MitoQ ameliorates testis injury from oxidative attack by repairing mitochondria and promoting the Keap1-Nrf2 pathway

Zhang, Jie; Bao, Xiaowen; Zhang, Mingya; Zhu, Zhiming; Zhou, Lvqi; Chen, Qiaohui; Zhang, Qi; Ma, Bo

doi:10.1016/j.taap.2019.03.001

Cited by 53 publications

(23 citation statements)

References 53 publications

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“…MitoQ, as a powerful activator of the Nrf2 pathway, plays a critical role in cytoprotective and antiapoptotic effect in various diseases, and these protective properties were associated with the decrease of inflammatory response and oxidative stress [7]. Our study demonstrated that MitoQ pretreatment can attenuate the intestinal injury induced by LPS.…”

Section: Discussionsupporting

confidence: 51%

“…Mitochondrial dysfunction induced by oxidative stress play an important role in the development of sepsis, leading to the impaired intestinal injury. A recent study demonstrated a strengthful effect of the mitochondrially targeted antioxidant MitoQ on alleviating oxidative injury and improving mitochondrial function [7]. However, no studies have provided strong evidence on the beneficial role of MitoQ in sepsis-induced gut injury.…”

Section: Introductionmentioning

confidence: 99%

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MitoQ Modulates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction via Regulating Nrf2 Signaling

Zhang

Zhou

et al. 2020

Mediators of Inflammation

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Background. Gut barrier dysfunction with alterant mucosal permeability during sepsis is a challenge problem in clinical practice. Intestinal epithelial cells (IECs) are strongly involved in mucosal oxidative stress and inflammatory response. The current study aimed at investigating the effect of MitoQ, a mitochondrial targeted antioxidant, in the treatment of intestinal injury and its potential mechanism during sepsis. Methods. 30 minutes before sepsis induction by lipopolysaccharide (LPS) treatment, mice were treated with MitoQ. Intestinal histopathology, mucosal permeability, inflammatory cytokines, and mucosal barrier proteins were evaluated in the present study. Results. MitoQ pretreatment significantly decreased the levels of plasma diamine oxidase, D-lactate, and intestinal histological damage and markedly restored the levels of tight junction proteins (ZO-1 and occludin) following LPS challenge. Furthermore, MitoQ inhibited the LPS-induced intestinal oxidative stress and inflammatory response, evidenced by increased levels of intestinal superoxide dismutase and glutathione, and decreased levels of intestinal IL-1, IL-6, TNF-α, and nitric oxide levels. Mechanically, we found that MitoQ inhibited the oxidative stress via activating nuclear factor E2-related factor 2 (Nrf2) signaling pathway and its downstream antioxidant genes, including HO-1, NQO-1, and GCLM. Conclusions. MitoQ exerts antioxidative and anti-inflammatory effects against sepsis-associated gut barrier injury by promoting Nrf2 signaling pathway.

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Section: Discussionsupporting

confidence: 51%

Section: Introductionmentioning

confidence: 99%

MitoQ Modulates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction via Regulating Nrf2 Signaling

Zhang

Zhou

et al. 2020

Mediators of Inflammation

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“…It is well known that oxidative stress leads to sperm dysfunction by inducing peroxidation damage to the plasma membrane. In this study, TP-induced increased MDA levels and decreased GSH-Px and SOD levels in mice, suggesting oxidative stress, which was consistent with the reports of some researchers [ 8 , 13 , 32 ]. As spermatozoa are high in polyunsaturated fatty acids (PUFAs), it is more sensitive to oxidative damage than other cells [ 33 ].…”

