2012
DOI: 10.3109/13880209.2012.716852
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Neuroprotective effects of luteolin against apoptosis induced by 6-hydroxydopamine on rat pheochromocytoma PC12 cells

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Cited by 50 publications
(31 citation statements)
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References 40 publications
(39 reference statements)
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“…Consistent with other studies, Mei et al indicated that neurotrophic factor prevented the apoptosis of PC12 cells induced by 6-OHDA through upregulation of Bcl-2/Bax ratio and downregulation of caspase-3activity [38]. Luteolin protected PC12 cells against 6-OHDA-induced apoptosis via suppressing the induction of Bax, inhibiting the reduction of Bcl-2, and reducing the induction of Bax/Bcl-2 ratio [39]. However, O'Malley et al suggested that 6-OHDA-induced neurotoxicity is not regulated by Bcl-2 in primary mice dopaminergic neurons cells [40].…”
Section: Discussionsupporting
confidence: 52%
“…Consistent with other studies, Mei et al indicated that neurotrophic factor prevented the apoptosis of PC12 cells induced by 6-OHDA through upregulation of Bcl-2/Bax ratio and downregulation of caspase-3activity [38]. Luteolin protected PC12 cells against 6-OHDA-induced apoptosis via suppressing the induction of Bax, inhibiting the reduction of Bcl-2, and reducing the induction of Bax/Bcl-2 ratio [39]. However, O'Malley et al suggested that 6-OHDA-induced neurotoxicity is not regulated by Bcl-2 in primary mice dopaminergic neurons cells [40].…”
Section: Discussionsupporting
confidence: 52%
“…The mitochondria-dependent pathway of apoptosis is regulated by members of the Bcl-2 family of proteins [29,30]. It has been demonstrated that increased Bax and lowered Bcl-2 expression play a critical role in reducing mitochondrial membrane potential and increasing ROS production in neurons [31,32]. Therefore, we investigated whether regulation of Bcl-2 family was involved in MCG-mediated reduction of ROS in H 2 O 2 -stimulated PC12 cells.…”
Section: Effect Of Mcg On H 2 O 2 -Induced Apoptosis In Pc12 Cellsmentioning
confidence: 97%
“…As 6-OHDA shares certain structural similarities with DA, it can enter dopaminergic neurons via DA transporters, and consequently cause toxicity (Shi et al, 2011). It produces diverse toxic effects, such as mitochondrial dysfunction and oxidative stress, apoptosis, neuroinflammation, and dopaminergic cell death (Chan et al, 2009; Liang et al, 2011; Shi et al, 2011; Thornton and Vink, 2012; Guo et al, 2013; Pyo et al, 2013; Wang J. Y. et al, 2013; Elyasi et al, 2014; Magalingam et al, 2014; Mu et al, 2014; De Jesús-Cortés et al, 2015; Liu et al, 2015; Yan et al, 2015; Zhang et al, 2015; Mirzaie et al, 2016). Disturbance of the dopaminergic system may also cause glutamatergic NMDARs imbalances in the brain (Hallett et al, 2006).…”
Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning
confidence: 99%