ArticleDrug design, development and therapy2020
Experimental Study on the Role of Apelin-13 in Alleviating Spinal Cord Ischemia Reperfusion Injury Through Suppressing Autophagy.
Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- The Fidelity Paradox in Spinal Cord Injury: Reframing Biomechanical Mimicry and Neurobiological Relevance for Clinical Translation.CNS neuroscience & therapeutics · 2026Review
- Apelin-13 confers Neuropeptide Y-mediated neuroprotection and preserves learning and allocentric memory in D-glutamic acid-induced excitotoxicity in rats.Molecular neurobiology · 2026Article
- Associations of FGF23 and Apelin-13 with osteoporosis and diabetic peripheral neuropathy in postmenopausal women with type 2 diabetes mellitus.Frontiers in medicine · 2026Article
- Differential effects of apelin-13 on lipid peroxidation and DNA oxidation in doxorubicin-treated rats: A preliminary study.Biomolecules & biomedicine · 2025Article
- Upregulated miR-125b mitigates inflammation, astrocyte activation, and dysfunction of spinal cord injury by inactivating the MAPK pathway.Histology and histopathology · 2024Article
- The Yin and Yang Effect of the Apelinergic System in Oxidative Stress.International journal of molecular sciences · 2023Review
- Crosstalk between exosomes and autophagy in spinal cord injury: fresh positive target for therapeutic application.Cell and tissue research · 2023Review
- Astaxanthin Modulates Autophagy, Apoptosis, and Neuronal Oxidative Stress in a Rat Model of Compression Spinal Cord Injury.Neurochemical research · 2022Article
- Apelin alleviated neuroinflammation and promoted endogenous neural stem cell proliferation and differentiation after spinal cord injury in rats.Journal of neuroinflammation · 2022Article
- Identification of the biological function of miR-9 in spinal cord ischemia-reperfusion injury in rats.PeerJ · 2021Article
- Preliminary study on a novel biological scaffold loaded with ApelinZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciencesArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aimed to explore the effect of Apelin-13 in protecting rats against spinal cord ischemia reperfusion injury (SCIR), as well as the related molecular mechanisms.
methodsOne week prior to the experiment, experimental Sprague-Dawley rats were injected with Apelin-13 and the autophagy activator rapamycin through the tail vein once a day for 7 consecutive days. The SCIR rat model was prepared through the abdominal aorta clamping method. At 72 h after injury, the spinal cord tissue water content, infarct volume, and normal neuron count were determined to evaluate the degree of spinal cord tissue injury in the rats. The Basso-Beattie-Bresnahan scoring standard was adopted for functional scoring of the rat hind leg, to reflect the post-injury motor function. At 72 h after injury, changes in mitochondrial membrane potential, reactive oxygen species content, and mitochondrial ATP were detected. ELISA was carried out to detect the malonaldehyde content, as well as catalase, superoxide dismutase, and glutathione catalase activities in spinal cord tissues at 72 h after injury. Quantitative chemistry was conducted to examine the contents of nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) in spinal cord tissues. Finally, the expression of autophagy-related proteins, Beclin1, ATG5, and LC3, in spinal cord tissues was detected through the Western blotting assay.
resultsApelin-13 pretreatment alleviated SCIR, promoted motor function recovery, suppressed mitochondrial dysfunction, resisted oxidative stress, and inhibited autophagy in spinal cord tissues following ischemia reperfusion injury.
conclusionApelin-3 exerts protection against SCIR by suppressing autophagy.
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