Section: Discussionsupporting

confidence: 93%

The Potential Protective Effect and Possible Mechanism of Peptides from Oyster (Crassostrea hongkongensis) Hydrolysate on Triptolide-Induced Testis Injury in Male Mice

et al. 2021

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Peptides from oyster hydrolysate (OPs) have a variety of biological activities. However, its protective effect and exact mechanism on testicular injury remain poorly understood. This study aimed to evaluate the protective effect of OPs on triptolide (TP)-induced testis damage and spermatogenesis dysfunction and investigate its underlying mechanism. In this work, the TP-induced testis injury model was created while OPs were gavaged in mice for 4 weeks. The results showed that OPs significantly improved the sperm count and motility of mice, and alleviated the seminiferous tubule injury. Further study showed that OPs decreased malonaldehyde (MDA) level and increased antioxidant enzyme (SOD and GPH-Px) activities, attenuating oxidative stress and thereby reducing the number of apoptotic cells in the testis. In addition, OPs improved the activities of enzymes (LDH, ALP and ACP) related to energy metabolism in the testis and restored the serum hormone level of mice to normal. Furthermore, OPs promoted the expression of Nrf2 protein, and then increased the expression of antioxidant enzyme regulatory protein (HO-1 and NQO1) in the testis. OPs inhibited JNK phosphorylation and Bcl-2/Bax-mediated apoptosis. In conclusion, OPs have a protective effect on testicular injury and spermatogenesis disorders caused by TP, suggesting the potential protection of OPs on male reproduction.

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“…concluded that, MitoQ 10 prevented intestinal cells damage by prevention OS through Nrf2/Keap 1 antioxidant related enzymes (ARE) pathway [ 43 ]. Furthermore, MitoQ 10 ameliorates testis injury from OS attack by repairing mitochondria and promoting the Nrf2/Keap1 pathway [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

Assessing the effect of MitoQ10 and Vitamin D3 on ovarian oxidative stress, steroidogenesis and histomorphology in DHEA induced PCOS mouse model

Kyei

Sobhani

Nekonam

et al. 2020

Heliyon

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Polycystic ovary syndrome (PCOS) continues to be one of the most complex reproductive and endocrine disorder among women of reproductive age. Recent reports have identified close interaction of Vitamin D deficiency and oxidative stress (OS) in exacerbating the pathophysiology of PCOS. This current study aims at assessing the combine effect of MitoQ 10 and Vitamin D3 on dehydroepiandrosterone (DHEA) induced PCOS. Following successful induction of PCOS using DHEA, mice were organized into five groups ( n = 8) namely: Negative Control (NC), Vitamin D3 Vehicle (VDV), Vitamin D3 (VD), MitoQ 10 (MQ), Vitamin D3 plus MitoQ 10 (V+M) and DHEA, ethanol and distilled water, Vitamin D3, MitoQ 10 and Vitamin D3 plus MitoQ 10 were respectively administered for 20 consecutive days. The study also included positive control (PC) group ( n = 8) in which no treatment was applied. Treatment effects were assessed using hormonal assays, biochemical assays, Real-Time PCR, western blotting and histological analysis. Combination of Vitamin D3 and MitoQ 10 significantly reduced levels of estradiol, progesterone, FSH, LH, LH/FSH, SOD and MDA. The expression rate of mRNAs of 3β-HSD, Cyp19a1, Cyp11a1, StAR, Keap1, HO-1 and Nrf2 were also significantly low in V+M group. Moreover, the histomorphological inspection of ovaries from this group revealed many healthy follicles at various stages of development including few atretic follicles, pre-antral and antral follicles and many corpora lutea. The characteristics observed in this group were in many ways similar to that of the PC group. The combination of MitoQ 10 and Vitamin D3 may be potential candidate to ameliorate PCOS.

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MitoQ ameliorates testis injury from oxidative attack by repairing mitochondria and promoting the Keap1-Nrf2 pathway

Cited by 53 publications

References 53 publications

MitoQ Modulates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction via Regulating Nrf2 Signaling

MitoQ Modulates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction via Regulating Nrf2 Signaling

The Potential Protective Effect and Possible Mechanism of Peptides from Oyster (Crassostrea hongkongensis) Hydrolysate on Triptolide-Induced Testis Injury in Male Mice

Assessing the effect of MitoQ10 and Vitamin D3 on ovarian oxidative stress, steroidogenesis and histomorphology in DHEA induced PCOS mouse model

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