6ʹʺ‐p‐Coumaroylspinosin protects PC12 neuronal cells from acrylamide‐induced oxidative stress and apoptosis

Li, Yaxin; Zhou, Aimin; Cui, Xusheng; Zhang, Yanqing; Xie, Junbo

doi:10.1111/jfbc.13321

Cited by 7 publications

(12 citation statements)

References 48 publications

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“…), hydrogen peroxide (H 2 O 2 ), and hydroxyl radicals (OH • ) [12], of which H 2 O 2 is a culprit, destroying neurons, and thus is widely used as a stimulant of neutral cells to establish an in vitro oxidative injury model [13,14]. In addition, acrylamide, a vinyl monomer formed in high-temperature foods [15], is applied as a neurotoxin in various cell and animal models for its overproduction of ROS. For instance, acrylamide was suggested to induce cell apoptosis in human neuroblastoma SH-SY5Y cells [16] and promote neurotoxicity in the zebrafish model [17].…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Protective Effect of Triphala against Oxidative Stress‐Induced Neurotoxicity

Ning

Tsering

et al. 2021

BioMed Research International

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Background. Oxidative stress is implicated in the progression of many neurological diseases, which could be induced by various chemicals, such as hydrogen peroxide (H2O2) and acrylamide. Triphala is a well-recognized Ayurvedic medicine that possesses different therapeutic properties (e.g., antihistamine, antioxidant, anticancer, anti-inflammatory, antibacterial, and anticariogenic effects). However, little information is available regarding the neuroprotective effect of Triphala on oxidative stress. Materials and Methods. An in vitro H2O2-induced SH-SY5Y cell model and an in vivo acrylamide-induced zebrafish model were established. Cell viability, apoptosis, and proliferation were examined by MTT assay, ELISA, and flow cytometric analysis, respectively. The molecular mechanism underlying the antioxidant activity of Triphala against H2O2 was investigated dose dependently by Western blotting. The in vivo neuroprotective effect of Triphala on acrylamide-induced oxidative injury in Danio rerio was determined using immunofluorescence staining. Results. The results indicated that Triphala plays a neuroprotective role against H2O2 toxicity in inhibiting cell apoptosis and promoting cell proliferation. Furthermore, Triphala pretreatment suppressed the phosphorylation of the mitogen-activated protein kinase (MARK) signal pathway (p-Erk1/2, p-JNK1/2, and p-p38), whereas it restored the activities of antioxidant enzymes (superoxide dismutase 1 (SOD1) and catalase) in the H2O2-treated SH-SY5Y cells. Consistently, similar protective effects of Triphala were observed in declining neuroapoptosis and scavenging free radicals in the zebrafish central neural system, possessing a critical neuroprotective property against acrylamide-induced oxidative stress. Conclusion. In summary, Triphala is a promising neuroprotective agent against oxidative stress in SH-SY5Y cells and zebrafishes with significant antiapoptosis and antioxidant activities.

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Section: Introductionmentioning

confidence: 99%

[Retracted] Protective Effect of Triphala against Oxidative Stress‐Induced Neurotoxicity

Ning

Tsering

et al. 2021

BioMed Research International

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“…In order to regulate the normal internal environment, cells are stable through a genetically spontaneous and orderly death called apoptosis 26 . It was reported that ACR exposure could activate the mitochondrial apoptotic pathway via activation of caspase 3 in PC12 cells and human neuroblastoma cells (SH‐SY5Y) 27,28 …”

Section: Resultsmentioning

confidence: 99%

“…Activation of caspase 9 was an early event in the mitochondrial involved apoptosis 5,32 . ACR has been reported that it could trigger the release of cleavage of caspase 9 and activate the mitochondrial apoptotic pathway in PC12 cells 27 . We used the activated caspase 9 antibody to determine the activated caspase 9 involved in the apoptosis pathway in PC12 and SK‐N‐SH cells treated with AA, ACR and AMPS.…”

Section: Resultsmentioning

confidence: 99%

Acrylamide, acrylic acid, or 2‐acrylamido‐2‐methyl‐1‐propanesulfonic acid induced cytotoxic in Photobacterium phosphoreum, PC12, and SK‐N‐SH cells

