Toxic effect of acrylamide on the development of hippocampal neurons of weaning rats

Lai, Sheng-min; Gu, Ziting; Zhao, Ming; Li, Xixia; Ma, Yuxin; Luo, Li; Liu, Jing

doi:10.4103/1673-5374.217345

Cited by 32 publications

(8 citation statements)

References 53 publications

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“…Nissl body, the important component of nerve cells, is involved in the regulation of advanced brain activities such as memory and learning 36 . The production of Nissl bodies is regarded to be essential for the maintenance of neuronal function 28 . Our present study revealed that SEV decreased the number of Nissl bodies, which were increased dramatically by engeletin in a concentration‐dependent way.…”

Section: Discussionsupporting

confidence: 46%

“…The Nissl body, a chromotropic substance in the cytoplasm of neuronal dendrites, usually presents in a fixed form that can be destroyed during brain injury. Hence, the morphology of Nissl body is commonly employed to identify the state of neurons 28 . Nissl staining analysis showed that compared with the Ctrl group, the SEV treatment notably damaged neurons, reduced the number of Nissl bodies, and disordered the granular cell layer and the arrangement of neurons with pyknotic nuclei in the hippocampal region.…”

Section: Resultsmentioning

confidence: 99%

“…Hence, the morphology of Nissl body is commonly employed to identify the state of neurons. 28 Nissl staining analysis showed that compared with the Ctrl group, the SEV treatment notably damaged neurons, reduced the number of Nissl bodies, and disordered the granular cell layer and the arrangement of neurons with pyknotic nuclei in the hippocampal region. However, the administration of engeletin effectively restored the injury of SEV to neurons and increased the number of Nissl bodies (Fig.…”

Section: Engeletin Ameliorates Sev-induced Neuroinflammation and Hipp...mentioning

confidence: 91%

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Engeletin ameliorates sevoflurane‐induced cognitive impairment by activating PPAR‐gamma in neonatal mice

Ying

Wang

2023

Neuropathology

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Sevoflurane (SEV) is a commonly used anesthetic in pediatric surgery. Recent studies reported that repeated use of SEV contributes to cognitive impairment. Engeletin has been discovered to exert anti‐inflammatory effects in various diseases. However, the detailed roles and mechanisms of engeletin in SEV‐induced cognitive dysfunction of neonatal mice remain unclear. In this study, C57BL/6 neonatal mice were randomly divided into Ctrl, SEV, SEV + Engeletin (10 mg /kg), SEV + Engeletin (20 mg/kg), and SEV + Engeletin (40 mg/kg) groups. The Morris water maze (MWM) test suggested that engeletin treatment significantly improved SEV‐induced cognitive impairment in neonatal mice. Employing ELISA and Nissl staining analysis, engeletin reduced neuroinflammation and loss of nerve cells caused by SEV, respectively. The treatment of engeletin dramatically suppressed the activation of microglia and apoptosis induced by SEV in the hippocampus of neonatal mice. Furthermore, the inhibition of PPAR‐γ obviously reversed the abovementioned effects of engeletin in the hippocampus of newborn mice. In conclusion, this study verified that engeletin notably ameliorated SEV‐induced cognitive deficiencies in neonatal mice at least partially by mediating the expression of PPAR‐γ.

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Section: Discussionsupporting

confidence: 46%

Section: Resultsmentioning

confidence: 99%

Section: Engeletin Ameliorates Sev-induced Neuroinflammation and Hipp...mentioning

confidence: 91%

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Engeletin ameliorates sevoflurane‐induced cognitive impairment by activating PPAR‐gamma in neonatal mice

Ying

Wang

2023

Neuropathology

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“…Cardiac output has two determinants: stroke volume and heart rate while peripheral resistance is determined by the vascular structure and function. The neural, endocrine/paracrine, and vascular mechanisms can potentially increase arterial pressure [36][37][38], and the toxic effects of AA on neuron regulation also include sympathetic autonomic neuropathy [6,39]. AA exposure can result in oxidative stress featured by a significant increase in reactive oxygen species (ROS) and malondialdehyde (MDA) levels and consumption of glutathione (GSH) [40].…”

