Protective effects of Cinnamomum verum, Cinnamomum cassia and cinnamaldehyde against 6-OHDA-induced apoptosis in PC12 cells

Neuroprotective potential of cinnamon and its metabolites in Parkinson's disease: Mechanistic insights, limitations, and novel therapeutic opportunities

“…[ 19 ] This is in accordance with other studies showing that sodium benzoate activates CREB pathway in the brain by upregulating protein kinase A. [ 10,28 ]…”

“…[ 28 ] Pretreatment of PC12 cells exposed to 6‐OHDA with hydro‐alcohol extracts and the essential oil of C. verum and C. cassia at 20 μg/ml, as well as 5 and 10 μM cinnamaldehyde for 25 h, resulted in enhanced cell viability, decreased apoptosis, and reduced reactive oxygen species (ROS) generation in a dose‐dependent manner. [ 28 ] The cell viability was assessed by flow cytometry, resazurin assay, and western blot analysis. [ 28 ] Regarding the underlying molecular mechanisms, these effects were accompanied by increased survivin and reduced cytochrome c (cyt‐c) levels, while pretreatment with the essential oil was further associated with downregulation of p44/42 pathway.…”

“…[ 28 ] The cell viability was assessed by flow cytometry, resazurin assay, and western blot analysis. [ 28 ] Regarding the underlying molecular mechanisms, these effects were accompanied by increased survivin and reduced cytochrome c (cyt‐c) levels, while pretreatment with the essential oil was further associated with downregulation of p44/42 pathway. [ 28 ] P44/42 is a mitogen‐activated protein kinase (MAPK), known as extracellular signal‐regulated protein kinase (ERK1/2), which can be activated by excessive ROS generation and mediate oxidative stress‐induced neuronal apoptosis.…”

“…[ 28 ] Regarding the underlying molecular mechanisms, these effects were accompanied by increased survivin and reduced cytochrome c (cyt‐c) levels, while pretreatment with the essential oil was further associated with downregulation of p44/42 pathway. [ 28 ] P44/42 is a mitogen‐activated protein kinase (MAPK), known as extracellular signal‐regulated protein kinase (ERK1/2), which can be activated by excessive ROS generation and mediate oxidative stress‐induced neuronal apoptosis. [ 29 ] Furthermore, activated P44/42 pathway has been shown to induce the release of cyt‐c from mitochondria to cytosol via Bax activation.…”

“…[6,8,9] A growing body of evidence suggests that cinnamon may exert its neuroprotective effects and delay the progression of several neurological disorders, by modulating several intracellular pathways including oxidative stress, apoptosis, mitochondrial function, autophagy, and neuroinflammation. [11][12][13] More specifically, cinnamon extracts exert anti-inflammatory effects by suppressing the production of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), IL-6, and nitric oxide (NO) in activated microglial cells. [14] They also act as inhibitors of tau aggregation, [15] blocking the formation, accumulation, and neurotoxicity of Aβ plaques in vitro, the two hallmarks of Alzheimer's disease pathogenesis.…”