Genistein protects epilepsy-induced brain injury through regulating the JAK2/STAT3 and Keap1/Nrf2 signaling pathways in the developing rats

Hu, Qing-peng; Yan, Hong-xia; Peng, Fang; Feng, Wei; Chen, Fenfang; Huang, Xiangyi; Zhang, Xin; Zhou, Yang; Chen, Yi-Shui

doi:10.1016/j.ejphar.2021.174620

Cited by 23 publications

(9 citation statements)

References 59 publications

(14 reference statements)

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“…Genistein is the main ingredient of isoflavone from soybean and is also used as a tyrosine kinase inhibitor. It has potent effects of antioxidant, anti-inflammatory, anti-angiogenesis, and anti-cancer [ 131 ]. Studies have shown that genistein can increase GSH levels and GPX activity along with decreased oxidative stress in diabetic cardiomyopathy and DOX-mediated cardiomyopathy [ 132 , 133 ].…”

Section: Strategies For Gsh System Activationmentioning

confidence: 99%

“…Meanwhile, genistein increased the levels of Nrf2, which is vital to the GSH system [ 132 – 134 ]. Genistein administration induced Nrf2 enhancement by activation/phosphorylation of keap1, sirt1, MAPK-ERK1/2, PKC, and estrogen receptor in other cells or tissues, such as: hippocampal tissue, hypothalamic paraventricular nucleus, ovary, and Caco-2 cells [ 131 , 135 – 137 ]. However, it is unclear why genistein upregulates the levels of Nrf2 in the myocardium.…”

Section: Strategies For Gsh System Activationmentioning

confidence: 99%

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Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Tan

Yin

et al. 2023

Cell Death Dis

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The glutathione (GSH) system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species (ROS). Numerous investigations have suggested that disruption of the GSH system is a critical element in the pathogenesis of myocardial injury. Meanwhile, a newly proposed type of cell death, ferroptosis, has been demonstrated to be closely related to the GSH system, which affects the process and outcome of myocardial injury. Moreover, in facing various pathological challenges, the mammalian heart, which possesses high levels of mitochondria and weak antioxidant capacity, is susceptible to oxidant production and oxidative damage. Therefore, targeted enhancement of the GSH system along with prevention of ferroptosis in the myocardium is a promising therapeutic strategy. In this review, we first systematically describe the physiological functions and anabolism of the GSH system, as well as its effects on cardiac injury. Then, we discuss the relationship between the GSH system and ferroptosis in myocardial injury. Moreover, a comprehensive summary of the activation strategies of the GSH system is presented, where we mainly identify several promising herbal monomers, which may provide valuable guidelines for the exploration of new therapeutic approaches.

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Section: Strategies For Gsh System Activationmentioning

confidence: 99%

Section: Strategies For Gsh System Activationmentioning

confidence: 99%

Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Tan

Yin

et al. 2023

Cell Death Dis

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“…A recent study by Kishore M et al suggested that the development of EP might be inhibited by modulating the Keap1/Nrf2 axis, 12 but they did not experimentally validate this. In addition, a study by Hu QP et al found that Genistein protects EP-induced brain injury by regulating the JAK2/STAT3 and Keap1/Nrf2 signaling pathways in the developing rats, 13 which further confirmed the important role of Keap1/Nrf2 in EP. However, although these studies have preliminarily confirmed the relationship between Keap1/Nrf2 and EP, the mechanism of Keap1/Nrf2′s effect on EP needs to be studied and analyzed in greater depth.…”

Section: Introductionmentioning

confidence: 81%

Keap1/Nrf2 signaling pathway participating in the progression of epilepsy via regulation of oxidative stress and ferroptosis in neurons

Wang,

Cui,

Gao

et al. 2024

Clinics

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“…The ability of quercetin, genistein, and procyanidin B2 to activate the Nrf2/ARE pathway has been previously demonstrated in numerous experimental models [ 63 , 64 , 65 , 66 , 67 ]. In this study, both quercetin and genistein treatments alone did not increase the p-Nrf2/Nrf2 ratio in BEAS-2B cells significantly ( p > 0.05).…”

Section: Discussionmentioning

confidence: 99%

Genistein and Procyanidin B2 Reduce Carcinogen-Induced Reactive Oxygen Species and DNA Damage through the Activation of Nrf2/ARE Cell Signaling in Bronchial Epithelial Cells In Vitro

Suraweera

Merlin

Dellaire

et al. 2023

IJMS

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Cancer is one of the leading causes of death worldwide. Chemotherapy and radiation therapy are currently providing the basis for cancer therapies, although both are associated with significant side effects. Thus, cancer prevention through dietary modifications has been receiving growing interest. The potential of selected flavonoids in reducing carcinogen-induced reactive oxygen species (ROS) and DNA damage through the activation of nuclear factor erythroid 2 p45 (NF-E2)-related factor (Nrf2)/antioxidant response element (ARE) pathway was studied in vitro. Dose-dependent effects of pre-incubated flavonoids on pro-carcinogen 4-[(acetoxymethyl)nitrosamino]-1-(3-pyridyl)-1-butanone (NNKAc)-induced ROS and DNA damage in human bronchial epithelial cells were studied in comparison to non-flavonoids. The most effective flavonoids were assessed for the activation of Nrf2/ARE pathway. Genistein, procyanidin B2 (PCB2), and quercetin significantly suppressed the NNKAc-induced ROS and DNA damage. Quercetin significantly upregulated the phosphorylated protein kinase B/Akt. PCB2 significantly upregulated the activation of Nrf2 and Akt through phosphorylation. Genistein and PCB2 significantly upregulated the phospho-Nrf2 nuclear translocation and catalase activity. In summary, genistein and PCB2 reduced the NNKAc-induced ROS and DNA damage through the activation of Nrf2. Further studies are required to understand the role of dietary flavonoids on the regulation of the Nrf2/ARE pathway in relation to carcinogenesis.

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Genistein protects epilepsy-induced brain injury through regulating the JAK2/STAT3 and Keap1/Nrf2 signaling pathways in the developing rats

Cited by 23 publications

References 59 publications

Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Keap1/Nrf2 signaling pathway participating in the progression of epilepsy via regulation of oxidative stress and ferroptosis in neurons

Genistein and Procyanidin B2 Reduce Carcinogen-Induced Reactive Oxygen Species and DNA Damage through the Activation of Nrf2/ARE Cell Signaling in Bronchial Epithelial Cells In Vitro

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