ArticleMolecular neurobiology2017
Upregulating the Expression of Survivin-HBXIP Complex Contributes to the Protective Role of IMM-H004 in Transient Global Cerebral Ischemia/Reperfusion.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
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- Gastrodin: a potential natural product for the prevention and treatment of cerebral ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Upregulated miR‑378a‑3p expression suppresses energy metabolism and promotes apoptosis by targeting a GLUT‑1/ALDOA/PKM2 axis in esophageal carcinoma.Oncology letters · 2023Article
- Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2023Review
- Over-expression of survivin could prevent the oxidative stress and toxicity of rotenone in SH-SY5Y cells.Iranian journal of basic medical sciences · 2022Article
- Role of Forkhead Box Protein O1 (FoxO1) in Stroke: A Literature Review.Aging and disease · 2022Review
- Pelargonidin ameliorates MCAO-induced cerebral ischemia/reperfusion injury in rats by the action on the Nrf2/HO-1 pathway.Translational neuroscience · 2021Article
- Effects of ginsenoside Rb1 on spinal cord ischemia-reperfusion injury in rats.Journal of orthopaedic surgery and research · 2019Article
- Neuroprotection of hydroxysafflor yellow A in experimental cerebral ischemia/reperfusion injury via metabolic inhibition of phenylalanine and mitochondrial biogenesis.Molecular medicine reports · 2019Article
- Low‑dose lipopolysaccharide inhibits neuronal apoptosis induced by cerebral ischemia/reperfusion injury via the PI3K/Akt/FoxO1 signaling pathway in rats.Molecular medicine reports · 2019Article
- Metabolism of IMM-H004 and Its Pharmacokinetic-Pharmacodynamic Analysis in Cerebral Ischemia/Reperfusion Injured Rats.Frontiers in pharmacology · 2019Article
- Ginsenoside Rg1 protects against ischemic/reperfusion-induced neuronal injury through miR-144/Nrf2/ARE pathway.Acta pharmacologica Sinica · 2019Article
- Co-Administration of Progesterone and Melatonin Attenuates Ischemia-Induced Hippocampal Damage in Rats.Journal of molecular neuroscience : MN · 2018Article
- BIRC5 is a novel target of peroxisome proliferator‑activated receptor γ in brain microvascular endothelium cells during cerebral ischemia.Molecular medicine reports · 2017Article
- Inflammatory factor TNF-α promotes the growth of breast cancer via the positive feedback loop of TNFR1/NF-κB (and/or p38)/p-STAT3/HBXIP/TNFR1.Oncotarget · 2017Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IMM-H004, a 3-piperazinylcoumarin compound derived from coumarin, has been proved effective against CA1 cell loss and spatial learning impairments resulting from transient global ischemia/reperfusion (TGCI/R), while the mechanism is still largely unknown. Here, we confirmed that treatment of rats with IMM-H004 immediately after TGCI/R ameliorated delayed neuronal death (DND) in the CA1 of hippocampus and cortex. Further study suggested that IMM-H004 contributed to the expression of antiapoptotic protein survivin through the activation of PI3K-dependent protein kinase B (PKB/Akt), which led to the phosphorylation of forkhead box O1 (FoxO1), then relieved the inhibiting effect on survivin promoter. Additionally, IMM-H004 also enhanced the expression of hepatitis B X-interacting protein (HBXIP), which formed a complex with survivin to prevent the activation of caspase death cascade, thereby halting apoptotic cell death. Finally, we injected a HBXIP siRNA into hippocampus and performed microelectroporation before ischemia/reperfusion, which abolished the protective effect of IMM-H004. Further study revealed that HBXIP maintained the high expression of Akt and survivin. Collectively, our findings demonstrated that DND after TGCI/R was alleviated by IMM-H004 through promoting the formation of survivin-HBXIP complex, which further emphasized the importance of endogenous protein involved in self-repair after stroke.
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