Glycosides of Buyang Huanwu decoction inhibits pyroptosis associated with cerebral ischemia-reperfusion through Nrf2-mediated antioxidant signaling pathway both in vivo and in vitro

She, Yan; Shao, Le; Jiao, Kai; Sun, Ruiting; Láng, Tibor; Long, Hong‐Ping; Tang, Yinghong; Zhang, Wei; Ding, Changsong; Deng, Chang-Qing

doi:10.1016/j.phymed.2023.155001

Cited by 5 publications

(3 citation statements)

References 19 publications

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“… Crebabine, an alkaloid with neuroprotective effects, was shown to be effective in a murine model of stroke, reducing cerebral damage by suppressing NADPH and NOX2 activity and through the inhibition of the NF-κB and MAPK pathways [ 87 ]. Glycosides, derived from the Buyang Huanwu Decoction, exert a neuroprotective effect in murine stroke models by reducing pyroptosis by regulating the Nrf2 pathway [ 88 ]. The Krüppel-like factor 4 (KLF4) is a transcription factor related to several cell processes, such as cell proliferation and apoptosis.…”

Section: Antioxidant Bioactive Molecules Against Ischemic Strokementioning

confidence: 99%

“…Glycosides, derived from the Buyang Huanwu Decoction, exert a neuroprotective effect in murine stroke models by reducing pyroptosis by regulating the Nrf2 pathway [ 88 ].…”

Section: Antioxidant Bioactive Molecules Against Ischemic Strokementioning

confidence: 99%

“…Glycosides, derived from the Buyang Huanwu Decoction, exert a neuroprotective effect in murine stroke models by reducing pyroptosis by regulating the Nrf2 pathway [88]. • The Krüppel-like factor 4 (KLF4) is a transcription factor related to several cell processes, such as cell proliferation and apoptosis.…”

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confidence: 99%

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Novel Multi-Antioxidant Approach for Ischemic Stroke Therapy Targeting the Role of Oxidative Stress

Briones-Valdivieso,

Briones,

Orellana-Urzúa

et al. 2024

Biomedicines

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Stroke is a major contributor to global mortality and disability. While reperfusion is essential for preventing neuronal death in the penumbra, it also triggers cerebral ischemia-reperfusion injury, a paradoxical injury primarily caused by oxidative stress, inflammation, and blood–brain barrier disruption. An oxidative burst inflicts marked cellular damage, ranging from alterations in mitochondrial function to lipid peroxidation and the activation of intricate signalling pathways that can even lead to cell death. Thus, given the pivotal role of oxidative stress in the mechanisms of cerebral ischemia-reperfusion injury, the reinforcement of the antioxidant defence system has been proposed as a protective approach. Although this strategy has proven to be successful in experimental models, its translation into clinical practice has yielded inconsistent results. However, it should be considered that the availability of numerous antioxidant molecules with a wide range of chemical properties can affect the extent of injury; several groups of antioxidant molecules, including polyphenols, carotenoids, and vitamins, among other antioxidant compounds, can mitigate this damage by intervening in multiple signalling pathways at various stages. Multiple clinical trials have previously been conducted to evaluate these properties using melatonin, acetyl-L-carnitine, chrysanthemum extract, edaravone dexborneol, saffron, coenzyme Q10, and oleoylethanolamide, among other treatments. Therefore, multi-antioxidant therapy emerges as a promising novel therapeutic option due to the potential synergistic effect provided by the simultaneous roles of the individual compounds.

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Section: Antioxidant Bioactive Molecules Against Ischemic Strokementioning

confidence: 99%

“…Glycosides, derived from the Buyang Huanwu Decoction, exert a neuroprotective effect in murine stroke models by reducing pyroptosis by regulating the Nrf2 pathway [ 88 ].…”

Section: Antioxidant Bioactive Molecules Against Ischemic Strokementioning

confidence: 99%