Shen

Wang

Zhao

et al. 2022

Environmental Toxicology

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In enhancing oil recovery, more and more new water-soluble polymers are developed to replace the high toxicity and low stability acrylamide (ACR) monomer. The common replacement monomer is acrylic acid (AA) and 2-acrylamido-2-methylamido-2-methyl-1-propanesulfonic acid (AMPS), which are considered safe and efficient. In this study, AA, ACR and AMPS caused remarkable cytotoxicity in Photobacterium phosphoreum, the rat pheochromocytoma cells (PC12) and the Human neuroblastoma cells (SK-N-SH). ACR is much more lethal than AA and AMPS in PC12 and SK-N-SH cells, meanwhile, the toxicity of AA and AMPS decreases with the decrease of acid.Furthermore, similar to ACR, AA, and AMPS can induce severe DNA double-strand breakage in PC12 and SK-N-SH cells. Both AA and ACR can cause cell cycle arrest in the G0/G1 phase in PC12 and SK-N-SH cells. In addition, like ACR, AA, and AMPS can generate reactive oxygen species (ROS) accumulation, mitochondrial dysfunction and mitochondrial-dependent apoptosis in both PC12 and SK-N-SH cells. The acute toxicity of AA and AMPS is lower than ACR, however, the decline in acute toxicity in monomers does not mean toxic-free. We should focus on the toxicity of AA and ACR and reduce occupational contact to protect employee occupational health.2-acrylamido-2-methyl-1-propanesulfonic acid, acrylamide, acrylic acid, cytotoxicity | INTRODUCTIONPolymer flooding is an effective method of enhancing oil recovery in the middle and later stages of oil recovery water flooding. Polyacrylamide is one of the most widely used water-soluble polymers in enhancing oil recovery. Due to the high salt concentration, the high temperature and the long recovery time of tertiary oil, the stability of the polymer is an important peculiarity. The new polymers with acrylic acid (AA), acrylamide (ACR), and 2-acrylamido-2-methyl-1-propanes ulfonic acid (AMPS) as widely used monomers have been developed widely, which is called with the characteristics of salt tolerance, heat resistance and stability water-soluble. [1][2][3] Since the extremely toxic acrylamide has been all or partly replaced with a less harmful monomer that is, AA and/or AMPS, the new polymers were thought to be more suitable. 4 Due to the environmental and occupational exposure to the raw material, the residual and released monomer from the polymers, are they safe? Acrylamide (ACR) is a water-soluble vinyl monomer, which is a low molecular weight, colorless and odorless crystalline substance. 5,6 ACR is vastly produced for the synthesis of polyacrylamides and widely used in various industries, such as water and wastewater management, soil coagulation, cosmetic manufacturing, dye synthesis and scientific laboratories for the gel electrophoretic separation of macromolecules. 6,7 In 1994, acrylamide was classified as potentially carcinogenic to humans by the International Agency for Research on Cancer (IARC).

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“…Administration of 6ʹʺ-p-coumaroylspinosin (P-CS) (flavonoid isolated from Ziziphi Spinosae Semen) on PC12 neuronal cells significantly prevents acrylamide-induced cell death, decreases GSH content, and ROS overproduction. P-CS was also suppressing the expression of Bax (apoptosis regulator) and Bim (pro-apoptotic protein) induced by acrylamide and inhibits the JNKs pathway [16].…”

Section: Role Of Flavonoids In Oxidative Stressmentioning

confidence: 96%

Flavonoids: Potential Candidates for the Treatment of Neuro-Degenerative Disorders

Devi¹,

Kumar²,

Singh³

et al. 2021

Preprint

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Neurodegenerative disorders such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Amyloidal lateral sclerosis (ALS), and Huntington disease (HD) are the most concerned disorders due to the lack of effective therapeutics and dramatic rise in affected cases. Although these disorders have diverse clinical manifestations, yet they all share a common cellular stress response. These cellular stress responses including neuroinflammation, oxidative stress, proteotoxicity, and ER-stress, which combats with stress conditions, but the overwhelming cellular stress response induces cell damage. Small molecules such as flavonoids could reduce cellular stress and have gained much attention in recent years. Evidence has shown the potential use of flavonoids in several ways such as antioxidants, anti-inflammatory, and anti-apoptotic, yet their mechanism is still elusive. This review provides an insight into the mechanistic ways of flavonoids against cellular stress response that prevent the pathogenesis of neurodegenerative disorders.

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6ʹʺ‐p‐Coumaroylspinosin protects PC12 neuronal cells from acrylamide‐induced oxidative stress and apoptosis

Cited by 7 publications

References 48 publications

[Retracted] Protective Effect of Triphala against Oxidative Stress‐Induced Neurotoxicity

[Retracted] Protective Effect of Triphala against Oxidative Stress‐Induced Neurotoxicity

Acrylamide, acrylic acid, or 2‐acrylamido‐2‐methyl‐1‐propanesulfonic acid induced cytotoxic in Photobacterium phosphoreum, PC12, and SK‐N‐SH cells

Flavonoids: Potential Candidates for the Treatment of Neuro-Degenerative Disorders

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