2023
DOI: 10.1016/j.freeradbiomed.2023.05.021
|View full text |Cite
|
Sign up to set email alerts
|

β-carotene targets IP3R/GRP75/VDAC1-MCU axis to renovate LPS-induced mitochondrial oxidative damage by regulating STIM1

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

2
1
0

Year Published

2023
2023
2025
2025

Publication Types

Select...
7

Relationship

0
7

Authors

Journals

citations
Cited by 14 publications
(3 citation statements)
references
References 62 publications
2
1
0
Order By: Relevance
“…As shown in Figure A, there were no obvious influences of cell viability by TPP, TPS, and TB since the concentrations lower than 100 μg/mL and 50 μg/mL were selected for follow-up study. It has been reported that excessive ROS was produced by mitochondria in the LPS-induced cell inflammatory model, which promoted mitochondrial membrane damage and cause apoptosis . In agreement with this view, as shown in Figure B, excessive ROS accumulation caused by LPS in RAW264.7 cells was detected using a flow cytometer and quantified by fluorescence intensity.…”
Section: Resultssupporting
confidence: 82%
See 1 more Smart Citation
“…As shown in Figure A, there were no obvious influences of cell viability by TPP, TPS, and TB since the concentrations lower than 100 μg/mL and 50 μg/mL were selected for follow-up study. It has been reported that excessive ROS was produced by mitochondria in the LPS-induced cell inflammatory model, which promoted mitochondrial membrane damage and cause apoptosis . In agreement with this view, as shown in Figure B, excessive ROS accumulation caused by LPS in RAW264.7 cells was detected using a flow cytometer and quantified by fluorescence intensity.…”
Section: Resultssupporting
confidence: 82%
“…It has been reported that excessive ROS was produced by mitochondria in the LPS-induced cell inflammatory model, which promoted mitochondrial membrane damage and cause apoptosis. 32 In agreement with this view, as shown in Figure 7B, excessive ROS accumulation caused by LPS in RAW264.7 cells was detected using a flow cytometer and quantified by fluorescence intensity. Apparently, Figure 7D demonstrates that TPP, TPS, and TB could effectively reverse the enhancement of ROS level by LPS.…”
Section: Pearson Correlation Analysis Between Gut Microbiota and Coli...supporting
confidence: 78%
“…The binding of LPS to the Toll-like receptor 4 (TLR4) receptor on macrophage surfaces can activate the NF-κB pathway, leading to upregulation of gene expressions such as IL-6, TNF-ɑ, and iNOS, thereby inducing an inflammatory reaction in the body [ 26 ]. Simultaneously, LPS can also induce ROS outbreak and oxidative stress in cells by activating the NOX2/ROS pathway [ 27 ], interfering with mitochondria [ 28 ], and downregulating antioxidant enzymes [ 29 ]. An appropriate inflammatory reaction and oxidative stress are beneficial for pathogen elimination, while excessive or chronic inflammation and oxidative stress may contribute to diseases like fibrosis [ 30 ], diabetes [ 31 ], cancer [ 32 ], and Alzheimer’s disease [ 33 ].…”
Section: Resultsmentioning
confidence: 99%