Neuroprotective effect of apocynin nitrone in oxygen glucose deprivation-treated SH-SY5Y cells and rats with ischemic stroke

Liu, Wu; Feng, Guoshuai; Ou, Yvonne; Xu, Jianxing; Zhang, Zaijun; Zhang, Gaoxiao; Sun, Yi; Li, Sha; Jiang, Jie

doi:10.4314/tjpr.v15i8.13

Cited by 5 publications

(7 citation statements)

References 25 publications

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“…At the same time, 100 µM AP pretreatment conferred significant protection up to 94% against Fb1-induced cell loss (Figure 6 A(c)). This result is in agreement with a previous report by Liu et al (2016) that demonstrated the neuroprotective effect of AP nitrone in oxygen glucose deprivation-treated SH-SY5Y cells and rats with ischemic stroke. The protective effect of AP was confirmed by morphological observation using a bright-field microscope (Figure 6B).…”

Section: Mtt and Ldhsupporting

confidence: 94%

Apocynin exerts neuroprotective effects in fumonisin b1–induced neurotoxicity via attenuation of oxidative stress and apoptosis in an animal model

Krishnaswamy,

Manasa,

Khan

et al. 2024

Journal of Food Science

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The Fusarium verticillioides produces a mycotoxin, that is, fumonisin b1 (Fb1), which commonly infects corn and agricultural commodities. The Fb1 showed hepatotoxicity, neurotoxicity, and carcinogenicity in animals. Hence, the present investigation aimed to evaluate the effect of apocynin (AP) on Fb1‐induced neurotoxic effects and its mechanism in the mice model and cell line. The male Balb/c mice, with the 6.75 mg/kg bwt of Fb1 were injected subcutaneously for 5 days to induce neurotoxicity. A significant elevation of serotonin (5‐HT) was observed in mice treated with Fb1 in the whole brain showing biogenic amines may reflect Fb1 neurotoxicity, but the negatively regulated mechanisms were attenuated by the pretreatment of AP. In addition, AP pretreatment normalized apoptotic changes in histology and immunohistochemistry studies. In Western blotting studies, apoptotic genes were upregulated and oxidative stress genes were downregulated due to Fb1 treatment; while treating with AP, these gene expressions were rectified. Further cell cytotoxicity was investigated by MTT and lactate dehydrogenase (LDH) assays in SH‐SY5Y cell line. MTT and LDH assays indicated the IC50 value to be 150 µM of Fb1, which was protected by 100 µg of AP. The electron microscopy evaluated the Fb1‐induced apoptotic conditions and its cell morphology recovery by AP. These results suggest that nicotinamide adenine dinucleotide phosphate hydrogen oxidase–mediated reactive oxygen species is the primary upstream signal leading to increased Fb1‐mediated neurotoxicity in mice. The use of the antioxidant AP reversed the toxin‐induced oxidative stress and apoptosis by its antioxidant potency.

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Section: Mtt and Ldhsupporting

confidence: 94%

Apocynin exerts neuroprotective effects in fumonisin b1–induced neurotoxicity via attenuation of oxidative stress and apoptosis in an animal model

Krishnaswamy,

Manasa,

Khan

et al. 2024

Journal of Food Science

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“…Several steps of the ischemic cascade have been targeted by pharmacological treatment strategies to prevent irreversible neuronal damage. Thirty-six studies in undifferentiated SH-SY5Y cell models (Chen et al 2021b ; Dong et al 2021 ; Gao et al 2017 ; Hao et al 2015 ; Hong et al 2017 ; Hsieh et al 2021 ; Huang et al 2021 ; Janssen et al 2021 ; Jiang et al 2012 ; Jimenez-Almarza et al 2019 ; Lai et al 2020 ; Landgraf et al 2020 ; Li et al 2019a , b , 2020a ; Lin-Holderer et al 2016 ; Liu et al 2016 , 2019a , b ; Liu 2016 ; Luan et al 2013 ; Marutani et al 2012 ; Park et al 2017 ; Ruan et al 2021 ; Shi et al 2019 ; Song et al 2019 ; Wang et al 2013 , 2019b , c , 2021a ; Wu et al 2020a , b ; Xu et al 2020b ; Yang et al 2014 ; Zappala et al 2021 ; Zhi et al 2020 ), seven in differentiated SH-SY5Y cell models (Cheng et al 2014 , 2019 ; Fu et al 2020 ; Lin et al 2011 ; Sriwastva et al 2020 ; Zeng et al 2019 ; Zhang et al 2019b ), two in undifferentiated SK-N-SH cell models (Lehane et al 2013 ; Soh et al 2007 ), and one in hiPSC-derived neurons (Pires Monteiro et al 2021 ) included treatment with a pharmacological compound. Treatment targets were neuronal activity, oxidative/nitrosative stress, inflammation, autophagy or cell death.…”

