Neuroprotection by Taurine on HBCD-Induced Apoptosis in PC12 Cells

Li, Yachen; Li, Shuangyue; Xie, Xizhe; Xiu, Hang; Liu, Xiaohui; Shao, Jing; Zhang, Xiuli

doi:10.1007/978-94-024-1079-2_9

Cited by 7 publications

(3 citation statements)

References 38 publications

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“…Bax, cleaved Caspase-3, and cleaved PARP are pro-apoptotic proteins, while Bcl-2 is an anti-apoptotic protein. 29,30 Results showed that hypoxia increased expression of Bax, cleaved Caspase-3, and cleaved PARP and decreased expression of Bcl-2. Differently, TPP administration reversed the expression trend, which could explain the finding in apoptosis.…”

Section: R E T R a C T E Dmentioning

confidence: 99%

RETRACTED: Typhae pollen polysaccharides protect hypoxia-induced PC12 cell injury via regulation of miR-34a/SIRT1

Wang

Tang

et al. 2020

Int J Immunopathol Pharmacol

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This current research was performed to investigate the role of typhae pollen polysaccharides (TPP) in hypoxia-treated PC12 cell which was an in vitro cell model of cerebral ischemia. Hypoxia-treated cells were treated with TPP for 12 h. Cell viability and apoptosis were detected by 3-(4,5-dimethylthiazol-2-yl)-2 5-diphenyl-2H-tetrazolium bromide (MTT) assay and flow cytometry, respectively. Cell apoptotic proteins and PI3K/AKT and Ras/Raf/MEK/ERK signal pathway–associated proteins were also examined by western blot. Furthermore, abnormal expression of miR-34a and silent information regulator 1 (SIRT1) was achieved by transfection. Besides, the expression of miR-34a and SIRT1 was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of SIRT1 was detected by qRT-PCR and western blot. The relationship between miR-34a and SIRT1 was verified by luciferase assay. We found that TPP enhanced cell viability and inhibited apoptosis in hypoxia-treated PC12 cells. Moreover, TPP increased the accumulated levels of Bcl-2 while decreased expression of Bax, cleaved Caspase-3, and cleaved PARP. TPP downregulated miR-34a expression while induced by hypoxia. Further results showed that miR-34a overexpression reversed the results led by TPP in cell viability, apoptosis, and its related proteins. In addition, SIRT1 was upregulated by TPP and was verified to be a target of miR-34a. Silence of SIRT1 led to the opposite results led by TPP. In the end, TPP activated PI3K/AKT and Ras/Raf/MEK/ERK signal pathways. In conclusion, TPP plays important roles in regulating cell viability and apoptosis in hypoxia-treated PC12 cells via modulating miR-34a/SIRT1, as well as activating PI3K/AKT and Ras/Raf/MEK/ERK signal pathways.

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Section: R E T R a C T E Dmentioning

confidence: 99%

RETRACTED: Typhae pollen polysaccharides protect hypoxia-induced PC12 cell injury via regulation of miR-34a/SIRT1

Wang

Tang

et al. 2020

Int J Immunopathol Pharmacol

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“…Induced growth of BG‐1 ovarian cancer cells by 17beta‐estradiol or various endocrine disrupting chemicals was reversed by resveratrol via downregulation of cell cycle progression.Treatment of BG‐1 cells with HBCDDs resulted in an increase of cell growth.Li et al. (2017c). Neuroprotection by Taurine on HBCD‐Induced Apoptosis in PC12.Exposure of PC12 cells to 10 μM HBCDDs reduced protein expression of Bcl‐2, increased expression in Bax protein and activity of caspase‐3.…”

Section: Appendix D – Mode Of Action Studiesmentioning

confidence: 99%

“…Treatment of BG-1 cells with HBCDDs resulted in an increase of cell growth. Li et al (2017c). Neuroprotection by Taurine on HBCD-Induced Apoptosis in PC12.…”

Section: Referencementioning

confidence: 99%

Update of the risk assessment of hexabromocyclododecanes (HBCDDs) in food

Schrenk

Bignami

Bodin³

et al. 2021

EFS2

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The European Commission asked EFSA to update its 2011 risk assessment on hexabromocyclododecanes ( HBCDD s) in food. HBCDD s, predominantly mixtures of the stereoisomers α‐, β‐ and γ‐ HBCDD , were widely used additive flame retardants. Concern has been raised because of the occurrence of HBCDD s in the environment, food and in humans. Main targets for toxicity are neurodevelopment, the liver, thyroid hormone homeostasis and the reproductive and immune systems. The CONTAM Panel concluded that the neurodevelopmental effects on behaviour in mice can be considered the critical effects. Based on effects on spontaneous behaviour in mice, the Panel identified a lowest observed adverse effect level ( LOAEL ) of 0.9 mg/kg body weight (bw) as the Reference Point, corresponding to a body burden of 0.75 mg/kg bw. The chronic intake that would lead to the same body burden in humans was calculated to be 2.35 μg/kg bw per day. The derivation of a health‐based guidance value ( HBGV ) was not considered appropriate. Instead, the margin of exposure ( MOE ) approach was applied to assess possible health concerns. Over 6,000 analytical results for HBCDD s in food were used to estimate the exposure across dietary surveys and age groups of the European population. The most important contributors to the chronic dietary LB exposure to HBCDD s were fish meat, eggs, livestock meat and poultry. The CONTAM Panel concluded that the resulting MOE values support the conclusion that current dietary exposure to HBCDD s across European countries does not raise a health concern. An exception is breastfed infants with high milk consumption, for which the lowest MOE values may raise a health concern.

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