Mechanisms of CDDO-imidazolide-mediated cytoprotection against acrolein-induced neurocytotoxicity in SH-SY5Y cells and primary human astrocytes

Speen, Adam M.; Jones, Colton; Patel, Ruby; Shah, Halley; Nallasamy, Palanisamy; Brooke, Elizabeth A.S.; Zhu, Hong; Li, Y. Robert; Jia, Zhenquan

doi:10.1016/j.toxlet.2015.07.005

Cited by 17 publications

(7 citation statements)

References 64 publications

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“…These results agree well with published data demonstrated that cyano-enone-bearing triterpenoids (CETs), including SM’s position isomer CDDO-Me, CDDO-Im, NZ, dh404, and SO1989, effectively inhibit the release of NO and iNOS expression in LPS/IFNγ-activated RAW264.7 cells [ 103 , 104 , 105 , 106 , 107 , 108 , 109 ] and LPS-challenged primary peritoneal macrophages [ 110 ], decreased the production of ROS, and activated the expression of HO-1 in unstimulated [ 105 , 107 ], LPS-stimulated, and tert-butyl hydroperoxide-stimulated RAW264.7 cells [ 106 , 107 , 108 , 109 ] as well as LPS-induced neutrophils [ 111 , 112 ]. Moreover, CDDO-Me and CDDO-MA were found to increase the production of GSH in human primary astrocytes [ 113 ] and block 3-NP neurotoxin-induced striatal GSH depletion in rats, respectively [ 114 ].…”

Section: Discussionmentioning

confidence: 99%

Dual Effect of Soloxolone Methyl on LPS-Induced Inflammation In Vitro and In Vivo

Markov

Sen’kova

Babich

et al. 2020

IJMS

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Plant-extracted triterpenoids belong to a class of bioactive compounds with pleotropic functions, including antioxidant, anti-cancer, and anti-inflammatory effects. In this work, we investigated the anti-inflammatory and anti-oxidative activities of a semisynthetic derivative of 18βH-glycyrrhetinic acid (18βH-GA), soloxolone methyl (methyl 2-cyano-3,12-dioxo-18βH-olean-9(11),1(2)-dien-30-oate, or SM) in vitro on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and in vivo in models of acute inflammation: LPS-induced endotoxemia and carrageenan-induced peritonitis. SM used at non-cytotoxic concentrations was found to attenuate the production of reactive oxygen species and nitric oxide (II) and increase the level of reduced glutathione production by LPS-stimulated RAW264.7 cells. Moreover, SM strongly suppressed the phagocytic and migration activity of activated macrophages. These effects were found to be associated with the stimulation of heme oxigenase-1 (HO-1) expression, as well as with the inhibition of nuclear factor-κB (NF-κB) and Akt phosphorylation. Surprisingly, it was found that SM significantly enhanced LPS-induced expression of the pro-inflammatory cytokines interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in RAW264.7 cells via activation of the c-Jun/Toll-like receptor 4 (TLR4) signaling axis. In vivo pre-exposure treatment with SM effectively inhibited the development of carrageenan-induced acute inflammation in the peritoneal cavity, but it did not improve LPS-induced inflammation in the endotoxemia model.

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Section: Discussionmentioning

confidence: 99%

Dual Effect of Soloxolone Methyl on LPS-Induced Inflammation In Vitro and In Vivo

Markov

Sen’kova

Babich

et al. 2020

IJMS

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“…The selection of tolfenamic acid/Nrf2 siRNA/ML385/BSO/3-NP doses and action times were based on the studies by Adwan et al, Huang et al, Zhang et al, Kulasekaran and Ganapasam, Jiang et al, and Speen et al [15–20] and our preliminary experiments.…”

Section: Methodsmentioning

confidence: 99%

Prevention of Huntington’s Disease-Like Behavioral Deficits in R6/1 Mouse by Tolfenamic Acid Is Associated with Decreases in Mutant Huntingtin and Oxidative Stress

