ArticleToxicology research2022
Zoletil promotes apoptosis in BV-2 microglial cells via induction of oxidative stress and neural inflammation.
Article in Toxicology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 1 citations in OpenAlex.
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3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Zoletil® (ZOL) is a combination drug of tiletamine, a dissociative anesthetic and zolazepam, a minor tranquilize, which has been used to induce short-term anesthesia in various animals. Depending on the administered dose, the effects of ZOL can range from sedation to anesthesia. Here, we aimed to determine the neurotoxicity of ZOL and elucidate its mechanism of action using BV-2 microglial cells. The results of MTT reduction assay and TUNEL staining revealed that ZOL induced neuronal toxicity and apoptosis in BV-2 cells. ZOL caused apoptosis via phosphorylation of c-Jun N-terminal kinase, increased ratio of Bax to Bcl-2, disruption of mitochondrial membrane potential, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase. Furthermore, reactive oxygen species were involved in ZOL-induced neuronal cell death as assessed by 2',7'-dichlorofluorescein diacetate staining. Moreover, BV-2 cells treated with ZOL exhibited increased expression of inflammatory enzymes, such as inducible nitric oxide synthase and cyclooxygenase-2, along with subsequent production of nitric oxide and prostaglandin E
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