Protective Effects of Genistein against Mono-(2-ethylhexyl) Phthalate-Induced Oxidative Damage in Prepubertal Sertoli Cells

Zhang, Liandong; Gao, Ming; Zhang, Tongdian; Chong, Tie; Wang, Ziming; Zhai, Xiaoqiang; Wu, Zhi‐Zhong; Li, Hecheng

doi:10.1155/2017/2032697

Cited by 31 publications

(16 citation statements)

References 38 publications

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“…30 Previous studies have investigated the role of genistein in brain injury and found that genistein has significant anti-inflammatory and anti-oxidative properties. [31][32][33] However, the poor water solubility of genistein restricted its wide use in the clinic.…”

Section: Discussionmentioning

confidence: 99%

Genistein‐3′‐sodium sulphonate protects against lipopolysaccharide‐induced lung vascular endothelial cell apoptosis and acute lung injury via BCL‐2 signalling

Lee

Chang

Zhao

et al. 2019

J Cellular Molecular Medi

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Under septic conditions, Lipopolysaccharide (LPS)‐induced apoptosis of lung vascular endothelial cells (ECs) triggers and aggravates acute lung injury (ALI), which so far has no effective therapeutic options. Genistein‐3′‐sodium sulphonate (GSS) is a derivative of native soy isoflavone, which has neuro‐protective effects through its anti‐apoptotic property. However, whether GSS protects against sepsis‐induced lung vascular endothelial cell apoptosis and ALI has not been determined. In this study, we found that LPS‐induced Myd88/NF‐κB/BCL‐2 signalling pathway activation and subsequent EC apoptosis were effectively down‐regulated by GSS in vitro. Furthermore, GSS not only reversed the sepsis‐induced BCL‐2 changes in expression in mouse lungs but also blocked sepsis‐associated lung vascular barrier disruption and ALI in vivo. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis‐induced ALI via its regulating effects on Myd88/NF‐κB/BCL‐2 signalling in lung ECs.

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Section: Discussionmentioning

confidence: 99%

Genistein‐3′‐sodium sulphonate protects against lipopolysaccharide‐induced lung vascular endothelial cell apoptosis and acute lung injury via BCL‐2 signalling

Lee

Chang

Zhao

et al. 2019

J Cellular Molecular Medi

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“…In addition, treatment of neonatal rats with low levels of di (2-ethylhexyl) phthalate (DEHP) and its metabolite, MEHP, induces a decrease in Sertoli cell proliferation accompanied by a decrease in cyclin D2 levels (306). More recently, it has been shown that MEHP can disrupt prepubertal Sertoli cell proliferation by increasing intracellular ROS levels (307). On the other hand, it has been shown that another plasticizer of the phthalate family, mono-n-butyl phthalate (MBP), induces immature Sertoli cell proliferation up-regulating ERK1/2 signaling pathway (308).…”

Section: Pharmacological Agents and Xenobiotics May Affect Sertoli Cementioning

confidence: 99%

Molecular Mechanisms and Signaling Pathways Involved in Sertoli Cell Proliferation

et al. 2019

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Sertoli cells are somatic cells present in seminiferous tubules which have essential roles in regulating spermatogenesis. Considering that each Sertoli cell is able to support a limited number of germ cells, the final number of Sertoli cells reached during the proliferative period determines sperm production capacity. Only immature Sertoli cells, which have not established the blood-testis barrier, proliferate. A number of hormonal cues regulate Sertoli cell proliferation. Among them, FSH, the insulin family of growth factors, activin, and cytokines action must be highlighted. It has been demonstrated that cAMP/PKA, ERK1/2, PI3K/Akt, and mTORC1/p70SK6 pathways are the main signal transduction pathways involved in Sertoli cell proliferation. Additionally, c-Myc and hypoxia inducible factor are transcription factors which participate in the induction by FSH of various genes of relevance in cell cycle progression. Cessation of proliferation is a pre-requisite to Sertoli cell maturation accompanied by the establishment of the blood-testis barrier. With respect to this barrier, the participation of androgens, estrogens, thyroid hormones, retinoic acid and opioids has been reported. Additionally, two central enzymes that are involved in sensing cell energy status have been associated with the suppression of Sertoli cell proliferation, namely AMPK and Sirtuin 1 (SIRT1). Among the molecular mechanisms involved in the cessation of proliferation and in the maturation of Sertoli cells, it is worth mentioning the up-regulation of the cell cycle inhibitors p21Cip1, p27Kip, and p19INK4, and of the gap junction protein connexin 43. A decrease in Sertoli cell proliferation due to administration of certain therapeutic drugs and exposure to xenobiotic agents before puberty has been experimentally demonstrated. This review focuses on the hormones, locally produced factors, signal transduction pathways, and molecular mechanisms controlling Sertoli cell proliferation and maturation. The comprehension of how the final number of Sertoli cells in adulthood is established constitutes a pre-requisite to understand the underlying causes responsible for the progressive decrease in sperm production that has been observed during the last 50 years in humans.

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“…Increased cytokines, such as TNF-α and IL-6, are hallmarks of many human inflammatory states, including sepsis [30,31]. Previous data have suggested protective effects of genistein such as antitumor, antioxidative, and antiapoptotic functions [32][33][34]; however, the anti-inflammatory effect of GSS, a new compound derived from genistein, is still incompletely understood. In the present study, we demonstrated that the GSS was able to inhibit LPS-induced lung microvascular EC injury and sepsis-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-αand IL-6

Lee

Zhou

Zheng

et al. 2019

Mediators of Inflammation

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Background. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3′-sodium sulfonate (GSS) is a derivative of native soy isoflavone, which exhibits neuroprotective effects via its antiapoptosis property. However, whether GSS protect against sepsis-induced EC injury and release of inflammatory mediators has not been determined. In this study, we found that GSS not only downregulated the levels of TNF-α and IL-6 in the lung and serum of mice in vivo but also inhibited the expression and secretion of TNF-α and IL-6 in ECs. Importantly, we also found that GSS blocked LPS-induced TNF-α and IL-6 expression in ECs via the Myd88/NF-κB signaling pathway. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis-induced ALI via its regulating effects on inflammatory response in lung ECs.

show abstract

Protective Effects of Genistein against Mono-(2-ethylhexyl) Phthalate-Induced Oxidative Damage in Prepubertal Sertoli Cells

Cited by 31 publications

References 38 publications

Genistein‐3′‐sodium sulphonate protects against lipopolysaccharide‐induced lung vascular endothelial cell apoptosis and acute lung injury via BCL‐2 signalling

Genistein‐3′‐sodium sulphonate protects against lipopolysaccharide‐induced lung vascular endothelial cell apoptosis and acute lung injury via BCL‐2 signalling

Molecular Mechanisms and Signaling Pathways Involved in Sertoli Cell Proliferation

Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-αand IL-6

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