Coenzyme Q10 inhibits RANKL‐induced osteoclastogenesis by regulation of mitochondrial apoptosis and oxidative stress in RAW264.7 cells

Author(s):  
Delu Zheng ◽  
Chenli Cui ◽  
Chen Shao ◽  
Yanqiu Wang ◽  
Chengsong Ye ◽  
...  
Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 2
Author(s):  
David Mantle ◽  
Robert A. Heaton ◽  
Iain P. Hargreaves

The ageing brain is characterised by changes at the physical, histological, biochemical and physiological levels. This ageing process is associated with an increased risk of developing a number of neurological disorders, notably Alzheimer’s disease and Parkinson’s disease. There is evidence that mitochondrial dysfunction and oxidative stress play a key role in the pathogenesis of such disorders. In this article, we review the potential therapeutic role in these age-related neurological disorders of supplementary coenzyme Q10, a vitamin-like substance of vital importance for normal mitochondrial function and as an antioxidant. This review is concerned primarily with studies in humans rather than in vitro studies or studies in animal models of neurological disease. In particular, the reasons why the outcomes of clinical trials supplementing coenzyme Q10 in these neurological disorders is discussed.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yang Ruan ◽  
Hong Li ◽  
Lianmei Pu ◽  
Tao Shen ◽  
Zening Jin

Aim. To investigate the function of Tremella fuciformis polysaccharides (TFPS) in LPS-induced inflammation and oxidative stress of macrophages. Methods. RAW264.7 cells were pretreated with TFPS and then stimulated with 0.1 μg/ml LPS. NFκB, Akt, p38MAPK, MCP-1, and SOD-1 were analyzed by Western blotting. Cell viability was measured using MTT assays. Reactive oxygen species (ROS) production, real-time PCR, ELISA, and immunofluorescence staining were performed on RAW264.7 cells that were treated with LPS and/or TFPS to investigate the anti-inflammatory effect of TFPS. Results. LPS induced inflammation and ROS production and promoted the secretion of cytokines such as TNF-α and IL-6. LPS also enhanced the nuclear translocation of NFκB, which promoted inflammation by oxidative stress. However, pretreatment with TFPS profoundly inhibited the activation of Akt, p38MAPK, and NFκB and attenuated the expression of MCP-1 in macrophages. Meanwhile, TFPS also decreased cytokine and ROS levels and attenuated cell inflammation after treatment with LPS. Moreover, miR-155, one of the key small RNAs which regulate NFκB and inflammation in macrophages, was significantly downregulated. Conclusion. TFPS inhibits LPS-induced oxidative stress and inflammation by inhibiting miR-155 expression and NFκB activation in macrophages, which suggests that TFPS may be a potential reagent for inhibiting the development of inflammation.


2019 ◽  
Vol 25 (4) ◽  
pp. 256-269
Author(s):  
Yeganeh Feizi ◽  
◽  
Mohammad Esmaeil Afzalpur ◽  
Seyed-Hosein Abtahi-Eivary ◽  
◽  
...  

Aims Physical activity is usually accompanied by free radicals’ production and oxidative stress. Moreover, to prevent adverse effects, coaches and athletes have to use proper supplementation. Therefore, the present study aimed to investigate the effect of short-term coenzyme Q10 supplementation on malondialdehyde and serum catalase enzyme activity following moderate and severe acute resistance training in inactive female students. Methods & Materials In total, 27 female students were randomly divided into three groups; the groups were homogeneous and equal (two groups of resistance training and one control group). The experimental groups were subjected to moderate-intensity acute (70% 1RM) acute and severe acute activity (85% 1RM) and supplemented with coenzyme Q10 (30 mg /d). CAT and MDA were measured in ELISA using a human kit. Findings Moderate and severe acute resistance activities did not alter MDA and catalytic activity (P>0.05); however, after 2 weeks of coenzyme Q10 supplementation, those resulted in a significant decrease in MDA (0.006 and 0.01, respectively) and CAT (0.04 and 0.007, respectively). There were no significant differences between the effects of two exercises (P>0.05). Conclusion Short-term (two weeks) supplementation of coenzyme Q10 and severe acute resistance activity could reduce two important oxidative stress indexes (MDA and CAT).


2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Jie Tang ◽  
Ping Diao ◽  
Xiaohong Shu ◽  
Li Li ◽  
Lidan Xiong

Background. Nowadays, atmospheric pollutants, ultraviolet rays, and other factors cause the imbalance of cell redox, resulting in skin oxidative damage. There is an interaction between inflammatory response and oxidative stress, which often involve networks of reactions and serve to amplify each other. Quercetin and quercitrin, with strong antioxidant and anti-inflammatory properties, were widely applied in cardiovascular disease, osteoporsis, pulmonary disease, etc. However, the regulation mechanism of quercetin and quercitrin on various inflammatory skin diseases is still not clear. Purpose. In this study, quercetin and quercitrin were used to investigate whether they had anti-inflammatory and anti-ROS effects. Besides, theoretical calculation method was also adopted to preliminarily explore the mechanism of the anti-inflammatory and antioxidant effects of these two substances. Methods. CCK-8 assay was employed to investigate the cytotoxicity. The concentration of NO measured by Griess Reaction System. Moreover, the inflammatory factors (TNF-α, IL-1β, and IL-6) were reduced in LPS-stimulated RAW264.7 cells were tested by ELISA kits. The trend of ROS changes was detected by DCFH-DA method. Finally, the mechanism of the anti-inflammatory and antioxidant effects of these two substances was carried out by DMol3 package in Materials Studio. Results. CCK-8 assay results guided that the safe concentration of quercetin and quercitrin was lower than 15.0 μg/mL and 22.4 μg/mL, respectively. Also, the concentration of NO could significantly be inhibited by quercetin and quercitrin. Besides, the ELISA results showed that TNF-α, IL-1β, and IL-6 were reduced in LPS-stimulated RAW264.7 cells after interfering with quercetin and quercitrin. The trend of ROS changes was similar to that of inflammatory factors. Finally, the theoretical calculation illustrated that the oxygen atom on B rings may be the main site of electron cloud density changes, which may suggest a possible mechanism for the anti-inflammatory and ROS scavenging effects of quercetin and quercitrin. Conclusions. This experiment shows that LPS can induce the overactivating of macrophages and the activated macrophages can subsequently induce inflammatory storms and oxidative stress. Both quercetin and quercitrin can inhibit LPS-induced macrophage inflammation and oxidative stress by experiment and theoretical calculations.


2011 ◽  
Vol 51 (7) ◽  
pp. 791-799 ◽  
Author(s):  
Javier Díaz-Castro ◽  
Rafael Guisado ◽  
Naroa Kajarabille ◽  
Carmen García ◽  
Isabel M. Guisado ◽  
...  

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