&lt;p&gt;Piceatannol inhibits oxidative stress through modification of Nrf2-signaling pathway in testes and attenuates spermatogenesis and steroidogenesis in rats exposed to cadmium during adulthood&lt;/p&gt;

Shi, Xiaoxue; Fu, Lei

doi:10.2147/dddt.s198444

Cited by 37 publications

(25 citation statements)

References 41 publications

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“…The cytoprotective effect of Nrf2 is achieved by promoting the synthesis of antioxidant enzymes to detoxify and eradicate the excessive ROS and other electrophilic molecules through conjugative reactions, as well as enhancing cellular antioxidant defense capacity (Chen et al., 2019). The downregulation of Nrf2 gene expression following CdCl 2 administration comes in line with the former studies (He et al., 2018; Shi & Fu, 2019). Pre‐administration of FA was found to significantly upregulate the Nrf2/ARE signaling pathway.…”

Section: Discussionsupporting

confidence: 87%

“…To evaluate the molecular changes that underlying the protective effect of FA on CdgCl 2 -induced toxicity, we analyzed the Nfe2l2 ing cellular antioxidant defense capacity (Chen et al, 2019). The downregulation of Nrf2 gene expression following CdCl 2 administration comes in line with the former studies (He et al, 2018;Shi & Fu, 2019). Pre-administration of FA was found to significantly upregulate the Nrf2/ARE signaling pathway.…”

Section: F I G U R Esupporting

confidence: 85%

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Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium‐induced oxidative challenge, inflammation, and apoptosis in rats

et al. 2020

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Here, we examined the protective effect of ferulic acid (FA) on cadmium chloride (CdCl 2)-mediated reproductive toxicity in male rats. Animals were divided into four groups: control, FA (20 mg/kg), CdCl 2 (6.5 mg/kg), and FA + CdCl 2. CdCl 2 treatment evoked a significant increase in testis cadmium concentration in addition to obvious increase in testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Moreover, CdCl 2-induced oxidative damage through exhausting the cellular defenses (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione) and downregulating the nuclear factor erythroid 2-related factor 2 (Nrf2) expression accompanied by increases of malondialdehyde and nitric oxide contents. Testicular inflammation was evident indicated by increased levels of interleukin-1β and tumor necrosis factor-α in CdCl 2-treated rats. CdCl 2 exposure also decreased the expression of the proliferating cell nuclear antigen and augmented apoptotic events associated with prominent histopathological alterations. However, FA coadministration mitigated the impaired hormonal level, apoptotic and inflammatory injuries elicited by CdCl 2, and maintained the oxidant/antioxidant balance in testicular tissue via Nrf2 activation. Practical applications Cadmium is an environmental toxicant and known to cause adverse effects including reproductive toxicity. However, antioxidant application has been found to protect against heavy metals-mediated toxic effects. Here, we examined the potential protective efficacy of ferulic acid against cadmium-mediated testicular impairments through estimating the amount of cadmium in the testis, hormonal profile, oxidative status, inflammatory response, apoptotic and proliferating markers in addition to the histopathological alterations. The obtained findings revealed that ferulic acid supplementation was able to abolish the testicular damages coupled with cadmium exposure. The protective efficiency of ferulic acid may correlated with its strong antioxidant, anti-inflammatory, and antiapoptotic activities; suggesting that ferulic acid may be used to ameliorate cadmium-induced testicular deficits. How to cite this article: Kassab RB, Lokman MS, Daabo HMA, et al. Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium-induced oxidative challenge, inflammation, and apoptosis in rats.

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Section: Discussionsupporting

confidence: 87%

Section: F I G U R Esupporting

confidence: 85%

Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium‐induced oxidative challenge, inflammation, and apoptosis in rats

et al. 2020

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“…Therefore, improving Nrf2 activity is effective for providing cytoprotection against different chronic and inflammatory conditions, including PM 2.5 -induced tissue damage [ 15 , 22 , 24 , 25 ]. Nrf2 is involved in the signaling pathway that results in PM-elicited spermatogenesis dysfunction [ 56 ]. In lung cells, Nrf2 protects against diverse PM components-triggered mitochondrial oxidative damage [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

Nrf2 mitigates prolonged PM2.5 exposure-triggered liver inflammation by positively regulating SIKE activity: Protection by Juglanin

