ArticleNeurochemical research2019
TGF-β2/Smad3 Signaling Pathway Activation Through Enhancing VEGF and CD34 Ameliorates Cerebral Ischemia/Reperfusion Injury After Isoflurane Post-conditioning in Rats.
Article in Neurochemical research, 2019. 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, 27 citations in OpenAlex.
- Sevoflurane ameliorates cerebral ischemia-reperfusion injury by modulating mitochondrial dynamics and attenuating apoptosis via Shh-YAP1 signaling pathway.Molecular brain · 2026Article
- Isoflurane Enhances Autophagy by Activating AMPK/ULK1, Inhibits NLRP3, and Reduces Cognitive Impairment After Cerebral Ischemia-Reperfusion Injury in Rats.Journal of molecular neuroscience : MN · 2023Article
- Gli2-induced lncRNA Peg13 alleviates cerebral ischemia-reperfusion injury by suppressing Yy1 transcription in a PRC2 complex-dependent manner.Metabolic brain disease · 2023Article
- Circular RNAs in organ injury: recent development.Journal of translational medicine · 2022Review
- Effect of Metformin on Myocardial Injury Induced by Hepatic Ischemia-Reperfusion in Rats.Frontiers in pharmacology · 2022Article
- Protective Effects of Remimazolam on Cerebral Ischemia/Reperfusion Injury in Rats by Inhibiting of NLRP3 Inflammasome-Dependent Pyroptosis.Drug design, development and therapy · 2022Article
- 1α,25-Dihydroxyvitamin D3 Promotes Angiogenesis After Cerebral Ischemia Injury in Rats by Upregulating the TGF-β/Smad2/3 Signaling Pathway.Frontiers in cardiovascular medicine · 2022Article
- miRNA Involvement in Cerebral Ischemia-Reperfusion Injury.Frontiers in neuroscience · 2022Review
- Cryptotanshinone possesses therapeutic effects on ischaemic stroke through regulating STAT5 in a rat model.Pharmaceutical biology · 2021Article
- Isoflurane upregulates microRNA-9-3p to protect rats from hepatic ischemia-reperfusion injury through inhibiting fibronectin type III domain containing 3B.Cell cycle (Georgetown, Tex.) · 2021Article
- Article
- Punicalin Alleviates OGD/R-Triggered Cell Injury via TGF-Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Overexpression of circRNA circUCK2 Attenuates Cell Apoptosis in Cerebral Ischemia-Reperfusion Injury via miR-125b-5p/GDF11 Signaling.Molecular therapy. Nucleic acids · 2020Article
- microRNA-195 attenuates neuronal apoptosis in rats with ischemic stroke through inhibiting KLF5-mediated activation of the JNK signaling pathway.Molecular medicine (Cambridge, Mass.) · 2020Article
- Intrauterine Injection of Umbilical Cord Mesenchymal Stem Cell Exosome Gel Significantly Improves the Pregnancy Rate in Thin Endometrium Rats.Cell transplantationArticle
- Current research progress of isoflurane in cerebral ischemia/reperfusion injury: a narrative review.Medical gas researchReview
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Evidence has shown the therapeutic potential of isoflurane (ISO) in cerebral stroke. The present study investigated the mechanism of ISO on vascular endothelial growth factor (VEGF) and CD34 expression in a rat model of stroke. Transient focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion for 24 h in rats. ISO was administered for 1.5 h when the reperfusion was initiated. Neurologic deficit scores, infarct volumes, HE staining, Nissl staining, and TUNEL staining were evaluated at 24 h after reperfusion. The levels of transforming growth factor (TGF)-β2, Smad3, p-Smad3, VEGF, and CD34 proteins were detected by immunofluorescence (IF) staining and Western blot assay. Administration of ISO significantly reduced the neurologic deficit scores, infarct volumes, and damaged and apoptotic cells after cerebral ischemia/reperfusion (I/R) injury (P < 0.05). Meanwhile, ISO post-conditioning significantly increased the expression levels of TGF-β2, p-Smad3, VEGF, and CD34 (P < 0.05), whereas the expression of Smad3 showed no difference (P > 0.05). However, Pirfenidone, a TGF-β2 inhibitor, decreased the expression levels of TGF-β2, p-Smad3, VEGF, and CD34 (P < 0.05). Moreover, the protective effects of ISO post-conditioning were negated by the inhibitor. The present study indicated that ISO attenuates brain damage by activating the TGF-β2/Smad3 signaling pathway and increasing the protein expression of VEGF and CD34 in the rat MCAO model.
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