Sulforaphane Rescues Ethanol-Suppressed Angiogenesis through Oxidative and Endoplasmic Reticulum Stress in Chick Embryos

Wang, Guang; Nie, Jiajia; Bao, Yongping; Yang, Xuesong

doi:10.1021/acs.jafc.8b02949

Cited by 24 publications

(16 citation statements)

References 45 publications

(113 reference statements)

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“…Sulforaphane (SFN) is a natural isothiocyanate extracted from cruciferous plants. SFN has been used in the treatment of diabetic cardiomyopathy (5), angiogenesis (6) and cancer (7). The main pathway regulated by SFN is the Keap-1/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway (8).…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1

Wang

Liu

2020

Int J Mol Med

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FAT atypical cadherin 1 (FAT1) regulates complex mechanisms for the promotion of oncogenesis or the suppression of malignancies. Sulforaphane (SFN) has antioxidant and anti-tumor activities. The present study investigated the roles of SFN and FAT1 in bladder cancer (Bc). The expression of FAT1 in Bc cell lines and tissues was measured by western blot analysis and reverse transcription-quantitative PcR (RT-qPcR). The association between FAT1 expression and the 5-year survival rate of patients with Bc was evaluated. The viability of and FAT1 expression in T24 and SW780 cells exposed to various concentrations of SFN were detected by MTT assay, and western blot analysis and RT-qPcR, respectively. Furthermore, the viability, migration, invasion and apoptosis of and FAT1 expression in Bc cells subjected to FAT1 overexpression or knockdown, and with or without SFN stimulation, were examined. The results revealed that FAT1 expression in Bc cells and tissues was increased, and patients with a high FAT-1 expression had a shorter 5-year survival time than those with a low FAT-1 expression. Bc cell viability and FAT1 expression were suppressed by SFN in a concentration-dependent manner. The knockdown of FAT1 inhibited the viability, migration and invasion, and promoted the apoptosis of Bc cells, whereas the overexpression of FAT1 produced opposite effects. In addition, cells exposed to SFN exhibited a reduced viability, migration, invasion and an increased apoptosis, effects which were promoted by FAT1 knockdown; however, the overexpression of FAT1 blocked the above-mentioned effects of SFN on the cells. On the whole, the present study demonstrates that SFN suppresses the progression of Bc by inhibiting the expression of FAT-1; thus, SFN may be used as a potential drug for the treatment of Bc.

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Section: Introductionmentioning

confidence: 99%

Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1

Wang

Liu

2020

Int J Mol Med

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“…It is effective against oxidative-induced cardiomyocyte damage ( 51 ). Moreover, SFN has been shown to be effective against ERS in different models of cell injury, including chick yolk sac membrane and chorioallantoic membrane models ( 52 ). It inhibits ERS by suppressing the apoptosis of cells in type 1 diabetes mellitus ( 53 ).…”

Section: Discussionmentioning

confidence: 99%

“…The anti-apoptotic effect of SFN was also found to be present in human hepatocytes ( 54 ). Wang et al ( 52 ) reported that SFN ameliorates ethanol-suppressed embryonic angiogenesis by alleviating excessive ROS production and ERS. Moreover, Li et al ( 26 ) documented that SFN suppresses expression levels of ERS-associated apoptosis proteins by activating SIRT1.…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis

