scholarly journals Daphnetin Protects against Cerebral Ischemia/Reperfusion Injury in Mice via Inhibition of TLR4/NF-κB Signaling Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Jia Liu ◽  
Qianxue Chen ◽  
Zhihong Jian ◽  
Xiaoxing Xiong ◽  
Lingmin Shao ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Signaling Pathway ◽  
Nuclear Translocation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coumarin Derivative ◽  
Neural Cells ◽  
Cerebral Ischemia Reperfusion ◽  
Anti Inflammatory

Growing evidences indicate that immune-mediated mechanisms contribute to the development of cerebral ischemia/reperfusion (I/R) injury. Daphnetin (DAP) is a coumarin derivative extracted from Daphne odora var., which displays anti-inflammatory properties. However, the effect of DAP on cerebral I/R injury is not yet clear. Recent studies have demonstrated that TLR4/NF-κB signaling pathway takes part in the damaging inflammatory process of cerebral I/R injury. The present study aimed to investigate the effect of DAP on cerebral I/R injury in vivo and its possible mechanisms. DAP was administered before middle cerebral artery occlusion and reperfusion in mice. The neurological scores, cerebral infarct sizes, the levels of inflammatory cytokines, apoptotic neural cells, and the levels of TLR4, NF-κB p65, and IκBα were estimated. The results showed that an obvious improvement of neurological scores and infarct sizes was observed in DAP-treated mice after MCAO/R. DAP treatment decreased the overexpression of TNF-α, IL-1β, and IL-6 and attenuated neural cells apoptosis. Moreover, DAP treatment decreased the TLR4 expression, IκB-α degradation, and nuclear translocation of NF-κB. Taken together, our results suggested that DAP exerted neuroprotective and anti-inflammatory effects on cerebral I/R injury. The potential mechanism was involved in the inhibition of TLR4/NF-κB mediated inflammatory signaling pathway.

scholarly journals Anti-inflammatory Effect of Heat-sensitive Moxibustion via the NF-κB Signaling Pathway on Cerebral Ischemia/Reperfusion Injury in Rats

2018 ◽  
Vol 1 (3) ◽  
pp. 67
Author(s):  
Aijiao Xiaoa ◽  
Yisheng Xiaoa ◽  
Xin OuYang ◽  
Lin He ◽  
Mingren Chen
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Temperature Increase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Suspended Moxibustion ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Anti Inflammatory

Ischemic stroke is universally acknowledged as a common cause of long-term disability or even death. Suspended moxibustion, an indirect form of moxibustion, is when moxibustion is placed superfcially over the skin without being in contact with it. Some researchers have used this method to treat stroke patients, but strong evidence of its therapeutic effectiveness is lacking.However, the effect of traditional suspended moxibustion has recently been improved with the development of heat-sensitive suspended moxibustion. Our previous studies showed that moxibustion for 35 min provided a more effective treatment strategy than moxibustion for 15 min, and moxibustion by 35 min with tail temperature increase had a better outcome than that without, however,the mechanism underlying the effect is not clear. In this study, we treated the stroke rats with moxibustion by 35min and divided them into non-heat sensitive moxibustion(NHSM) group and heat sensitive moxibustion (HSM) group according to difference in the tail temperature increase, then we compared the effect and investigated the mechanisms between NHSM and HSM. We found that HSM signifcantly decreased tail-flick latency, increased neurological function score, decreased infarct volume, reduced inflammatory cells,decreased the expression of inflammatory factor ICAM-1 and reduced the expression of NF-κB p65 and p-IKKα/β in rats with focal cerebral ischemia/reperfusion injury. Our experimental fndings revealed that HSM exerted its anti-inflammatory and neuroprotective effects from MCAO-induced injury by decreasing the expression of the NF-κB signaling pathway.

scholarly journals LINGO-1 shRNA protects the brain against ischemia/reperfusion injury by inhibiting the activation of NF-κB and JAK2/STAT3

Human Cell ◽  
2021 ◽  
Author(s):  
Jiaying Zhu ◽  
Zhu Zhu ◽  
Yipin Ren ◽  
Yukang Dong ◽  
Yaqi Li ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nuclear Translocation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Mice Model ◽  
Down Regulation

AbstractLINGO-1 may be involved in the pathogenesis of cerebral ischemia. However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose deprivation/reperfusion (OGD/R) were established to simulate the pathological process of cerebral ischemia in vivo and in vitro and to detect the relevant mechanism. We found that LINGO-1 mRNA and protein were upregulated in mice and cell models. Down-regulation LINGO-1 improved the neurological symptoms and reduced pathological changes and the infarct size of the mice after MACO/R. In addition, LINGO-1 interference alleviated apoptosis and promoted cell proliferation in HT22 of OGD/R. Moreover, down-regulation of LINGO-1 proved to inhibit nuclear translocation of p-NF-κB and reduce the expression level of p-JAK2 and p-STAT3. In conclusion, our data suggest that shLINGO-1 attenuated ischemic injury by negatively regulating NF-KB and JAK2/STAT3 pathways, highlighting a novel therapeutic target for ischemic stroke.

scholarly journals Up-regulation of miR-499a-5p decreases cerebral ischemia/reperfusion injury by targeting PDCD4

2021 ◽  
Author(s):  
Weifeng Shan ◽  
Huifeng Ge ◽  
Bingquan Chen ◽  
Linger Huang ◽  
Shaojun Zhu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Artery Occlusion ◽  
Tunel Staining ◽  
Cerebral Ischemia Reperfusion

Abstract MiR-499a-5p was significantly down-regulated in degenerative tissues and correlated with apoptosis. Nonetheless, the biological function of miR-499a-5p in acute ischemic stroke has been still unclear. In this study, we found the plasma levels of miR-499a-5p were significantly down-regulated in 64 ischemic stroke patients and negatively correlated with the National Institutes of Health Stroke Scale score. Then, we constructed cerebral ischemia/reperfusion (I/R) injury in rats after middle cerebral artery occlusion and subsequent reperfusion and oxygen-glucose deprivation and reoxygenation (OGD/R) treated SH-SY5Y cell model. Transfection with miR-499a-5p mimic was accomplished by intracerebroventricular injection in the in vivo I/R injury model. We further found miR-499a-5p overexpression decreased infarct volumes and cell apoptosis in the in vivo I/R stroke model using TTC and TUNEL staining. PDCD4 was a direct target of miR-499a-5p by luciferase report assay and western blotting. Knockdown of PDCD4 reduced the infarct damage and cortical neuron apoptosis caused by I/R injury. MiR-499a-5p exerted neuroprotective roles mainly through inhibiting PDCD4-mediated apoptosis by CCK-8 assay, LDH release assay and flow cytometry analysis. These findings suggest that miR-499a-5p might represent a novel target that regulates brain injury by inhibiting PDCD4-mediating apoptosis.

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