Section: Acrylamide Exposure and Cardiovascular Diseasementioning

confidence: 99%

Negative Association between Acrylamide Exposure and Metabolic Syndrome Markers in Adult Population

Hung

Cheng

Chen

et al. 2021

IJERPH

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Metabolic syndrome encompasses multiple conditions that increase the risk of cardiovascular disease, and exposure to environmental chemicals can cause metabolic syndrome. This cross-sectional study analyzed data from the US National Health and Nutrition Examination Survey (2003–2006) on 4318 adult participants to assess the association between acrylamide (AA) exposure and metabolic syndrome. Concentrations of hemoglobin-adducted AA (HbAA) and hemoglobin-adducted glycidamide (HbGA) were evaluated. Metabolic syndrome markers related to HbAA and HbGA and the effect of exposure to AA and GA on the prevalence of metabolic syndrome were studied by ANOVA and multivariate logistic regression analyses, respectively. HbAA concentration inversely correlated with the number of metabolic syndrome markers (p < 0.05). An increased HbAA concentration was noted with reduced high triglyceride and low high-density lipoprotein cholesterol levels in the adjusted model (p < 0.05). High fasting plasma glucose level significantly correlated with HbGA concentration in the adjusted model. In conclusion, AA exposure alters metabolic syndrome markers in adults. Additional clinical and animal studies will clarify the role of AA exposure at different stages in the progression of metabolic syndrome-related diseases.

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“…Some studies show that ACR may induce developmental neurotoxicity (DNT). Prenatal and perinatal ACR exposure affect average horizontal motor activity, auditory startle response and cerebellar development rats 9 , 10 , learning and memory function are impaired in young mice that have been exposed with low doses of ACR 11 , prenatal ACR exposure in rats induces lipid peroxidation and oxidative stress 9 and impairs development of hippocampal neurons in weaning rats 12 . In vitro studies have shown that ACR interferes with neuronal differentiation and alters transcriptional markers for neurodevelopment in the C17.2 neural progenitor cell model 13 , attenuates neurite outgrowth in PC12 cells 14 , delays maturation of primary neurons 11 and impairs synaptic function 15 .…”

Section: Introductionmentioning

confidence: 99%

Acrylamide alters CREB and retinoic acid signalling pathways during differentiation of the human neuroblastoma SH-SY5Y cell line

Attoff

Johansson

Cediel-Ulloa

et al. 2020

Sci Rep

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Acrylamide (ACR) is a known neurotoxicant which crosses the blood–brain barrier, passes the placenta and has been detected in breast milk. Hence, early-life exposure to ACR could lead to developmental neurotoxicity. The aim of this study was to elucidate if non-cytotoxic concentrations of ACR alter neuronal differentiation by studying gene expression of markers significant for neurodevelopment in the human neuroblastoma SH-SY5Y cell model. Firstly, by using RNASeq we identified two relevant pathways that are activated during 9 days of retinoic acid (RA) induced differentiation i.e. RA receptor (RAR) activation and the cAMP response element-binding protein (CREB) signalling pathways. Next, by qPCR we showed that 1 and 70 µM ACR after 9 days exposure alter the expression of 13 out of 36 genes in the RAR activation pathway and 18 out of 47 in the CREB signalling pathway. Furthermore, the expression of established neuronal markers i.e. BDNF, STXBP2, STX3, TGFB1 and CHAT were down-regulated. Decreased protein expression of BDNF and altered ratio of phosphorylated CREB to total CREB were confirmed by western blot. Our results reveal that micromolar concentrations of ACR sustain proliferation, decrease neurite outgrowth and interfere with signalling pathways involved in neuronal differentiation in the SH-SY5Y cell model.

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Toxic effect of acrylamide on the development of hippocampal neurons of weaning rats

Cited by 32 publications

References 53 publications

Engeletin ameliorates sevoflurane‐induced cognitive impairment by activating PPAR‐gamma in neonatal mice

Engeletin ameliorates sevoflurane‐induced cognitive impairment by activating PPAR‐gamma in neonatal mice

Negative Association between Acrylamide Exposure and Metabolic Syndrome Markers in Adult Population

Acrylamide alters CREB and retinoic acid signalling pathways during differentiation of the human neuroblastoma SH-SY5Y cell line

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