ArticleNeurochemical research2014
Neuroprotection of up-regulated carbon monoxide by electrical acupuncture on perinatal hypoxic-ischemic brain damage in rats.
Article in Neurochemical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The Interaction between Carbon Monoxide and Hydrogen Sulfide during Chronic Joint Pain in Young Female Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Interaction among Hydrogen Sulfide and Other Gasotransmitters in Mammalian Physiology and Pathophysiology.Advances in experimental medicine and biology · 2021Review
- CBS-Induced HEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Inhaled Gases for Neuroprotection of Neonates: A Review.Frontiers in pediatrics · 2019Review
- Exploring the Mechanisms of Electroacupuncture-Induced Analgesia through RNA Sequencing of the Periaqueductal Gray.International journal of molecular sciences · 2017Article
- Acupuncture for Children with Cerebral Palsy: A Systematic Review Protocol.JMIR research protocols · 2017Article
- Carbon monoxide treatment reduces microglial activation in the ischemic rat retina.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2016Article
- Carbon monoxide as a promising molecule to promote nerve regeneration after traumatic brain injury.Medical gas researchReview
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the neuroprotection and potential mechanism of carbon monoxide (CO) against perinatal hypoxic-ischemic brain damage in rats by electrical acupuncture (EA). Animal behavior, morphological changes, cystathionine beta-synthase (CBS), hypoxia-inducible factor-1α (HIF-1α), and heme oxygenase-1 (HO-1) expression levels, and CO content in rat cortex cells were determined. Results demonstrated that EA treatment decreased the slope behavior and increased the overhang behavior of perinatal rats. The treatment also decreased the number of positive cells. The activator and inhibitor of CBS aggravated and remitted the hypoxic damage in cortex cells, respectively. EA treatment decreased CBS expression level and increased HO-1 and HIF-1α expression levels in perinatal rat cortex cells. Compared with the control groups, the CO content of cortex cells in the EA treatment group significantly increased (**p < 0.01). We hypothesized that EA treatment increases cortical CO content to protect against hypoxic damage via the hydrogen sulfide/CBS-CO/HO-1-HIF-1α system. This study provided a significant reference for EA therapy and cued a novel protective mechanism for cerebral palsy.
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Registered trials
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