The Possibility and Molecular Mechanisms of Cell Pyroptosis After Cerebral Ischemia

Dong, Zhaofei; Pan, Kuang; Pan, Jianke; Peng, Qingxia; Wang, Yidong

doi:10.1007/s12264-018-0294-7

Cited by 57 publications

(45 citation statements)

References 61 publications

(73 reference statements)

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“…Recently, more and more studies have shown that cell pyroptosis, also known as in ammatory death, can be caused by cerebral ischemia-reperfusion injury [27]. A hallmark of pyroptosis is GSDMD-NT-dependent membrane rupture due to Caspase-1 activation, which, unlike apoptosis, allows the release of intracellular pathogens such as pro-in ammatory mediators (e.g., IL-1β and IL-18) [28].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of Indobufen against pyroptosis following cerebral ischemia-reperfusion injury both in vivo and in vitro

Tian

et al. 2020

Preprint

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Background: Indobufen is a new generation of antiplatelet agents and has been shown to have antithrombotic effects in animal models. However, the efficacy of Indobufen on cerebral ischemia/reperfusion (I/R) injury and its mechanisms remain to be investigated. Methods: In this study, the efficacy of Indobufen with both pre- (5days) and post- (15days) treatment on rats suffering middle cerebral artery occlusion/reperfusion (MCAO/R, 2h of ischemia and 24h/15days of reperfusion) was investigated. Furthermore, human umbilical vein endothelial cells (HUVECs) were cultured and underwent oxygen glucose deprivation/reoxygenation (OGD/R) injury for in vitro studies. Relationship between Indobufen and pyroptosis associated NF-κB/Caspase-1/GSDMD pathway was preliminarily discussed. Results: The pharmacodynamic tests revealed that Indobufen ameliorated I/R injury by decreasing the platelet aggregation, infarct size, brain edema and neurologic impairment in rats and rescuing cell apoptosis/pyroptosis in HUVECs. The underlying mechanisms were probably related to pyroptosis suppression by platelet inhibition induced regulation of the NF-κB/Caspase-1/GSDMD pathway. Conclusion: Overall, these studies indicates that Indobufen exerts protective and therapeutic effects against I/R injury by pyroptosis suppression via downregulating NF-κB/Caspase-1/GSDMD pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of Indobufen against pyroptosis following cerebral ischemia-reperfusion injury both in vivo and in vitro

Tian

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…Recently, more and more studies have shown that cell pyroptosis, also known as in ammatory death, can be caused by cerebral ischemia-reperfusion injury [28]. A hallmark of pyroptosis is GSDMD-NT-dependent membrane rupture due to Caspase-1 activation, which, unlike apoptosis, allows the release of intracellular pathogens such as pro-in ammatory mediators (e.g., IL-1β and IL-18) [29].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of Indobufen against pyroptosis following cerebral ischemia-reperfusion injury both in vivo and in vitro

Tian

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Indobufen is a new generation of antiplatelet agents and has been shown to have antithrombotic effects in animal models. However, the efficacy of Indobufen on cerebral ischemia/reperfusion (I/R) injury and its mechanisms remain to be investigated. Methods: In this study, the efficacy of Indobufen with both pre- (5days) and post- (15days) treatment on rats suffering middle cerebral artery occlusion/reperfusion (MCAO/R, 2h of ischemia and 24h/15days of reperfusion) was investigated. Furthermore, human umbilical vein endothelial cells (HUVECs) were cultured and underwent oxygen glucose deprivation/reoxygenation (OGD/R) injury for in vitro studies. Relationship between Indobufen and pyroptosis associated NF-κB/Caspase-1/GSDMD pathway was preliminarily discussed. Results: The pharmacodynamic tests revealed that Indobufen ameliorated I/R injury by decreasing the platelet aggregation, infarct size, brain edema and neurologic impairment in rats and rescuing cell apoptosis/pyroptosis in HUVECs. The underlying mechanisms were probably related to pyroptosis suppression by platelet inhibition induced regulation of the NF-κB/Caspase-1/GSDMD pathway.Conclusion: Overall, these studies indicates that Indobufen exerts protective and therapeutic effects against I/R injury by pyroptosis suppression via downregulating NF-κB/Caspase-1/GSDMD pathway.

show abstract

“…The reduction of I/R injury and the improvement of motor, memory and learning abilities are all closely related to the reduction of brain cell injury and death by Indobufen. Recently, more and more studies have shown that cell pyroptosis, also known as in ammatory death, can be caused by cerebral ischemia-reperfusion injury [23]. A hallmark of pyroptosis is GSDMD-NT-dependent membrane rupture due to Caspase-1 activation, which, unlike apoptosis, allows the release of intracellular pathogens such as pro-in ammatory mediators (e.g., IL-1β and IL-18) [24].…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of Indobufen against pyroptosis following cerebral ischemia-reperfusion injury both in vivo and in vitro

Zhang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Indobufen is a new generation of antiplatelet agents and has been shown to have antithrombotic effects in animal models. However, the efficacy of Indobufen on cerebral ischemia/reperfusion (I/R) injury and its mechanisms remain to be investigated. Methods: In this study, the efficacy of Indobufen with both pre- and post-treatment on rats suffering middle cerebral artery occlusion/reperfusion (MCAO/R) was investigated. Furthermore, human umbilical vein endothelial cells (HUVECs) were cultured and underwent oxygen glucose deprivation/reoxygenation (OGD/R) injury for in vitro studies. Relationship between Indobufen and pyroptosis associated NF-κB/Caspase-1/GSDMD pathway was preliminarily discussed. Results: The pharmacodynamic tests revealed that Indobufen ameliorated I/R injury by decreasing the platelet aggregation, infarct size, brain edema and neurologic impairment in rats and rescuing cell apoptosis/pyroptosis in HUVECs. The underlying mechanisms were probably related to pyroptosis suppression by regulating the NF-κB/Caspase-1/GSDMD pathway. Conclusion: Overall, these studies indicates that Indobufen exerts protective and therapeutic effects against I/R injury by pyroptosis suppression via downregulating NF-κB/Caspase-1/GSDMD pathway.

show abstract

The Possibility and Molecular Mechanisms of Cell Pyroptosis After Cerebral Ischemia

Cited by 57 publications

References 61 publications

Neuroprotective effect of Indobufen against pyroptosis following cerebral ischemia-reperfusion injury both in vivo and in vitro

Neuroprotective effect of Indobufen against pyroptosis following cerebral ischemia-reperfusion injury both in vivo and in vitro

Neuroprotective effect of Indobufen against pyroptosis following cerebral ischemia-reperfusion injury both in vivo and in vitro

Neuroprotective effect of Indobufen against pyroptosis following cerebral ischemia-reperfusion injury both in vivo and in vitro

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