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Kechun Liu

Researcher at Qilu University of Technology

Publications -  120
Citations -  1640

Kechun Liu is an academic researcher from Qilu University of Technology. The author has contributed to research in topics: Zebrafish & Medicine. The author has an hindex of 16, co-authored 90 publications receiving 743 citations. Previous affiliations of Kechun Liu include Chinese Academy of Sciences.

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Berberine protects against 6-OHDA-induced neurotoxicity in PC12 cells and zebrafish through hormetic mechanisms involving PI3K/AKT/Bcl-2 and Nrf2/HO-1 pathways.

TL;DR: The results demonstrated that BBR induced a typical hormetic response in PC12 cells, and strongly suggested that the neuroprotection of BBR were attributable to the hormetic mechanisms via activating cell survival and antioxidant signaling pathways.
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Mechanism of isoniazid-induced hepatotoxicity in zebrafish larvae: Activation of ROS-mediated ERS, apoptosis and the Nrf2 pathway

TL;DR: INH may act on hepatotoxicity in zebrafish by increasing ROS content, which weakens the antioxidant capacity, leading to ERS, cell apoptosis and liver injury, and the Nrf2 signalling pathway is activated as a stress compensation mechanism during INH-induced liver injury.
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Hormetic effect of panaxatriol saponins confers neuroprotection in PC12 cells and zebrafish through PI3K/AKT/mTOR and AMPK/SIRT1/FOXO3 pathways

TL;DR: Low dose PTS could significantly prevent the 6-OHDA-induced dopaminergic neuron loss and improve the behavior movement deficiency in zebrafish, whereas relative high dose PTS exhibited neural toxicity, further supporting the hormetic and neuroprotective effects of PTS.
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Isoliquiritigenin triggers developmental toxicity and oxidative stress–mediated apoptosis in zebrafish embryos/larvae via Nrf2-HO1/JNK-ERK/mitochondrion pathway

TL;DR: First evidence that demonstrate ISL-induced dose-dependent developmental toxicity in zebrafish embryos is provided, and gene expression patterns in the embryos correlate the above and reveal potential genetic mechanisms of developmental toxicity.
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Toxicity of different zinc oxide nanomaterials and dose-dependent onset and development of Parkinson's disease-like symptoms induced by zinc oxide nanorods.

TL;DR: The results indicated that l-ZnO NRs induced developmental neurotoxicity with hallmarks linked to Parkinson's disease (PD)-like symptoms at relatively high doses, including the disruption of locomotor activity as well as neurodevelopmental and PD responsive genes expression, and the induction of dopaminergic neuronal loss and apoptosis in zebrafish brain.