Isoliquiritigenin alleviates cerebral ischemia-reperfusion injury by reducing oxidative stress and ameliorating mitochondrial dysfunction via activating the Nrf2 pathway

Lan, Xiaobing; Wang, Qing; Liu, Yue; You, Qing; Wei, Wei; Zhu, Chunhao; Hai, Dongmei; Cai, Zhenyu; Yu, Jianqiang; Zhang, Jian; Liu, Ning

doi:10.1016/j.redox.2024.103406

Redox Biology

2024

DOI: 10.1016/j.redox.2024.103406

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Isoliquiritigenin alleviates cerebral ischemia-reperfusion injury by reducing oxidative stress and ameliorating mitochondrial dysfunction via activating the Nrf2 pathway

Xiaobing Lan,

Qing Wang,

Yue Liu

et al.

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2024

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Isoliquiritigenin attenuated cognitive impairment, cerebral tau phosphorylation and oxidative stress in a streptozotocin-induced mouse model of Alzheimer’s disease

Tang,

Sha,

Wang

et al. 2024

Preprint

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Introduction Tau hyperphosphorylation, mitochondrial dysfunction and oxidative stress play important roles in Alzheimer′s disease (AD). Isoliquiritigenin, a natural flavonoid isolated from the root of liquorice, has been shown to exert inhibitory effects on oxidative stress. Here, we assessed the neuroprotective effects of isoliquiritigenin on a streptozotocin-injected mouse model. Method Molecular docking analysis performed for isoliquiritigenin with mTOR and ERK2. The mice (n = 27, male) were intracerebroventricularly injected with streptozotocin, treated with isoliquiritigenin (intraperitoneal, 2 days) and assessed using the Morris water maze. Oxidative stress, tau phosphorylation, mitochondrial dysfunction and synaptic impairment were evaluated in the cortex and hippocampal tissues of the mice by using biochemical assays and immunofluorescence staining. Results Isoliquiritigenin treatment mitigated the spatial memory capacity of streptozotocin-injected mice and alleviated tau phosphorylation at Ser396; the production of reactive oxygen species; the mitochondrial fission proteins Mfn1 and Mfn2; neuronal loss; and synaptic impairment (PSD95, SNAP25). Isoliquiritigenin treatment reduced the levels of mTOR Ser2448 and ERK1/2 T202/Y204 and upregulated the level of GSK-3βSer9 in the cortex and hippocampus of streptozotocin-injected mice. Conclusion In conclusion, our findings suggest that isoliquiritigenin ameliorates streptozotocin-induced cognitive impairment, hyperphosphorylated tau, oxidative stress, mitochondrial dysfunction and synaptic impairment by decreasing mTOR and ERK activity and increasing GSK-3β activity.

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Isoliquiritigenin attenuated cognitive impairment, cerebral tau phosphorylation and oxidative stress in a streptozotocin-induced mouse model of Alzheimer’s disease

Tang,

Sha,

Wang

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

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Isoliquiritigenin alleviates cerebral ischemia-reperfusion injury by reducing oxidative stress and ameliorating mitochondrial dysfunction via activating the Nrf2 pathway

Cited by 1 publication

References 77 publications

Isoliquiritigenin attenuated cognitive impairment, cerebral tau phosphorylation and oxidative stress in a streptozotocin-induced mouse model of Alzheimer’s disease

Isoliquiritigenin attenuated cognitive impairment, cerebral tau phosphorylation and oxidative stress in a streptozotocin-induced mouse model of Alzheimer’s disease

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