Vitamin E protects against cadmium-induced sub-chronic liver injury associated with the inhibition of oxidative stress and activation of Nrf2 pathway

Fang, Jing; Yin, Heng; Yang, Ziyuan; Tan, Maoyun; Wang, Fengyuan; Chen, Kejie; Zuo, Zhuang; Shu, Gang; Cui, Hengmin; Ouyang, Ping; Guo, Hongrui; Chen, Zhengli; Huang, Chao; Geng, Yi; Liu, Wentao

doi:10.1016/j.ecoenv.2020.111610

Cited by 43 publications

(26 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The VitE antioxidant effect has been related to Nrf2 modulation in different experimental models [159][160][161], but it has not been fully explored in NAFLD models. For example, it has been reported that VitE protects against oxidative stress-related liver injury in rats treated with cadmium, promoting the expression of genes and proteins of the Nrf2 pathway [162]. Furthermore, recent evidence demonstrates that VitE treatment reduces hepatic steatosis in mice with NAFLD induced by fructose feeding, and this therapeutic effect seems to be dependent on the activation of Nrf2/CES1 signalling, which was also observed in in vitro experiments [163].…”

Section: Classical Antioxidants: Vitamin C and Vitamin Ementioning

confidence: 71%

Role of Oxidative Stress in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: Implications for Prevention and Therapy

et al. 2021

View full text Add to dashboard Cite

Oxidative stress (OxS) is considered a major factor in the pathophysiology of inflammatory chronic liver diseases, including non-alcoholic liver disease (NAFLD). Chronic impairment of lipid metabolism is closely related to alterations of the oxidant/antioxidant balance, which affect metabolism-related organelles, leading to cellular lipotoxicity, lipid peroxidation, chronic endoplasmic reticulum (ER) stress, and mitochondrial dysfunction. Increased OxS also triggers hepatocytes stress pathways, leading to inflammation and fibrogenesis, contributing to the progression of non-alcoholic steatohepatitis (NASH). The antioxidant response, regulated by the Nrf2/ARE pathway, is a key component in this process and counteracts oxidative stress-induced damage, contributing to the restoration of normal lipid metabolism. Therefore, modulation of the antioxidant response emerges as an interesting target to prevent NAFLD development and progression. This review highlights the link between disturbed lipid metabolism and oxidative stress in the context of NAFLD. In addition, emerging potential therapies based on antioxidant effects and their likely molecular targets are discussed.

show abstract

Section: Classical Antioxidants: Vitamin C and Vitamin Ementioning

confidence: 71%

Role of Oxidative Stress in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: Implications for Prevention and Therapy

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Under normal conditions, NRF2 is bound to its inhibitor Keap1 protein and resided in the cytoplasm. However, when stimulated, it dissociates from Keap1, translocates to the nucleus, and then binds to the antioxidant response element (ARE), thus regulating the transcript abundance of its downstream antioxidant genes (NQO1, GCLM, GCLC, and HO-1) (Bellezza et al, 2018 exposure inhibited the activation of NRF2 (Ma et al, 2019), whereas VE might protect cells against apoptosis by activating the NRF2 and its downstream genes (Duan et al, 2017;Fang, Yin, et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Vitamin E regulates bovine granulosa cell apoptosis via NRF2‐mediated defence mechanism by activating PI3K/AKT and ERK1/2 signalling pathways

