2017
DOI: 10.1007/s10787-016-0305-0
|View full text |Cite
|
Sign up to set email alerts
|

Implication of Nrf2/HO-1 pathway in the coloprotective effect of coenzyme Q10 against experimentally induced ulcerative colitis

Abstract: Coenzyme Q10 dose-dependently protects against AA-induced UC mainly via modulation of Nrf2/HO-1 and caspase-3 pathways. Antioxidant, anti-inflammatory and anti-apoptotic properties of CoQ10 are implicated in its observed therapeutic benefit.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

2
27
0

Year Published

2017
2017
2023
2023

Publication Types

Select...
8

Relationship

0
8

Authors

Journals

citations
Cited by 42 publications
(29 citation statements)
references
References 46 publications
2
27
0
Order By: Relevance
“…This effect was shown to be triggered by the activation of (ERK1/2)- and JNK signalling and subsequent phosphorylation of Nrf2 in macrophages [ 96 ]. Khodir and co-workers [ 97 ] investigated the coloprotective potential of coenzyme Q10 in a rat model of experimental colitis and documented the Nrf2/HO-1 pathway to be mainly responsible for the suppression of inflammatory marker release and the recovery of the oxidant/antioxidant homeostasis. Additionally, luteolin (3’, 4’, 5, 7-tetrahydroxyflavone) attenuated disease patterns of a DSS-induced colitis in mice and activated Nrf2-dependent gene expression of HO-1 and NQO1 [ 98 ].…”
Section: Protection Against Colitis By Targeting Nrf2mentioning
confidence: 99%
“…This effect was shown to be triggered by the activation of (ERK1/2)- and JNK signalling and subsequent phosphorylation of Nrf2 in macrophages [ 96 ]. Khodir and co-workers [ 97 ] investigated the coloprotective potential of coenzyme Q10 in a rat model of experimental colitis and documented the Nrf2/HO-1 pathway to be mainly responsible for the suppression of inflammatory marker release and the recovery of the oxidant/antioxidant homeostasis. Additionally, luteolin (3’, 4’, 5, 7-tetrahydroxyflavone) attenuated disease patterns of a DSS-induced colitis in mice and activated Nrf2-dependent gene expression of HO-1 and NQO1 [ 98 ].…”
Section: Protection Against Colitis By Targeting Nrf2mentioning
confidence: 99%
“…SOD is a key antioxidant enzyme that plays a crucial role in the protection of the cells from oxidative stress [ 1 , 3 ]. On the first line of defense against oxidative stress [ 9 ], SOD consecutively catalyzes the dismutation of superoxide ion into the less reactive metabolite hydrogen peroxide, which attenuates free radical impairment in the eukaryotic cells [ 1 , 3 , 18 , 20 ]. Glutathione peroxidase (GSH-PX) is an enzyme that can protect the cells from oxidative injury [ 3 ].…”
Section: Resultsmentioning
confidence: 99%
“…Glutathione peroxidase (GSH-PX) is an enzyme that can protect the cells from oxidative injury [ 3 ]. Glutathione (GSH) is a tripeptide and a fundamental provider in cellular antioxidative defense, which serves for scavenging free radicals [ 20 ]. The GSH-PX converts hydrogen peroxide into water and oxygen; it also oxidizes glutathione (GSH) to oxidized glutathione (GSSG) [ 5 , 13 , 37 ], averting the production of reactive hydroxyl radical and protecting the cells against ROS [ 18 ].…”
Section: Resultsmentioning
confidence: 99%
See 1 more Smart Citation
“…In normal conditions, Nrf2 combines with kelch-like ECH-associated protein 1 (Keap-1), and this combined form of Nrf2 is degraded. Degradation effectively controls the level of Nrf2 in cells (18). Heme oxygenase-1 (HO-1) is located downstream of Nrf2 (19); therefore, alterations in the levels of Nrf2 subsequently affect the expression of HO-1.…”
Section: Protective Effects Of Osthole Against Inflammation Induced Bmentioning
confidence: 99%