LncRNA MALAT1 Promoted Neuronal Necroptosis in Cerebral Ischemia-reperfusion Mice by Stabilizing HSP90

Huang, Shan; Hou, Dan; Zhang, Lei; Pei, Chaoying; Liang, Jing; Li, Junqi; Yang, Guoshuai; Yu, Dan

doi:10.1007/s11064-023-03991-z

Cited by 4 publications

(3 citation statements)

References 59 publications

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“…22 In this study, we investigated the neuroprotective role of Sal B against ischemic brain damage using a mouse tMCAO model as a classical model that mimics human stroke. 11 Sal B improved neurological dysfunction, reduced the size of cerebral infarcts and cerebral edema, and inhibited the TLRs are coreceptors of the innate immune response and are triggered when infectious microbes invade mammals. They are also activated by host-derived molecules.…”

Section: Discussionmentioning

confidence: 99%

“…It has been demonstrated that the TLR‐MyD88 association activates MAPKs and NF‐κB pathway cascades, which are necessary for the expression of inflammatory mediators such as IL‐1β 22 . In this study, we investigated the neuroprotective role of Sal B against ischemic brain damage using a mouse tMCAO model as a classical model that mimics human stroke 11 . Sal B improved neurological dysfunction, reduced the size of cerebral infarcts and cerebral edema, and inhibited the inflammatory response following cerebral I/R injury by downregulating TLR4, p‐p38MAPK, p‐JNK, nuclear NF‐κB, and IL‐1β production.…”

Section: Discussionmentioning

confidence: 99%

“…At first, animals were anesthetized with chloral hydrate (10%, 400 mg/kg, intraperitoneally). The mouse tMCAO model was established by right middle cerebral artery occlusion (60 min) followed by reperfusion, as described previously 11,12 . Body temperatures were monitored and maintained at 37 ± 0.5°C during surgery.…”

Section: Methodsmentioning

confidence: 99%

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Neuroprotective mechanism of salvianolic acid B against cerebral ischemia–reperfusion injury in mice through downregulation of TLR4, p‐p38MAPK, p‐JNK, NF‐κB, and IL‐1β

Zheng,

Zhang,

Dong

et al. 2023

Immunity Inflam & Disease

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ObjectiveTissue injury and inflammation are two potential outcomes of cerebral ischemia–reperfusion (I/R) injury. Salvianolic acid B (Sal B), isolated from the roots of Salvia miltiorrhiza, is one of the major water‐soluble compounds with a wide range of pharmacological effects including antioxidant, anti‐inflammatory, antiproliferative, and neuroprotective effects. In the present study, we explored the neuroprotective effects and potential mechanisms of Sal B after I/R injury.MethodsWe induced cerebral ischemia in male CD‐1 mice through transient (60 min) middle cerebral artery occlusion (tMCAO), and then injected Sal B (30 mg/kg) intraperitoneally. Neurological deficits, infarct volumes, and brain edema were assessed at 24 and 72 h after tMCAO. We detected the expression of Toll‐like receptor 4 (TLR4), phosphorylated‐p38 mitogen‐activated protein kinase (P‐p38 MAPK), phosphorylated c‐Jun amino (N)‐terminal kinases (p‐JNK), nuclear factor‐κB (NF‐κB), and interleukin‐1β (IL‐1β) in the brain tissue.ResultsCompared with the tMCAO group, Sal B significantly improved neurological deficits, reduced infarct size, attenuated cerebral edema, and downregulated the expression of pro‐inflammatory mediators TLR4, p‐p38MAPK, p‐JNK, nuclear NF‐κB, and IL‐1β in brain tissue after I/R injury.ConclusionWe found that Sal B protects brain tissues from I/R injury by activating its anti‐inflammatory properties.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%