Ge¹,

Tan

Zhong

et al. 2020

Redox Biology

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Air pollution containing particulate matter (PM) less than 2.5 μm (PM 2.5 ) plays an essential role in regulating hepatic disease. However, its molecular mechanism is not yet clear, lacking effective therapeutic strategies. In this study, we attempted to investigate the effects and mechanisms of PM 2.5 exposure on hepatic injury by the in vitro and in vivo experiments. At first, we found that PM 2.5 incubation led to a significant reduction of nuclear factor erythroid-derived 2-related factor 2 (Nrf2), along with markedly reduced expression of different anti-oxidants. Notably, suppressor of IKKε (SIKE), known as a negative regulator of the interferon pathway, was decreased in PM 2.5 -incubated cells, accompanied with increased activation of TANK-binding kinase 1 (TBK1) and nuclear factor-κB (NF-κB). The in vitro studies showed that Nrf2 positively regulated SIKE expression under the conditions with or without PM 2.5 . After PM 2.5 treatment, Nrf2 knockdown further accelerated SIEK decrease and TBK1/NF-κB activation, and opposite results were observed in cells with Nrf2 over-expression. Subsequently, the gene loss- and gain-function analysis demonstrated that SIKE deficiency further aggravated inflammation and TBK1/NF-κB activation caused by PM 2.5 , which could be abrogated by SIKE over-expression. Importantly, SIKE-alleviated inflammation was mainly dependent on TBK1 activation. The in vivo studies confirmed that SIKE- and Nrf2-knockout mice showed significantly accelerated hepatic injury after long-term PM 2.5 exposure through reducing inflammatory response and oxidative stress. Juglanin (Jug), mainly isolated from Polygonum aviculare , exhibits anti-inflammatory and anti-oxidant effects. We found that Jug could increase Nrf2 activation, and then up-regulated SIKE in cells and liver tissues, mitigating PM 2.5 -induced liver injury. Together, all these data demonstrated that Nrf2 might positively meditate SIKE to inhibit inflammatory and oxidative damage, ameliorating PM 2.5 -induced liver injury. Jug could be considered as an effective therapeutic strategy against this disease by improving Nrf2/SIKE signaling pathway.

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“…Studies related to the direct effect of Cd on several sperm parameters have been well documented in the literature. A significant increase in the number of dead and abnormal sperm, with a marked decrease in the motility and concentration of sperm via Cd‐mediated oxidative damage in rat testes has been documented (Bashir et al, 2019; El‐Demerdash, Yousef, Kedwany, & Baghdadi, 2004; Olufemi, Tams, & Dolapo, 2014; Shi & Fu, 2019). In both in vivo and in vitro studies of Cd on human and mouse sperm, Cd significantly decreased the viability, motility, acrosome reaction, and fertilization capacity of sperm by interfering with the functioning of sperm‐specific Ca 2+ channel (CatSper) in a dose‐ and time‐dependent manner (Wang et al, 2017; Zhao et al, 2017).…”

Section: Cadmium‐mediated Toxicity In Testesmentioning

confidence: 99%

“…Inhibition of Cd-mediated testicular steroidogenesis has been shown by the substantial decrease in the mRNA levels of steroid acute regulatory (StAR) protein, 3β-and17β-hydroxysteroid dehydrogenase (HSD) enzymes activities, as well as reduced serum concentration of testosterone in rats(Habib, Wahdan, Gad, & Azab, 2019;Sen Gupta, Sen Gupta, Dhakal, Thakur, & Ahnn, 2004;Shi & Fu, 2019). In a recent study, chronic administration of Cd showed an initial increase (with low and medium dose) and subsequent decrease (with a higher dose) in the expression level of luteinizing hormone receptor (LHR), 17α-hydroxylase, and endothelial NO synthase (eNOS) in the rat(Ren et al, 2019).…”

mentioning

confidence: 99%

Cadmium as a testicular toxicant: A Review

Bhardwaj

Panchal

Saraf

2020

J of Applied Toxicology

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Cadmium (Cd) is a toxic heavy metal with no known biological functions in the human body. Due to a considerably long biological half-life and very low rate of excretion, accumulation of Cd in different body organs (eg, liver, kidney, and testes) over time is associated with perturbed functioning of these organs. Recent studies have shown the extreme sensitivity of the testes to Cd toxicity. In testes, Cd has been reported to induce oxidative stress, apoptosis of spermatogenic cells, reduction in androgen production and sperm functions. Moreover, Cd in combination with other environmental toxicants may be responsible for the declining fertility of males in both animals and humans. Pinpointing how Cd toxicity affects various testicular processes will be imperative for the development of preventative measures to promote fertility among males. Therefore, in the present review, we summarize the recent findings related to the Cd-induced oxidative toxicity, apoptotic toxicity, steroidogenic toxicity, and spermatotoxicity, along with their possible mechanisms in testicular tissue of different animal species. In addition, the utilization of various antioxidant compounds, medicinal plants and other compounds for the management of Cd toxicity in testes is discussed.

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<p>Piceatannol inhibits oxidative stress through modification of Nrf2-signaling pathway in testes and attenuates spermatogenesis and steroidogenesis in rats exposed to cadmium during adulthood</p>

Cited by 37 publications

References 41 publications

Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium‐induced oxidative challenge, inflammation, and apoptosis in rats

Ferulic acid influences Nrf2 activation to restore testicular tissue from cadmium‐induced oxidative challenge, inflammation, and apoptosis in rats

Nrf2 mitigates prolonged PM2.5 exposure-triggered liver inflammation by positively regulating SIKE activity: Protection by Juglanin

Cadmium as a testicular toxicant: A Review

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