Antiapoptotic effect of gangliosides on PC12 cells exposed to bacterial lipopolysaccharide

Bayunova, L. V.; Парнова, Р. Г.; Аврова, Н. Ф.

doi:10.1134/s0022093015020027

Cited by 1 publication

(1 citation statement)

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“…These cells can release neurotransmitters and exhibit properties similar to neurons, providing a model to study neuronal pharmacology. In line with references (Ye et al, 2013;Bayunova et al, 2015), we conducted experiments on a PC12 cell model of LPS-induced injury to study infection in the central nervous system (Mao et al, 2011). MTT results indicated that the injury was concentration-dependent.…”

Section: Discussionmentioning

confidence: 99%

NF-κB in mitochondria regulates PC12 cell apoptosis following lipopolysaccharide-induced injury

Song

Ding

et al. 2018

J. Zhejiang Univ. Sci. B

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Objective: To determine the relationship between nuclear transcription factor κB (NF-κB) expression in mitochondria and neuronal cell apoptosis after lipopolysaccharide (LPS)-induced injury. Methods: The effect of drug administration on PC12 cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and Hoechst 33342 staining. The morphology and function of mitochondria were investigated with electron microscopy and rhodamine 123, respectively. The activity of adenine nucleotide translocase 1 (ANT1), lipid peroxide, and antiperoxidase enzymes was measured by enzyme-linked immunosorbent assay (ELISA). Relative expression levels of NF-κB were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Results: Pyrrolidine dithiocarbamate (PDTC, an NF-κB inhibitor) and nerve growth factor (NGF) not only reduced apoptosis but also had a protective effect on mitochondrial structure and function in a PC12 cell LPS damage model. The subcellular distribution of NF-κB demonstrated that NGF, diterpene acid atractyloside (ATR, an ANT1 antagonist), and PDTC alleviated increases in mitochondrial NF-κB after LPS-induced injury. Conclusions: (1) NF-κB is activated in mitochondria via uptake of ANT1 during apoptosis following LPS-induced injury in neuronal cells; (2) NGF not only decreases the activity of NF-κB but also reduces ANT1 activity, which in turn decreases NF-κB levels in mitochondria and suppresses mitochondria-mediated apoptosis.

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Section: Discussionmentioning

confidence: 99%