kukoamine-b and acetovanillone

kukoamine-b has been researched along with acetovanillone* in 1 studies

Other Studies

1 other study(ies) available for kukoamine-b and acetovanillone

Article	Year
Kukoamine B, an amide alkaloid, protects against NMDA-induced neurotoxicity and potential mechanisms in vitro. Neurochemistry international, 2015, Volume: 87 A major cause of cerebral ischemia is overactivation of the N-methyl-D-aspartate receptors (NMDARs). Therefore, NMDAR antagonists are needed for the treatment of cerebral ischemia. In our research, KuB protected the SH-SY5Y cells against NMDA-induced injury, apoptosis, LDH release and MMP loss. In addition, KuB could decrease MDA levels while increasing SOD activity. Meanwhile, KuB decreased NADPH oxidase-mediated ROS production, inhibited Ca(2+) influx, and increased the Bcl-2/Bax ratio. Furthermore, KuB not only down-regulated expression of the NR2B subunit of NMDAR but also actively modulated expression of the signaling molecules downstream of NR2B, including p-ERK, p-CREB, p-AKT and SAPKs. Finally, docking results showed that KuB had a high affinity for NR2B-containing NMDARs. Therefore, we conclude that KuB protected the SH-SY5Y cells from NMDA-induced injury likely by antagonizing NMDARs and reducing oxidative stress. Topics: Acetophenones; Apoptosis; bcl-2-Associated X Protein; Caffeic Acids; Calcium; Cell Line, Tumor; Dizocilpine Maleate; Humans; In Vitro Techniques; Ion Transport; L-Lactate Dehydrogenase; Malondialdehyde; Matrix Metalloproteinases; N-Methylaspartate; Neurons; Reactive Oxygen Species; Spermine; Superoxide Dismutase	2015

Article

Year

Kukoamine B, an amide alkaloid, protects against NMDA-induced neurotoxicity and potential mechanisms in vitro.

Neurochemistry international, 2015, Volume: 87

A major cause of cerebral ischemia is overactivation of the N-methyl-D-aspartate receptors (NMDARs). Therefore, NMDAR antagonists are needed for the treatment of cerebral ischemia. In our research, KuB protected the SH-SY5Y cells against NMDA-induced injury, apoptosis, LDH release and MMP loss. In addition, KuB could decrease MDA levels while increasing SOD activity. Meanwhile, KuB decreased NADPH oxidase-mediated ROS production, inhibited Ca(2+) influx, and increased the Bcl-2/Bax ratio. Furthermore, KuB not only down-regulated expression of the NR2B subunit of NMDAR but also actively modulated expression of the signaling molecules downstream of NR2B, including p-ERK, p-CREB, p-AKT and SAPKs. Finally, docking results showed that KuB had a high affinity for NR2B-containing NMDARs. Therefore, we conclude that KuB protected the SH-SY5Y cells from NMDA-induced injury likely by antagonizing NMDARs and reducing oxidative stress.

Topics: Acetophenones; Apoptosis; bcl-2-Associated X Protein; Caffeic Acids; Calcium; Cell Line, Tumor; Dizocilpine Maleate; Humans; In Vitro Techniques; Ion Transport; L-Lactate Dehydrogenase; Malondialdehyde; Matrix Metalloproteinases; N-Methylaspartate; Neurons; Reactive Oxygen Species; Spermine; Superoxide Dismutase

2015