ArticlePloS one2013
The neuroprotective effects of intramuscular insulin-like growth factor-I treatment in brain ischemic rats.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Intranasal Administration of Insulin and IGF-1 Protects Hippocampal CA1 Neurons Against Transient Global Forebrain Ischemia by Inhibiting Autophagy, Apoptosis and Neuroinflammation: A Comparative Study.International journal of molecular sciences · 2026Article
- Protective effects of early low-intensity exercise on the antigravity soleus muscle following focal cerebral infarction in rats.Frontiers in rehabilitation sciences · 2026Article
- Meteorin-like facilitates skeletal muscle repair through a Stat3/IGF-1 mechanism.Nature metabolism · 2020Article
- Combined network pharmacology and virtual reverse pharmacology approaches for identification of potential targets to treat vascular dementia.Scientific reports · 2020Article
- The Role of Insulin-Like Growth Factors and Insulin-Like Growth Factor-Binding Proteins in the Nervous System.Biochemistry insights · 2019Review
- Involvement of GSK-3β Phosphorylation Through PI3-K/Akt in Cerebral Ischemia-Induced Neurogenesis in Rats.Molecular neurobiology · 2017Article
- Specific titin and myomesin domains stimulate myoblast proliferation.Biochemistry and biophysics reports · 2017Article
- IGF-1-Involved Negative Feedback of NR2B NMDA Subunits Protects Cultured Hippocampal Neurons Against NMDA-Induced Excitotoxicity.Molecular neurobiology · 2017Article
- Growth factors for the treatment of ischemic brain injury (growth factor treatment).Brain sciences · 2015Review
- Activation of IGF-1 and insulin signaling pathways ameliorate mitochondrial function and energy metabolism in Huntington's Disease human lymphoblasts.Molecular neurobiology · 2015Article
- Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia.Neural plasticity · 2015Article
- IGF-1 Protects Neurons in the Cortex and Subventricular Zone in a Periventricular Leucomalacia Model.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain ischemia leads to muscle inactivity-induced atrophy and may exacerbate motor function deficits. Intramuscular insulin-like growth factor I (IGF-I) injection has been shown to alleviate the brain ischemia-induced muscle atrophy and thus improve the motor function. Motor function is normally gauged by the integrity and coordination of the central nervous system and peripheral muscles. Whether brain ischemic regions are adaptively changed by the intramuscular IGF-I injection is not well understood. In this study, the effect of intramuscular IGF-I injection was examined on the central nervous system of brain ischemic rats. Rats were divided into 4 groups: sham control, brain ischemia control, brain ischemia with IGF-I treatment, and brain ischemia with IGF-I plus IGF-I receptor inhibitor treatment. Brain ischemia was induced by right middle cerebral artery occlusion. IGF-I and an IGF-1 receptor inhibitor were injected into the affected calf and anterior tibialis muscles of the treated rats for 4 times. There was an interval of 2 days between each injection. Motor function was examined and measured at the 24 hours and 7 days following a brain ischemia. The affected hind-limb muscles, sciatic nerve, lumbar spinal cord, and motor cortex were collected for examination after euthanizing the rats. IGF-I expression in the central nervous system and affected muscles were significantly decreased after brain ischemia. Intramuscular IGF-I injection increased the IGF-I expression in the affected muscles, sciatic nerve, lumbar spinal cord, and motor cortex. It also increased the p-Akt expression in the affected motor cortex. Furthermore, intramuscular IGF-I injection decreased the neuronal apoptosis and improved the motor function. However, co-administration of the IGF-I receptor inhibitor eliminated these effects. Intramuscular IGF-I injection after brain ischemia attenuated or reversed the decrease of IGF-I in both central and peripheral tissues, and these effects could contribute to neuroprotection and improve motor function.
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