ArticleWorld journal of emergency medicine2013
Effect of β-sodium aescinate on hypoxia-inducible factor-1α expression in rat brain cortex after cardiopulmonary resuscitation.
Article in World journal of emergency medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Neuroprotective effects of arctigenin on cerebral ischemia-reperfusion injury in rats via the EPO/EPOR-JAK2-STAT5 signaling pathway.Frontiers in pharmacology · 2025Article
- Sodium aescinate and its bioactive components induce degranulation via oxidative stress in RBL-2H3 mast cells.Toxicology research · 2020Article
- Type 2 diabetes mellitus worsens neurological injury following cardiac arrest: an animal experimental study.Intensive care medicine experimental · 2018Article
- Clinical effects of joint application of β-sodium aescinate and mannitol in treating early swelling after upper limb trauma surgery.Experimental and therapeutic medicine · 2016Article
- In Vivo Cardiotoxicity Induced by Sodium Aescinate in Zebrafish Larvae.Molecules (Basel, Switzerland) · 2016Article
- Article
- S100B protein in serum is elevated after global cerebral ischemic injury.World journal of emergency medicine · 2013Review
- Mesenteric infarction due to iatrogenic polycythemia.World journal of emergency medicine · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study was undertaken to investigate the expression of hypoxia-inducible factor-1α (HIF-1α) in rat cerebral cortex and the effects of β-sodium aescinate (SA) administration after return of spontaneous circulation (ROSC).
methodsSIXTY RATS WERE DIVIDED INTO THREE GROUPS: SA group, injected intraperitoneally with SA instantly after ROSC; control group, injected intraperitoneally with normal saline; and sham-operated group, without cardiac arrest or SA. The cardiac arrest model was established using asphyxiation and intravenous potassium chloride. Blood was sampled 1, 6, 12, and 24 hours after ROSC. Protein and mRNA levels of HIF-1α, VEGF and EPO were detected in the cerebral cortex by immunohistochemistry and real-time RT-PCR; serum levels of NSE and S100β were determined by enzyme-linked immunosorbent assays.
resultsSerum S100β and NSE were significantly increased in the control group versus the sham-operated group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were significantly increased in the control rats (P<0.05). Serum NSE and S100β were significantly decreased in the SA group versus the control group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were significantly increased in the SA group (P<0.05).
conclusionsThe expression of HIF-1α is increased in rat cerebral cortex after ROSC, and SA up-regulates the expression of HIF-1α. The up-regulation of HIF-1α improves the resistance of the cortex to ischemia and hypoxia and contributes to neuroprotection, possibly because of up-regulation of EPO and VEGF expression.
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