ArticleExperimental and therapeutic medicine2021
TIMP3 attenuates cerebral ischemia/reperfusion-induced apoptosis and oxidative stress in neurocytes by regulating the AKT pathway.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 13 citations in OpenAlex.
- Cationic microbubble loading hSIRT3 and hTIMP3 optimize cardiac-targeted delivery and myocardial protection in the porcine MI/R model.Materials today. Bio · 2025Article
- Proteomic analysis of Biliverdin protected cerebral ischemia-reperfusion injury in rats.Scientific reports · 2023Article
- Laser speckle contrast imaging for blood flow monitoring in predicting outcomes after cerebral ischemia-reperfusion injury in mice.BMC neuroscience · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Ischemic stroke seriously threatens human health and creates a large social burden. The present study investigated whether tissue inhibitor of metalloproteinases-3 (TIMP3) prevented cerebral ischemia/reperfusion (I/R), with the aim to explore the underlying mechanism. A transient middle cerebral artery occlusion model was conducted in mice, and oxygen glucose deprivation and reoxygenation (OGD/R) was investigated in PC12 cells to mimic cerebral ischemia-reperfusion injury (CIRI). Western blotting was used to determine the expression of TIMP3, Bax, Bcl-2 and AKT. TUNEL was used to detect apoptosis in cerebral tissues or cultured PC12 cells. Expression levels of reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) were detected to reveal oxidative stress. The results demonstrated that TIMP3 expression was significantly decreased after I/R
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