Wang

Gao

et al. 2021

Reprod Domestic Animals

View full text Add to dashboard Cite

High-yield dairy cows are usually subject to high-intensive cell metabolism and produce excessive reactive oxygen species (ROS). Once ROS is beyond the threshold of scavenging ability, it can induce oxidative stress, imperilling the reproductive performance of cows. The study was to investigate the effects of vitamin E (VE) on H 2 O 2 -induced proliferation and apoptosis of bovine granulosa cells and the underlying molecular mechanism. Granulosa cells were pretreated with VE for 24 hr and then treated with H 2 O 2 for 6 hr. The results showed that VE treatment decreased the intracellular ROS levels, increased the MDA content, and improved the antioxidant enzyme activity in a dose-dependent manner. Furthermore, VE treatment promoted the proliferation and inhibited apoptosis in granulosa cells by up-regulation of CCND1 and BCL2 levels and down-regulation of P21, BAX, and CASP3 levels. The cytoprotective effects of VE were attributed to the activation of the NRF2 signalling pathway. Knockdown of the NRF2 impaired the cytoprotective effects of VE on granulosa cells. Besides, the PI3K/AKT and ERK1/2, but not the p38 signalling pathway is involved in the regulation of VE-mediated cell proliferation and apoptosis. The PI3K/AKT inhibitor LY294002 and ERK1/2 inhibitor SCH772984 inhibited the VE-induced granulosa cell proliferation and promoted apoptosis, whereas the p38 inhibitor SB203580 had the opposite effects. These results were confirmed by proliferation and apoptosis-related gene expression at mRNA and protein levels.The results also showed that the PI3K/AKT inhibitor LY294002 and ERK1/2 inhibitor SCH772984 inhibited VE-induced NRF2, GCLC, GCLM, and HO-1 expression, whereas the p38 inhibitor SB203580 not. Overall, the results demonstrated that VE-regulated granulosa cell proliferation and apoptosis via NRF2-mediated defence system by activating the PI3K/AKT and ERK1/2 signalling pathway.

show abstract

“…It is believed that LXRα acts as a cholesterol sensor, and after SREBP-1c induction, fatty acids are produced in order to esterify cholesterol, which in turn balances the cholesterol amount in the organism [210]. omega-3 fatty acids: DHA traumatic brain injury [272] vitamin A cholestasis [273] vitamin E chronic liver injury [274] Nrf2 inhibition apigenin lung cancer [275] luteolin colon cancer [276] keampferol non-small cell lung cancer [277] chrysin breast cancer, glioblastoma [278,279] gallic acid psoriasis-like skin disease, respiratory diseases [280,281] vitamin E asthma [282] zinc diabetic nephropathy [283] chrysin bladder cancer [305] gallic acid non-small cell lung cancer [306] omega-3 fatty acids: DHA renal cancer, multiple myeloma, pancreatic cancer [254,307,308] sulforaphane nasopharyngeal cancer, glioblastoma multiforme [160,309] activation of p53 curcumin gastric cancer, neuroblastoma, renal cell carcinoma [310][311][312] resveratrol prostate cancer, colon cancer, hepatocellular carcinoma, glioblastoma multiform, neuroblastoma, thyroid cancer [313][314][315][316][317][318][319] epigallocatechin-3-gallate liver cancer [320] vitamin D endometrial cancer [321] inhibition of p53 resveratrol osteoporosis, breast cancer [322,323] vitamin E breast cancer [324] Beside carbohydrates and fats, proteins are the third most important class of macromolecules that need to be received with diet. Although higher organisms are able to synthetize some amin...…”

Section: Activation Of Transcription Factors By Nutrientsmentioning

confidence: 99%

Influence of the Bioactive Diet Components on the Gene Expression Regulation

et al. 2021

View full text Add to dashboard Cite

Diet bioactive components, in the concept of nutrigenetics and nutrigenomics, consist of food constituents, which can transfer information from the external environment and influence gene expression in the cell and thus the function of the whole organism. It is crucial to regard food not only as the source of energy and basic nutriments, crucial for living and organism development, but also as the factor influencing health/disease, biochemical mechanisms, and activation of biochemical pathways. Bioactive components of the diet regulate gene expression through changes in the chromatin structure (including DNA methylation and histone modification), non-coding RNA, activation of transcription factors by signalling cascades, or direct ligand binding to the nuclear receptors. Analysis of interactions between diet components and human genome structure and gene activity is a modern approach that will help to better understand these relations and will allow designing dietary guidances, which can help maintain good health.

show abstract

Vitamin E protects against cadmium-induced sub-chronic liver injury associated with the inhibition of oxidative stress and activation of Nrf2 pathway

Cited by 43 publications

References 48 publications

Role of Oxidative Stress in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: Implications for Prevention and Therapy

Role of Oxidative Stress in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: Implications for Prevention and Therapy

Vitamin E regulates bovine granulosa cell apoptosis via NRF2‐mediated defence mechanism by activating PI3K/AKT and ERK1/2 signalling pathways

Influence of the Bioactive Diet Components on the Gene Expression Regulation

Contact Info

Product

Resources

About