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- W4236645981 abstract "Abstract Background: The study was aimed to explore the effects and potential mechanisms of Dexmedetomidine (Dex) on hypoxia/reoxygenation (H/R) injury in human renal tubular epithelial HK-2 cells. Methods: Human renal tubular epithelial HK-2 cells were divided into four groups: control group, Dex group, H/R group, and Dex + H/R group. After treatment, cell viability rate and cell apoptosis rate were measured by MTT assay and flow cytometry, respectively. Afterwards, the expressions of Hypoxia-inducible factor 1 (HIF-1α), glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), caspase-12 and cleaved caspase-3 were determined by western blot. Malondialdehyde (MDA) concentration and Superoxide Dismutase (SOD) activity were determined by assay kits. Results: Compared with control group, the cell viability rate was decreased and cell apoptotic was increased in H/R group. Besides, cell viability rate was increased, and cell apoptotic rate of HK-2 cells was decreased in Dex + H/R group, compared with H/R group. Western blot analysis showed that the expression of HIF-1α was up-regulated, and the expressions of GRP78, CHOP, capase-12 and cleaved caspase-3 were down-regulated in Dex + H/R group. In addition, the concentrations of MDA in Dex + H/R group and H/R group were 1.68 ± 0.22 nmol/mgprot and 0.85 ± 0.16 nmol/mgprot, which showed a 49.4% decrease in Dex + H/R group. However, after Dex treatment, the SOD activity was rose to 121 ± 11 U/L, which was more than twice larger than that in H/R group (57 ± 10 U/L). Conclusions: Dex could inhibit cell apoptosis by up-regulating the expression of HIF-1α, reducing endoplasmic reticulum stress and regulating oxidative stress, thus ameliorating the H/R injury." @default.
- W4236645981 created "2022-05-12" @default.
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- W4236645981 date "2019-12-03" @default.
- W4236645981 modified "2023-10-18" @default.
- W4236645981 title "Dexmedetomidine protects human renal tubular epithelial HK-2 cells against hypoxia/reoxygenation injury by inactivating endoplasmic reticulum stress pathway" @default.
- W4236645981 doi "https://doi.org/10.21203/rs.2.17940/v1" @default.
- W4236645981 hasPublicationYear "2019" @default.
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