Quantitative iTRAQ-based proteomic analysis of piperine protected cerebral ischemia/reperfusion injury in rat brain

Zou, Yichun; Gong, Pian; Zhao, Wenyuan; Zhang, Jianjian; Wu, Xiaolin; Xin, Can; Xiong, Zhili; Wu, Xiaohui; Wan, Qi; Li, Xiang; Chen, Jincao

doi:10.1016/j.neuint.2018.12.010

Cited by 23 publications

(14 citation statements)

References 46 publications

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“…Interestingly, the latest study has indicated that PIP exerts pivotal effects on the pathological process of I/R as well 20,21 . For instance, in a rat model of cerebral I/R injury, Zou et al 32 uncovered that PIP pre‐treatment protected neurocytes from I/R damages by regulating complement and coagulation cascades. Vaibhav et al 33 found that PIP administration was able to salvage ischaemic penumbral zone neurons by virtue of its anti‐inflammatory property.…”

Section: Discussionmentioning

confidence: 99%

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Piperine protects against pyroptosis in myocardial ischaemia/reperfusion injury by regulating the miR‐383/RP105/AKT signalling pathway

Guo

Huang

Liu

et al. 2020

J Cellular Molecular Medi

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Section: Discussionmentioning

confidence: 99%

“…13 Interestingly, the latest study has indicated that PIP exerts pivotal effects on the pathological process of I/R as well. 20,21 For instance, in a rat model of cerebral I/R injury, Zou et al 32 Timely and effectively reperfusion acts as most efficacious remedy for AMI. 4,6 However, accompanying MIRI largely offset this beneficial effect.…”

Section: Discussionmentioning

confidence: 99%

Piperine protects against pyroptosis in myocardial ischaemia/reperfusion injury by regulating the miR‐383/RP105/AKT signalling pathway

Guo

Huang

Liu

et al. 2020

J Cellular Molecular Medi

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“…The cerebral infarct volume was evaluated by 2% 2, 3, 5-triphenyltetrazolium chloride (TTC, Sigma, St. Louis, MO, USA; dissolved in phosphate buffer saline) [33,34] staining. Rats were anesthetized by 5% iso urane 24 h after the MCAO surgery, and brains were collected quickly.…”

Section: Triphenyltetrazolium Chloride (Ttc) Stainingmentioning

confidence: 99%

The Neuroprotective Effects of Insulin-Like Growth Factor 1 via the Hippo/YAP Signaling Pathway is Mediated by the PI3K/AKT Pathway Following Cerebral Ischemia-Reperfusion Injury

Gong

Zou

Zhang

et al. 2021

Preprint

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Insulin-like growth factor 1 (IGF-1) exhibits neuroprotective properties, such as vasodilatory and anti-inflammatory effects following ischemic stroke. However, the specific molecular mechanisms of action of IGF-1 following ischemic stroke remain elusive. We wanted to explore whether IGF-1 regulates Hippo/YAP signaling pathway, potentially via activation of the PI3K/AKT signaling pathway to exert its neuroprotective effects following ischemic stroke. In the in vitro study, we used oxygen–glucose deprivation to injure cultured PC12 and SH-5YSY cells, and cortical primary neurons. Cell viability was measured using CCK-8 assay. For the in vivo analyses, Sprague–Dawley rats were subjected to middle cerebral artery occlusion; neurological function was assessed using the neurological deficit score; infarct volume was measured using triphenyltetrazolium chloride staining, and neuronal death and apoptosis was evaluated by TUNEL staining, H&E staining and Nissl staining. Western blot was used to measure the levels of YAP/TAZ, PI3K and phosphorylated AKT (p-AKT) both in vitro and in vivo. We found that IGF-1 induced activation of YAP/TAZ, which resulted in improved cell viability in vitro, and decreased neurological deficits, neuronal death and apoptosis, and cerebral infarct volume in vivo. Notably, the neuroprotective effects of IGF-1 were reversed by an inhibitor of the PI3K/AKT signaling pathway, LY294002, which not only reduced expressions of PI3K and p-AKT, but also down-regulated expression of YAP/TAZ, leading to aggravation of neurological dysfunction. These findings indicate that neuroprotective effect of IGF-1 is partly realized by up-regulation of YAP/TAZ, which is mediated by activation of the PI3K/AKT signaling pathway following cerebral ischemic stroke.

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“…In a case-control study, FGG was associated with a reduced risk of ischemic stroke [13]. FGG was also highly expressed in the ischemic penumbra of focal cerebral ischemia rats [14]. Trefoil factor 2 was upregulated in the plasma of atrial brillation patients with ischemic stroke [15].…”

Section: Prm Validation and Analysis Of Differentially Abundant Proteinsmentioning

confidence: 99%

Urinary Proteome Changes in Global Cerebral Ischemia-Reperfusion Injury Rat Model Using Proteomics

Sun

Wang

et al. 2021

Preprint

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Background Cerebral ischemia-reperfusion (I/R) injury is the leading cause of death in severe hypotension caused by cardiac arrest, drowning, and excessive blood loss. Urine can sensitively reflect pathophysiological changes in the brain even at an early stage. Methods In this study, a rat model of global cerebral I/R injury was established via Pulsinelli’s four-vessel occlusion (4-VO) method. The proteomics techniques of data-independent acquisition (DIA) and parallel reaction monitoring (PRM) were applied to profile the urinary proteome. The differentially expressed proteins were subjected to Gene Ontology (GO) and protein-protein interaction (PPI) analysis. Results One hundred and sixty-four proteins significantly differed in the 4-VO rat urine samples compared to the control samples (1.5-fold change, p<0.05). GO analysis showed that the acute-phase response, the ERK1 and ERK2 cascade, endopeptidase activity, blood coagulation, and angiogenesis were overrepresented. After PRM validation, fifteen differentially expressed proteins were identified, and their expression was consistent with the DIA quantification. The abundance of FGG, COMP, TFF2, and HG2A was significantly changed only at 12 h after I/R injury. APOE, FAIM3, FZD1, IL1R2, UROK and CD48 were upregulated only at 48 h after I/R injury. KNG1, CATZ, PTGDS, PRVA and HEPC showed an overall trend of upregulation or downregulation at 12 and 48 h after I/R injury, reflecting the progression of cerebral I/R injury. Conclusion In this study, fifteen differentially expressed urinary proteins were identified and validated in a 4-VO rat model. Eight of these proteins were reported to be associated with cerebral I/R injury. These findings provide important clues to inform the monitoring of cerebral I/R injury and further the current understanding of its molecular biological mechanisms.

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Quantitative iTRAQ-based proteomic analysis of piperine protected cerebral ischemia/reperfusion injury in rat brain

Cited by 23 publications

References 46 publications

Piperine protects against pyroptosis in myocardial ischaemia/reperfusion injury by regulating the miR‐383/RP105/AKT signalling pathway

Piperine protects against pyroptosis in myocardial ischaemia/reperfusion injury by regulating the miR‐383/RP105/AKT signalling pathway

The Neuroprotective Effects of Insulin-Like Growth Factor 1 via the Hippo/YAP Signaling Pathway is Mediated by the PI3K/AKT Pathway Following Cerebral Ischemia-Reperfusion Injury

Urinary Proteome Changes in Global Cerebral Ischemia-Reperfusion Injury Rat Model Using Proteomics

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