Preventive Effects of Sinigrin Against the Memory Deterioration in the Pentylenetetrazole-Kindled Male Wistar Rats: Possible Modulation of NLRP3 Pathway

Aghaie, Fatemeh; Rajabi, Mojgan; Hosseini, Amin; Moradifar, Fatemeh; Koneshlou, Samaneh; Hosseini, Abdolkarim

doi:10.1007/s12017-021-08690-y

Cited by 6 publications

(2 citation statements)

References 35 publications

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“…(Cong et al., 2021) Moreover, sinigrin has been reported to have memory‐improving and anticonvulsant effects on pentylenetetrazole‐induced epilepsy in rats. (Aghaie et al., 2021) However, the therapeutic effect of sinigrin on CIR injury is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Sinigrin improves cerebral ischaemia‐reperfusion injury by inhibiting the TLR4 pathway‐mediated oxidative stress

Guo,

Lei,

Yang

et al. 2024

Chem Biol Drug Des

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Cerebral ischaemia‐reperfusion (CIR) injury occurs in stroke patients after the restoration of cerebral perfusion. Sinigrin, a phytochemical found in cruciferous vegetables, exhibits strong antioxidant activity. This study investigated the role of sinigrin in oxidative stress using a CIR injury model. The effects of sinigrin were studied in middle cerebral artery occlusion (MCAO) rats and oxygen–glucose deprivation/reoxygenation (OGD/R)‐injured SH‐SY5Y cells. Sinigrin treatment improved brain injury and neurological deficits induced by MCAO surgery in rats. Sinigrin inhibited apoptosis in brain tissues and SH‐SY5Y cells following OGD/R induction. Additionally, sinigrin elevated the levels of superoxide dismutase (SOD), glutathione (GSH) and glutathione peroxidase (GSH‐Px) while reducing malondialdehyde (MDA) levels. Furthermore, sinigrin inhibited the toll‐like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signalling pathway. The anti‐apoptotic and antioxidant activities of sinigrin in OGD/R‐injured SH‐SY5Y cells were reversed by TLR4 overexpression. In conclusion, sinigrin inhibits oxidative stress in CIR injury by suppressing the TLR4/MyD88 signalling pathway.

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Section: Introductionmentioning

confidence: 99%

Sinigrin improves cerebral ischaemia‐reperfusion injury by inhibiting the TLR4 pathway‐mediated oxidative stress

Guo,

Lei,

Yang

et al. 2024

Chem Biol Drug Des

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show abstract

“…Similar to other avonoids, apigenin showed noteworthy antioxidant activities and potent free radical scavenging ability in in vitro and in vivo experimental models (Aghaie et al 2021, Singh et al 2020. In this study, apigenin pretreatment signi cantly restored enzymatic (SOD, CAT, GR and GPx) and nonenzymatic (GSH) antioxidants compared with MSG treatment.…”

Section: Discussionmentioning

confidence: 97%

Monosodium glutamate induces cortical oxidative, apoptotic, and inflammatory challenges in rats: the potential neuroprotective role of apigenin

Albrakati

2022

Environ Sci Pollut Res

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Monosodium glutamate (MSG) is used as a avor, and a taste enhancer was reported to evoke marked neuronal impairments. This study investigated the neuroprotective ability of avonoid apigenin against neural damage in MSG-administered rats. Adult male rats were allocated into four groups; control, apigenin (20 mg/kg, orally), MSG (4 g/kg, orally), and apigenin + MSG at the aforementioned doses for 30 days. Regarding the levels of neurotransmitters, our results revealed that apigenin augmented the activity of acetylcholinesterase (AChE) markedly, and levels of brain monoamines (dopamine, norepinephrine, and serotonin) accompanied by lessening the activity of monoamine oxidase (MAO) as compared to MSG treatment. Moreover, apigenin counteracted the MSG-mediated oxidative stress by decreasing the malondialdehyde (MDA) levels together with elevating the glutathione (GSH) levels. In addition, pretreatment with apigenin induced notable increases in the activities of cortical superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR). Further, apigenin attenuated the cortical in ammatory stress as indicated by lower levels of pro-in ammatory mediators as interleukin-1 b (IL-1b), tumor necrosis factor-α (TNF-α), and nitric oxide (NO) as well as downregulated inducible nitric oxide synthase (iNOS) expression levels. Histopathological screening validated the abovementioned results and revealed that apigenin restored the distorted cytoarchitecture of the brain cortex. Thus, the present ndings collectively suggest that apigenin exerted signi cant protection against MSG-induced neurotoxicity by enhancing the cellular antioxidant response and attenuating in ammatory machineries in the rat brain cortex.

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Neuroprotective role of chlorogenic acid against hippocampal neuroinflammation, oxidative stress, and apoptosis following acute seizures induced by pentylenetetrazole

Althagafi

2024

Metab Brain Dis

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Preventive Effects of Sinigrin Against the Memory Deterioration in the Pentylenetetrazole-Kindled Male Wistar Rats: Possible Modulation of NLRP3 Pathway

Cited by 6 publications

References 35 publications

Sinigrin improves cerebral ischaemia‐reperfusion injury by inhibiting the TLR4 pathway‐mediated oxidative stress

Sinigrin improves cerebral ischaemia‐reperfusion injury by inhibiting the TLR4 pathway‐mediated oxidative stress

Monosodium glutamate induces cortical oxidative, apoptotic, and inflammatory challenges in rats: the potential neuroprotective role of apigenin

Neuroprotective role of chlorogenic acid against hippocampal neuroinflammation, oxidative stress, and apoptosis following acute seizures induced by pentylenetetrazole

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