Coenzyme Q10 attenuates lung and liver fibrosis via modulation of autophagy in methotrexate treated rat

Mohamed, Doaa I.; Khairy, Eman; Tawfek, Sherin Shafik; Habib, Eman K.; Fetouh, Marwa A.

doi:10.1016/j.biopha.2018.10.133

Cited by 40 publications

(26 citation statements)

References 38 publications

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“…The asterisks immediately above each bar indicate significance from the control. The asterisks immediately above each line indicate significance between different groups linked by line with other studies showing that co-enzyme Q10 can protect cells by increasing autophagy during stress conditions (Liang et al 2017;Mohamed et al 2019).…”

Section: Discussionsupporting

confidence: 81%

Co-enzyme Q10 protects primary chicken myocardial cells from heat stress by upregulating autophagy and suppressing the PI3K/AKT/mTOR pathway

Huang

Tang

et al. 2019

Cell Stress and Chaperones

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In this study, we investigated the function of co-enzyme Q10 (Q10) in autophagy of primary chicken myocardial cells during heat stress. Cells were treated with Q10 (1 μΜ, 10 μΜ, and 20 μM) before exposure to heat stress. Pretreatment of chicken myocardial cells with Q10 suppressed the decline in cell viability during heat stress and suppressed the increase in apoptosis during heat stress. Treatment with 20 μM Q10 upregulated autophagy-associated genes during heat stress. The expression of LC3-II was highest in cells treated with 20 μM Q10. Pretreatment with Q10 decreased reactive oxygen species (ROS) levels during heat stress. The number of autophagosomes was significantly increased by 20 μM Q10 treatment, as demonstrated by electron microscopy or monodansylcadaverine (MDC) fluorescence. SQSTM1 accumulation was diminished by Q10 treatment during heat stress, and the number of LC3II puncta was increased. Treatment with 20 μM Q10 also decreased the activation of the PI3K/Akt/mTOR pathway. Our results showed that co-enzyme Q10 can protect primary chicken myocardial cells by upregulating autophagy and suppressing the PI3K/Akt/mTOR pathway during heat stress.

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Section: Discussionsupporting

confidence: 81%

Co-enzyme Q10 protects primary chicken myocardial cells from heat stress by upregulating autophagy and suppressing the PI3K/AKT/mTOR pathway

Huang

Tang

et al. 2019

Cell Stress and Chaperones

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“…A recent study has suggested that LKB1-AMPK-ULK1 axis-mediated autophagy plays a critical role in the BLM-induced lung fibrosis 111 . Several studies have shown that several antioxidant agents and bioactive natural products, such as coenzyme Q 10 (CoQ10), celastrol and ligustrazin, promoted autophagy, reduced expression of TGF-β and Col-1 and protected against different chemical compounds-induced IPF through the downregulation of the PI3K/Akt/mTOR pathways in animal models 112 - 114 . Du et al further suggested that dioscin activated autophagy, reduced the secretion of inflammatory factors and subsequently alleviated the abnormal collagen accumulation.…”

Section: Lung Fibrosis and Autophagymentioning

confidence: 99%

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

Liu¹,

Wu²,

Li³

2020

Theranostics

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Fibrosis occurs in most human organs including the liver, lung, heart and kidney, and is crucial for the progression of most chronic diseases. As an indispensable catabolic process for intracellular quality control and homeostasis, autophagy occurs in most mammalian cells and is implicated in many biological processes including fibrogenesis. Although advances have been made in understanding autophagy process, the potential role of autophagy in fibrotic diseases remains controversial and has recently attracted a great deal of attention. In the current review, we summarize the commonalities of autophagy affecting different types of fibrosis in different organs, including the liver, lung, heart, and kidney as well as in cystic fibrosis, systematically outline the contradictory results and highlight the distinct role of autophagy during the various stages of fibrosis. In summary, the exact role autophagy plays in fibrogenesis depends on specific cell types and different stimuli, and identifying and evaluating the pathogenic contribution of autophagy in fibrogenesis will promote the discovery of novel therapeutic strategies for the clinical management of these fibrotic diseases.

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“…However, compared to other techniques in the literature, our experimental model evaluated oxidative stress, adhesion and biomarkers in a different way (34,35). We measured the diamond adhesion score and investigated that clinical adhesion formation get decrease by the effect of coenzyme-Q-10 and we also obtained promising results of GSH-Px and SOD regarding anti-oxidant and anti-inflammatory process for pathological adhesion formation, we saw that utilization of coenzyme-Q-10 could be beneficial for intraabdominal protection after surgical procedures.…”

Section: Discussionmentioning

confidence: 99%

A novel coenzyme-Q approach for the prevention of postsurgical adhesion

et al. 2020

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Objective: Postoperative intraperitoneal adhesions are an unsolved and important problem in abdominal surgery. In the present study, the probable preventive role of coenzyme-Q in the development of peritoneal adhesions was investigated. Material and Methods: Sixteen Wistar Hannover male rats weighing 300-350 g were randomly separated into two groups of 8 rats each. The cecum was abraded with a sterile gauze until sub-serosal hemorrhage developed. A patch of peritoneum located opposite to the cecal abrasion was completely dissected. No treatment was given to Group 1. Group 2 received 30 mg/kg coenzyme-Q, which was injected 2 mL intraperitoneally. All the rats were sacrificed on the postoperative 21 st day, and after adhesions were scored macroscopically, tissue specimens of the peritoneum and bowel were subjected to histopathological investigation. Tissue and blood specimens were also taken for biochemical analysis to investigate antioxidant efficiency. Results: Adhesion scores were significantly different between the control group and the coenzyme-Q group (p= 0.001). According to the tissue levels of GSH-Px, MDA, and SOD levels, there was no significant difference between the study groups (p= 0.074, p= 0.208, p= 0.526). According to the plasma GSH-Px and SOD levels, there was significant difference between the groups (p= 0.002, p= 0.001), but the difference was not significant at MDA levels (p= 0.793). The differences between the pathological scores of the control and coenzyme-Q (p= 0.028 for fibrosis; p= 0.025 for inflammation) groups were statistically significant. Conclusion: This study confirms that coenzyme-Q is the potential application in the prevention of early postoperative adhesions.

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Coenzyme Q10 attenuates lung and liver fibrosis via modulation of autophagy in methotrexate treated rat

Cited by 40 publications

References 38 publications

Co-enzyme Q10 protects primary chicken myocardial cells from heat stress by upregulating autophagy and suppressing the PI3K/AKT/mTOR pathway

Co-enzyme Q10 protects primary chicken myocardial cells from heat stress by upregulating autophagy and suppressing the PI3K/AKT/mTOR pathway

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

A novel coenzyme-Q approach for the prevention of postsurgical adhesion

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