Role for the PI3K/Akt/Nrf2 signaling pathway in the protective effects of carnosic acid against methylglyoxal-induced neurotoxicity in SH-SY5Y neuroblastoma cells

Haem oxygenase‐1 up‐regulation by rosiglitazone via ROS‐dependent Nrf2‐antioxidant response elements axis or PPARγ attenuates LPS‐mediated lung inflammation

“…These results are consistent with the reports that expression of HO‐1, in response to up‐regulated Nrf2 in post‐transcriptional sites, protects cells from apoptosis in an Nrf2‐denpendent manner (Foresti et al ., ). Moreover, the Akt/Nrf2 signalling pathway protects against toxicity (de Oliveira et al ., ). Here, we reported that blockade of the NOX/ROS/c‐Src/Pyk2/Akt cascade by their respective inhibitors reduced rosiglitazone‐stimulated phosphorylation/nuclear translocation of Nrf2, HO‐1 promoter binding and ARE promoter activity in HPAEpiCs.…”

Anticancer Effects of Rosemary (Rosmarinus officinalis L.) Extract and Rosemary Extract Polyphenols

“…In IMR-32 neuroblastoma cells CA induced apoptosis by activation of caspases, PARP and the p38 MAPK pathway and inhibited cell viability, which was associated with decreased ERK activation [66]. Interestingly however, in SH-SY5Y neuroblastoma cells CA attenuated apoptosis induced by the neurotoxic compounds methylglyoxal and amyloid β, exerting a cytoprotective effect [67,68]. This protective effect was associated with increased activation of PI3K/Akt signaling, inhibition of cytochrome c release and inhibition of caspase cascades which results in a pro-survival effect on the cell [36,67].…”

“…Interestingly however, in SH-SY5Y neuroblastoma cells CA attenuated apoptosis induced by the neurotoxic compounds methylglyoxal and amyloid β, exerting a cytoprotective effect [67,68]. This protective effect was associated with increased activation of PI3K/Akt signaling, inhibition of cytochrome c release and inhibition of caspase cascades which results in a pro-survival effect on the cell [36,67]. Similarly, in U373MG astrocytoma cells CA inhibited amyloid β peptide production and release and this was associated, at least partially, with activation of the α-secretase TACE/ADAM17 [69].…”

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

“…Many natural compounds have been described to have therapeutic effects in preventing MG‐induced glycation, mainly due to MG‐scavenging and antioxidant properties, also increasing GLO1 activity. There are immense studies addressing this issue and a myriad of compounds including soy isoflavones, δ‐tocopherol, several flavonoids, phenols, xantonoids, and diterpenes and triterpenes from fruit and vegetables, phlorotannins, olive oil, polyunsaturated free fatty acids, and diverse plant, root and algae‐extracted compounds have been previously tested in in vitro and in vivo models of hyperglycemia and in presence of MG‐derived AGE. Such compounds were found to prevent from protein glycation by scavenging MG and, some of them, by activating GLO1.…”