Literature DB >> 30008063

Lupeol against high-glucose-induced apoptosis via enhancing the anti-oxidative stress in rabbit nucleus pulposus cells.

Ming-Bo Guo1, De-Chun Wang2, Hai-Fei Liu1, Long-Wei Chen1, Jian-Wei Wei1, Yong Lin1, Hui Xue1.   

Abstract

PURPOSE: This study aimed to investigate the potential mechanism and value of lupeol in inhibiting high-glucose-induced apoptosis in rabbit nucleus pulposus cells (NPCs).
METHODS: NPCs were divided into four groups: control (CON), high glucose (HG), LUP, and HG + LUP. Viability, reactive oxygen species (ROS) levels, and apoptosis were examined in NPCs. The protein expression levels of Bax, Bcl-2, cytochrome C, and caspase 9/3 were measured using reverse transcription-polymerase chain reaction and Western blot assay.
RESULTS: The apoptotic rate and total ROS level of the HG group significantly increased compared with the CON group (P < 0.01). The total ROS level in the HG + LUP group significantly decreased compared with the HG group(P < 0.05). The mRNA expression of Bcl-2 was significantly upregulated, whereas the expression of Bax, cytochrome C, and caspase 9/3 was downregulated in the HG + LUP group compared with those in the HG group(P < 0.05).The Western blot assay showed that the expression of Bcl-2 was upregulated, but the expression of Bax, cytochrome C, and caspase 9/3 was significantly downregulated in the HG + LUP group compared with the HG group (P < 0.05).
CONCLUSIONS: Lupeol inhibited high-glucose-induced apoptosis in NPCs by enhancing the anti-oxidative stress in the mitochondria. This study suggested lupeol as a potential therapeutic drug for treating intervertebral disc degeneration under hyperglycaemic conditions. These slides can be retrieved under Electronic Supplementary Material.

Entities:  

Keywords:  Anti-oxidative stress; Apoptosis; Intervertebral disc degeneration; Lupeol; Nucleus pulposus

Mesh:

Substances:

Year:  2018        PMID: 30008063     DOI: 10.1007/s00586-018-5687-9

Source DB:  PubMed          Journal:  Eur Spine J        ISSN: 0940-6719            Impact factor:   3.134


  41 in total

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