fredag 30 augusti 2019

Sent inkommet

Grävskopan Axel mejlar bloggen på kvällskvisten en ny forskningsrapport undertecknad inte hade en susning om...hmm.
Det handlar om alzheimerforskning 13 kinesiska forskare bedrivit och nu fått publicerat på det vetenskapliga forumet ScienceDirect.



Propofol prevents oxidative stress and apoptosis by regulating iron homeostasis and targeting JAK/STAT3 signaling in SH-SY5Y cells

Received 27 June 2019, Revised 9 August 2019, Accepted 26 August 2019, Available online 28 August 2019.

Abstract

The present study aimed to test the hypothesis that propofol (PRO) could exert a neuroprotective effect via inhibiting oxidative stress induced by iron accumulation. Human SH-SY5Y cells were pretreated with ferric citrate (FAC), and then were protected by PRO. Cell viability was measured by MTT method. Iron levels were assayed by ICP-MS. Cell apoptosis was examined by TUNEL and digital holographic technique. Malondialdehyde (MDA), reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) depolarization were measured by MDA, DCFH-DA and JC-1 kits, respectively. The expression of proteins or genes involved in iron metabolism such as ferritin, TfR1, DMT1, Fpn1 and hepcidin, and other apoptosis-related proteins including Bcl2, Bax, Bid, Cox2, IL-6, JAK1 and STAT3 were detected by western blot. Our results showed low concentration of PRO (5 μM) could significantly prevent FAC induced apoptosis via inhibiting oxidative stress and iron accumulation. PRO suppressed the increase of ROS and MDA and decrease of MMP induced by FAC. PRO significantly down-regulated the expression of ferritin and up-regulated the expression of TfR1and Fpn1, but had no effect of DMT1. Furthermore, this effect was not done by PRO chelating iron. Meanwhile, PRO suppressed the inflammatory response through inhibiting IL-6 and Cox2 expression and activating JAK/STAT3 signaling induced by iron overload. In conclusion, here we demonstrated a new antioxidation mechanism of PRO. PRO could protect against nerve cell injury induced by overload of iron through regulating iron metabolism and inhibiting stress oxidative and inflammation reaction pathways by targeting JAK/STAT3 signaling.

Som vanligt med dessa hyperintressanta studier måste man hosta upp stålar för att läsa hela rapporten.
Fast bloggen kört google stenhårt vill Mr G inte släppa mer info och heller inte vidimering på användande av PHI´s HoloMonitor.
Men som tur är har Axel tagit en screenshot via mobilsökningen så beviset finns där.

                                    Attans att man inte kan få samma info via datorsökning.

Edit 3/9. Nu har Mr G (google) behagat göra studien sökbar via dator.



                                            Mvh the99

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