Section: Resultsmentioning

confidence: 99%

Neuronal Responses to Ischemia: Scoping Review of Insights from Human-Derived In Vitro Models

2023

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Translation of neuroprotective treatment effects from experimental animal models to patients with cerebral ischemia has been challenging. Since pathophysiological processes may vary across species, an experimental model to clarify human-specific neuronal pathomechanisms may help. We conducted a scoping review of the literature on human neuronal in vitro models that have been used to study neuronal responses to ischemia or hypoxia, the parts of the pathophysiological cascade that have been investigated in those models, and evidence on effects of interventions. We included 147 studies on four different human neuronal models. The majority of the studies (132/147) was conducted in SH-SY5Y cells, which is a cancerous cell line derived from a single neuroblastoma patient. Of these, 119/132 used undifferentiated SH-SY5Y cells, that lack many neuronal characteristics. Two studies used healthy human induced pluripotent stem cell derived neuronal networks. Most studies used microscopic measures and established hypoxia induced cell death, oxidative stress, or inflammation. Only one study investigated the effect of hypoxia on neuronal network functionality using micro-electrode arrays. Treatment targets included oxidative stress, inflammation, cell death, and neuronal network stimulation. We discuss (dis)advantages of the various model systems and propose future perspectives for research into human neuronal responses to ischemia or hypoxia. Graphical Abstract

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“…A growing body of evidence supported that the occurrence of diverse brain diseases is closely related to oxidative stress [36] and the SH-SY5Y cells are recognized as a common model for evaluating the function of nerve cells [37]. In order to explore the neuroprotective activity of diosgenin-amino acids derivatives [38,39,40,41,42], the model of 2,4,5-Trihydroxybutyrophenone (TBHP)-induced neurotoxicity in SH-SY5Y cells has been used as an in vitro research platform in this study. The results were expressed as EC 50 values in Table 2.…”

Section: Resultsmentioning

confidence: 99%

Design, Synthesis and Biological Evaluation of Diosgenin-Amino Acid Derivatives with Dual Functions of Neuroprotection and Angiogenesis

Cai

Yang

et al. 2019

Molecules

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Diosgenin, a natural product with steroidal structure, has a wide range of clinical applications in China. It also shows great potential in the treatment of blood clots and nerve damage. To enhance the bioavailability as well as efficacy of diosgenin, eighteen diosgenin-amino acid derivatives were designed and synthesized. The neuroprotective effects of these compounds were evaluated by SH-SY5Y cell line and the biosafety was evaluated by H9c2 cell line. The results displayed that part of the derivatives’ activities (EC50 < 20 μM) were higher than positive control edaravone (EC50 = 21.60 ± 3.04 μM), among which, DG-15 (EC50 = 6.86 ± 0.69 μM) exhibited the best neuroprotection. Meanwhile, biosafety evaluation showed that DG-15 had no cytotoxicity on H9c2 cell lines. Interestingly, combined neuroprotective and cytotoxic results, part of the derivatives without their protecting group were superior to compounds with protecting group. Subsequently, Giemsa staining and DAPI (4′,6-diamidino-2-phenylindole) staining indicated that DG-15 had a protective effect on damaged SH-SY5Y cells by reducing apoptosis. Moreover, DG-15 showed a higher role in promoting angiogenesis at high concentrations (4 mg/mL) on the chorioallantoic membrane model. This finding displayed that DG-15 had dual functions of neuroprotection and angiogenesis, which provided further insight into designing agent for the application in treatment of ischemic stroke.

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Neuroprotective effect of apocynin nitrone in oxygen glucose deprivation-treated SH-SY5Y cells and rats with ischemic stroke

Cited by 5 publications

References 25 publications

Apocynin exerts neuroprotective effects in fumonisin b1–induced neurotoxicity via attenuation of oxidative stress and apoptosis in an animal model

Apocynin exerts neuroprotective effects in fumonisin b1–induced neurotoxicity via attenuation of oxidative stress and apoptosis in an animal model

Neuronal Responses to Ischemia: Scoping Review of Insights from Human-Derived In Vitro Models

Design, Synthesis and Biological Evaluation of Diosgenin-Amino Acid Derivatives with Dual Functions of Neuroprotection and Angiogenesis

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