Liu

Yang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Tolfenamic acid is a nonsteroidal anti-inflammatory drug with neuroprotective properties, and it alleviates learning and memory deficits in the APP transgenic mouse model of Alzheimer’s disease. However, whether tolfenamic acid can prevent motor and memory dysfunction in transgenic animal models of Huntington’s disease (HD) remains unclear. To this end, tolfenamic acid was orally administered to transgenic R6/1 mice from 10 to 20 weeks of age, followed by several behavioral tests to evaluate motor and memory function. Tolfenamic acid improved motor coordination in R6/1 mice as tested by rotarod, grip strength, and locomotor behavior tests and attenuated memory dysfunction as analyzed using the novel object recognition test and passive avoidance test. Tolfenamic acid decreased the expression of mutant huntingtin in the striatum of 20-week-old R6/1 mice by inhibiting specificity protein 1 expression and enhancing autophagic function. Furthermore, tolfenamic acid exhibited antioxidant effects in both R6/1 mice and PC12 cell models. Collectively, these results suggest that tolfenamic acid has a good therapeutic effect on R6/1 mice, and may be a potentially useful agent in the treatment of HD.

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“…This cell line was selected as an in vitro model because it was commonly used to study neurotoxicology of many toxicants, including METH (Huang et al, 2015; Speen et al, 2015). SH-SY5Y cells were cultured in DMEM/F12 (1:1) containing fetal bovine serum (Gibco, Grand Island, NY, USA).…”

Section: Methodsmentioning

confidence: 99%

SUMOylation of Alpha-Synuclein Influences on Alpha-Synuclein Aggregation Induced by Methamphetamine

Zhu

Qiao

Chen

et al. 2018

Front. Cell. Neurosci.

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Methamphetamine (METH) is an illegal and widely abused psychoactive stimulant. METH abusers are at high risk of neurodegenerative disorders, including Parkinson’s disease (PD). Previous studies have demonstrated that METH causes alpha-synuclein (α-syn) aggregation in the both laboratory animal and human. In this study, exposure to high METH doses increased the expression of α-syn and the small ubiquitin-related modifier 1 (SUMO-1). Therefore, we hypothesized that SUMOylation of α-syn is involved in high-dose METH-induced α-syn aggregation. We measured the levels of α-syn SUMOylation and these enzymes involved in the SUMOylation cycle in SH-SY5Y human neuroblastoma cells (SH-SY5Y cells), in cultures of C57 BL/6 primary mouse neurons and in brain tissues of mice exposure to METH. We also demonstrated the effect of α-syn SUMOylation on α-syn aggregation after METH exposure by overexpressing the key enzyme of the SUMOylation cycle or silencing SUMO-1 expression in vitro. Then, we make introduced mutations in the major SUMOylation acceptor sites of α-syn by transfecting a lentivirus containing the sequence of WT α-syn or K96/102R α-syn into SH-SY5Y cells and injecting an adenovirus containing the sequence of WT α-syn or K96/102R α-syn into the mouse striatum. Levels of the ubiquitin-proteasome system (UPS)-related makers ubiquitin (Ub) and UbE1, as well as the autophagy-lysosome pathway (ALP)-related markers LC3, P62 and lysosomal associated membrane protein 2A (LAMP2A), were also measured in SH-SY5Y cells transfected with lentivirus and mice injected with adenovirus. The results showed that METH exposure decreases the SUMOylation level of α-syn, although the expression of α-syn and SUMO-1 are increased. One possible cause is the reduction of UBC9 level. The increase in α-syn SUMOylation by UBC9 overexpression relieves METH-induced α-syn overexpression and aggregation, whereas the decrease in α-syn SUMOylation by SUMO-1 silencing exacerbates the same pathology. Furthermore, mutations in the major SUMOylation acceptor sites of α-syn also aggravate α-syn overexpression and aggregation by impairing degradation through the UPS and the ALP in vitro and in vivo. These results suggest that SUMOylation of α-syn plays a fundamental part in α-syn overexpression and aggregation induced by METH and could be a suitable target for the treatment of neurodegenerative diseases.

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Mechanisms of CDDO-imidazolide-mediated cytoprotection against acrolein-induced neurocytotoxicity in SH-SY5Y cells and primary human astrocytes

Cited by 17 publications

References 64 publications

Dual Effect of Soloxolone Methyl on LPS-Induced Inflammation In Vitro and In Vivo

Dual Effect of Soloxolone Methyl on LPS-Induced Inflammation In Vitro and In Vivo

Prevention of Huntington’s Disease-Like Behavioral Deficits in R6/1 Mouse by Tolfenamic Acid Is Associated with Decreases in Mutant Huntingtin and Oxidative Stress

SUMOylation of Alpha-Synuclein Influences on Alpha-Synuclein Aggregation Induced by Methamphetamine

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