Neuroprotective effects of genistein-3′-sodium sulfonate on focal cerebral ischemia in rats

Li, Liangdong; Xue, Jianming; Liu, Ruizhen; Xiao, Li; Lai, Lijuan; Xie, Jing; Huang, Zhihua; Huang, Cheng

doi:10.1016/j.neulet.2017.02.046

Cited by 24 publications

(28 citation statements)

References 15 publications

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“…Interestingly, a recent study reported that GSS could protect cortical neurons from focal cerebral ischaemia-induced apoptosis of neurons. 17 To explore the role of GSS on LPS-induced lung vascular EC apoptosis, we first explored the cytotoxicity of GSS in ECs using CCK-8 assays. The results demonstrated that although GSS slightly decreased cell viability in a dose-dependent manner, it had no obvious cytotoxicity to ECs.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have reported that GSS has a protective effect against focal cerebral ischaemia-induced cytotoxicity in rat cortical neurons by inhibiting cell apoptosis. 17 To determine whether GSS also protects ECs against LPS-induced apoptosis, the numbers of apoptotic ECs were quantified by an Annexin V/PI apoptosis kit. We found that LPS-induced EC apoptosis was significantly blocked by GSS (Figure 2A The BCL-2 family-mediated intrinsic apoptotic pathway plays a key role in LPS-induced EC apoptosis.…”

Section: Gss Protects Ecs Against Lps-induced Apoptosis Via Bcl-2mentioning

confidence: 99%

“…Genistein is a native isoflavone extracted from food sources such as tofu and beans, which has significant anti‐inflammatory and antioxidant pharmacological properties . Importantly, a recent study observed that genistein‐3′‐sodium sulphonate (GSS), a new derivative of genistein, has the anti‐apoptotic activity in focal cerebral ischaemia‐induced neuronal injury by inhibiting BCL‐2 family‐associated activation of the apoptotic pathway . These findings suggested that GSS might be involved in the regulation of LPS‐induced EC apoptosis processes.…”

Section: Introductionmentioning

confidence: 99%

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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%

Section: Gss Protects Ecs Against Lps-induced Apoptosis Via Bcl-2mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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“…Jeong et al demonstrated that genistein inhibited activation of microglial cells and release of inflammatory cytokines [19]. Other scholars recently revealed that GSS could protect cortical neurons from focal cerebral ischemia-induced apoptosis of neurocytes [5]. Therefore, it was of interest to understand the effects of GSS on LPS-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

“…Though genistein has many beneficial effects, its poor water solubility and fat solubility limits its widespread application [4]. To improve the bioavailability and activity of genistein, Li et al synthesized genistein-3 ′ -sodium sulfonate (GSS), a new compound derived from genistein that protected cortical neurons from ischemia-induced neuronal apoptosis [5]. However, there is no report about the effects of GSS on bacterial infection-induced acute lung injury (ALI) under sepsis condition until now.…”

Section: Introductionmentioning

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.

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Long‐term hypogonadism diminishes the neuroprotective effects of dietary genistein in young adult ovariectomized rats after transient focal ischemia

Oppong-Gyebi

Metzger

Doan

et al. 2021

J of Neuroscience Research

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Increasing age disproportionately increases the risk of stroke among women compared to men of similar age, especially after menopause. One of the reasons for this observation is a sharp drop in circulating estrogens. However, the timing of initiation of estrogen replacement after menopause is associated with mixed beneficial and detrimental effects, hence contributing to widespread mistrust of estrogen use. Agents including soy isoflavones are being assessed as viable alternatives to estrogen therapy. In this study, we hypothesized that the neuroprotective effects of genistein, a soy isoflavone are less sensitive to the length of hypogonadism in young adult ovariectomized rats following cerebral ischemia. We expected that long‐term hypogonadism will worsen motor and cognitive function, increase post‐stroke inflammation with no effect on the neuroprotection of genistein. We compared the effect of treatment with dietary genistein (GEN) on short‐term (2 weeks) and long‐term hypogonadism (12 weeks) in young adult ovariectomized Sprague–Dawley rats on sensorimotor function, cognition and inflammation after focal ischemia. Dorsal Silastic implant of 17β‐estradiol (E2) was used as a control for hormone therapy. Long‐term hypogonadism stroked rats performed worse than the short‐term hypogonadism stroked rats on the motor and cognitive function tests. GEN did not improve neurological assessment and motor learning after either short‐term or long‐term hypogonadism. GEN improved cognitive flexibility after short‐term hypogonadism but not after the long‐term. Both GEN and E2 reduced tissue loss after short‐term hypogonadism and reduced GFAP expression at the contralateral side of ischemia after long‐term hypogonadism. The length of hypogonadism may differentially influence the neuroprotective effects of both GEN and E2 on the motor and cognitive functions in young adult rats.

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Neuroprotective effects of genistein-3′-sodium sulfonate on focal cerebral ischemia in rats

Cited by 24 publications

References 15 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

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

Long‐term hypogonadism diminishes the neuroprotective effects of dietary genistein in young adult ovariectomized rats after transient focal ischemia

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