Section: Neat1 Directly Regulates Inflammation In the Central Nervous Systemmentioning

confidence: 99%

Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation

Pan

Wang

Zhao

et al. 2022

JIR

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Nuclear paraspeckle assembly transcript 1 (Neat1) located at chromosome 11 is a long non-coding RNA that is widely expressed in mammalian cell types, and which is overexpressed in several inflammation-related disorders. Inflammation implies a plethora of mutual interactions between both soluble factors and cells due to various stimuli including tissue injury. Although there is no doubt that inflammation is critically involved in multiple biological and pathological processes alike, the precise mechanisms being involved are still open for debate. In this context, the role of Neat1 as a regulator of inflammation, microglial activation, and lipid accumulation under various inflammatory conditions remains elusive. Herein, we review the regulation of Neat1 and how it modulates the expression of its target genes. Thereafter, we will review the impact of Neat1 on inflammation by activating or inhibiting various signaling pathways, such as microRNAs, AKT, TLR4, TRAF6, and NF-κB.

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Gastrodin Alleviates Cerebral Ischaemia/Reperfusion Injury by Inhibiting Pyroptosis by Regulating the lncRNA NEAT1/miR-22-3p Axis

Cited by 34 publications

References 53 publications

Chlorogenic Acid Prevents Microglia-Induced Neuronal Apoptosis and Oxidative Stress under Hypoxia-Ischemia Environment by Regulating the MIR497HG/miR-29b-3p/SIRT1 Axis

Chlorogenic Acid Prevents Microglia-Induced Neuronal Apoptosis and Oxidative Stress under Hypoxia-Ischemia Environment by Regulating the MIR497HG/miR-29b-3p/SIRT1 Axis

miRNA Involvement in Cerebral Ischemia-Reperfusion Injury

Novel Insights into the Emerging Role of Neat1 and Its Effects Downstream in the Regulation of Inflammation

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