Selenium protects against cadmium-induced kidney apoptosis in chickens by activating the PI3K/AKT/Bcl-2 signaling pathway

Bao, Rong-Kun; Zheng, Shufang; Wang, Xinyue

doi:10.1007/s11356-017-9422-6

Cited by 54 publications

(27 citation statements)

References 47 publications

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“…By investigating the effect of cadmium and selenium on cells, the interaction between these two in the cell can be found. The use of selenium simultaneously with the use of cadmium, due to its antioxidant properties, reduces cad- (17), which is consistent with the results of this research.…”

Section: Discussionsupporting

confidence: 92%

The Effect of Interval Training with Selenium Consumption on Gene Expression of Caspase- 3 and Cyclin-D in Liver Tissue of Cadmium-Exposed Rats

Fard

Hoseini

Azarbayjani

et al. 2019

Jundishapur J Health Sci

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Background: Cadmium is one of the heaviest metals in the natural environment that can increase DNA damage in liver cells, nevertheless, it has been reported that physical activity and nutrition can improve the damage of DNA in liver cells. Objectives: The aim of the present research was to review the effect of interval training and selenium on cyclin-D and caspase-3 gene expression in liver tissue of cadmium-exposed rats. Methods: In the present experimental research, 30 rats were divided to six groups of (1) control, (2) sham, (3) cadmium, (4) selenium consumption with cadmium, (5) interval training with cadmium consumption, and (6) interval training with selenium and cadmium consumption. For eight weeks, groups three to six received 2 mg/kg of cadmium per day; groups four and six consumed 0.23 mg/kg of selenium per day and groups five and six performed three sessions of selected interval training per week. Results: Cadmium consumption significantly increased cyclin-D and caspase-3 (P = 0.001); selenium consumption and interval training had a significant effect on decreasing caspase-3 and cyclin-D levels (P = 0.001); concurrent interval training with selenium consumption had interactive effects on the increase of cyclin-D (P = 0.001). However, there was no interactive effect on the reduction of caspase-3 (P = 0.75). Conclusions: It seems that interval training with selenium consumption has interactive effects on hepatocyte apoptotic factors in rats exposed to cadmium.

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Section: Discussionsupporting

confidence: 92%

The Effect of Interval Training with Selenium Consumption on Gene Expression of Caspase- 3 and Cyclin-D in Liver Tissue of Cadmium-Exposed Rats

Fard

Hoseini

Azarbayjani

et al. 2019

Jundishapur J Health Sci

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“…These findings were consistent with those of Bao et al . 42 , in which chicken kidney exposed to Cd showed decreased Bcl-2 and increased Bax and caspase 3 levels. However, RJ pretreatment effectively reversed this Cd-induced process, suggesting that RJ resisted apoptosis by enhancing the expression level of anti-apoptotic protein Bcl-2.…”

Section: Discussionmentioning

confidence: 98%

Royal jelly attenuates cadmium-induced nephrotoxicity in male mice

Almeer

Albasher

Alarifi

et al. 2019

Sci Rep

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Cadmium exposure induces nephrotoxicity by mediating oxidative stress, inflammation, and apoptosis. The purpose of this study was to examine the protective effect of royal jelly on Cd-induced nephrotoxicity. Adult male mice were distributed randomly into 4 clusters: untreated, royal jelly-treated (85 mg/kg, oral), CdCl 2 -treated (6.5 mg/kg, intraperitoneal), and pretreated with royal jelly (85 mg/kg) 2 h before CdCl 2 injection (6.5 mg/kg, intraperitoneal) for seven consecutive days. Cd concentration in the renal tissue and absolute kidney weight of the Cd-treated mice were significantly higher than those of control group. The levels of kidney function markers, kidney injury molecules-1 (KIM-1), metallothionein, lipid peroxidation, nitric oxide, tumor necrosis factor-α, interleukin-1β, and the apoptosis regulators Bax and caspases-3 also increased significantly in the renal tissue of Cd-treated mice, whereas the levels of glutathione, antioxidant enzyme activities, and the apoptosis inhibitor Bcl-2 were significantly reduced in the renal tissue of Cd-treated group. Histopathological studies showed vacuolation and congested glomeruli in the kidney tissue of Cd-treated mice. However, all aforementioned Cd-induced changes were attenuated by pretreatment with royal jelly. We therefore concluded that royal jelly attenuated Cd-induced nephrotoxicity and it is suggested that this nephroprotective effect could be linked to its ability to promote the nuclear factor erythroid 2–related factor 2 (Nrf2)/antioxidant responsive element (ARE) pathway.

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“…Previous studies have reported that PI3K/Akt signalling pathway is associated with cadmium‐induced apoptosis in different cell types . Notably, 3 studies have shown that activation of PI3K/Akt signalling pathway led to cadmium‐induced apoptosis in astrocytes, thyroid carcinoma cells and HK‐2 renal proximal tubular epithelial cells, respectively .…”

Section: Discussionmentioning

confidence: 99%

Modelling cadmium‐induced cardiotoxicity using human pluripotent stem cell‐derived cardiomyocytes

Shen

Wang

Zhou

et al. 2018

J Cellular Molecular Medi

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Cadmium, a highly ubiquitous toxic heavy metal, has been widely recognized as an environmental and industrial pollutant, which confers serious threats to human health. The molecular mechanisms of the cadmium‐induced cardiotoxicity (CIC) have not been studied in human cardiomyocytes at the cellular level. Here we showed that human pluripotent stem cell‐derived cardiomyocytes (hPSC‐CMs) can recapitulate the CIC at the cellular level. The cadmium‐treated hPSC‐CMs exhibited cellular phenotype including reduced cell viability, increased apoptosis, cardiac sarcomeric disorganization, elevated reactive oxygen species, altered action potential profile and cardiac arrhythmias. RNA‐sequencing analysis revealed a differential transcriptome profile and activated MAPK signalling pathway in cadmium‐treated hPSC‐CMs, and suppression of P38 MAPK but not ERK MAPK or JNK MAPK rescued CIC phenotype. We further identified that suppression of PI3K/Akt signalling pathway is sufficient to reverse the CIC phenotype, which may play an important role in CIC. Taken together, our data indicate that hPSC‐CMs can serve as a suitable model for the exploration of molecular mechanisms underlying CIC and for the discovery of CIC cardioprotective drugs.

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Selenium protects against cadmium-induced kidney apoptosis in chickens by activating the PI3K/AKT/Bcl-2 signaling pathway

Cited by 54 publications

References 47 publications

The Effect of Interval Training with Selenium Consumption on Gene Expression of Caspase- 3 and Cyclin-D in Liver Tissue of Cadmium-Exposed Rats

The Effect of Interval Training with Selenium Consumption on Gene Expression of Caspase- 3 and Cyclin-D in Liver Tissue of Cadmium-Exposed Rats

Royal jelly attenuates cadmium-induced nephrotoxicity in male mice

Modelling cadmium‐induced cardiotoxicity using human pluripotent stem cell‐derived cardiomyocytes

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