Chen

Huang

et al. 2021

Mol Med Rep

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osteoarthritis (oa), the most common form of human joint disease, is characterized by progressive degeneration of the articular cartilage, synovitis and subchondral osteoporosis. chondrocyte apoptosis is the primary pathogenic mechanism of oa and is considered to be a potential therapeutic target. Sulforaphane (SFn), a dietary isothiocyanate obtained from cruciferous vegetables, has been reported to exert an anti-apoptotic effect by activating sirtuin 1 (SirT1). To the best of our knowledge, however, the effects of SFn on apoptotic responses in oa have not been reported. in the present study, SFN was shown to significantly inhibit chondrocyte apoptosis while enhancing expression levels of SirT1 in a H 2 o 2 -induced oa mouse model. The anti-apoptotic effect of SFn was reversed by SirT1 small interfering rna, implying that SirT1 exerted a protective role against the effect of SFn on chondrocytes. The expression levels of c/eBP homologous protein, 78-kda glucose regulated protein, Bax, Bcl-2 and cleaved caspase 3 were found to be downregulated in SFn-treated mice. Furthermore, SFn ameliorated cartilage degradation in the OA mouse model. These findings indicate that SFn exerted an anti-apoptotic effect on chondrocytes and ameliorated oa in vivo by activating the SirT1 signaling pathway.

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“…Embryo mortality in the experimental groups of our study was the highest in the 200μM PhIP group in terms of the median lethal dose (LD50) and neural tube malformation rates. Therefore, 200μM PhIP was selected for the treatment group, and a 5μM Nano-SFN intervention was chosen based on existing literature (G. Wang et al, 2018). The results showed that Nano-SFN reduced PhIP-induced embryonic death and NTDs.…”

Section: Discussionmentioning

confidence: 99%

“…SFN can protect cells from DNA damage (Russo et al, 2018) and is a potent antioxidant (Negrette-Guzman, 2019;Negrette-Guzman et al, 2013), which inhibits oxidative damage caused by various factors in neurons, glial cells, microglia and astrocytes (Danilov et al, 2009;Greco et al, 2010;Hong et al, 2005;Innamorato et al, 2008;Kraft et al, 2004;Soriano et al, 2008). In our previous study, we found that 5-10μM SFN significantly rescued ethanol-suppressed angiogenesis in chick embryos (G. Wang et al, 2018). Nano-sized medicine, in comparison with conventional medicine, leads to increased active concentrations and bioavailability (Balakumar et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Nano-sulforaphane attenuates PhIP-induced early abnormal embryonic neuro-development

Zhang

Liu

et al. 2021

Annals of Anatomy - Anatomischer Anzeiger

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Background 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyrimidine (PhIP), one of the most abundant heterocyclic aromatic amines (HAA) formed by cooking meat at high temperatures, may modify humans and rodents through the metabolic process prior to affecting nervous system development. in humans and rodents may be modified by metabolic processes and then affecting nervous system development. MethodsIn this paper, PhIP was used to prepare a chicken embryo model with abnormal embryonic nervous system defects. Sulforaphane (SFN) is a derivative of a glucosinolate, which is abundant in cruciferous vegetables, and can pass through the placental barrier. Moreover, SFN has antioxidant and anti-apoptotic functions and is considered as a bioactive antioxidant with significant neuroprotective effects.Nano-sulforaphane (Nano-SFN, Sulforaphane nanoparticles) was prepared by self-assembly using biocompatible, biodegradable methoxy polyethylene glycol 5000-b-polyglutamic acid 10000 (mPEG5K-PGA10K) as the substrate, to explore the new application of Nano-SFN and its modified compounds as leading compounds in protecting against the abnormal development of the embryonic nervous system. ResultsThe results show that Nano-SFN could protect against PhIP-induced central nervous system (CNS, derived from neural tube) and peripheral nervous system (PNS, derived from neural crest cells, NCCs) defects and neural tube defects (NTDs), and increase the embryo survival rate. ConclusionsThis study indicates that Nano-SFN can effectively alleviate the developmental defects of embryonic nervous system induced by PhIP in the microenvironment and has a protective effect on embryonic development. It not only helps with expanding the application of SFN and improving its medicinal value, but also provides a possibility of SFN being developed as a novel drug for neuroprotection.

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Sulforaphane Rescues Ethanol-Suppressed Angiogenesis through Oxidative and Endoplasmic Reticulum Stress in Chick Embryos

Cited by 24 publications

References 45 publications

Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1

Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1

Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis

Nano-sulforaphane attenuates PhIP-induced early abnormal embryonic neuro-development

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