Neuroprotection Of Emodin Against Middle Cerebral Artery Occlusion Injury In Rats And Its Mechanism

ObejectiveRhubarb is one of the important components on relieving treatments for stroke.The emodin is the main effective components,have non-toxic in short-term.This topic research emodin on MCAO rats model of neural protection,explore the emodin PTEN/PI3K/AKT pathway protective effect of ischemic cerebral apoplexy rats and the effect of emodin from the level of molecular biology to elucidate part of brain protection mechanism.Methods(1)60 Male sprague dawley rats are administrated with Emodin for 7 days after 2h of the ischemia reperfusion.Zea-Longa neurological deficit score,Nissl's staining,RT-PCR,Western blot and fluorescent technique are used for detection.(2)To establish an inflammatory damage model of astrocytes induced by LPS and detect IL-6 production and inflammatory cytokines mRNA.At the same time,To establish an inflammatory damage model of BV2 and macrophages induced by LPS and detect IL-6 production.(3)To study PTEN/PI3K/AKT signaling pathway on neuroprotective effect of salidroside,72 Male sprague dawley rats are seperately injected into the left lateral ventricle PI3K inhibitor LY294002 and artificial cerebrospinal fluid with the help of ventricle stereotaxic apparatus.30 minutes later,the Models of MCAO are finished with 1 hour reperfusion,drug administration and intracerebroventricular injection for 1 day.At last,the expressions of PTEN,AKT,NF-KBp50,Bax and Bcl-xl were detected.(4)To establish an inflammatory damage model of astrocytes induced by PI3K inhibitor LY294002,and LPS.ELISA technique detect IL-6 production.Result(1)The rats undergo 2 hour ischemia reperfusion with 7 days Emodin treatments show that Emodin can improve the neurological deficit score,increase the number of positive cell of Nissl,decrease the nuber of apoptotic cells,inhibit the expressions of Bax,enhance the BDNF,NGF and Bcl-xl protein,inhibit the expressions of IL-6,IL-1?mRNA.(2)Emodin can inhibit astrocytes the expression of inflammatory cytokines mRNA and IL-6 production.Emodin can inhibit BV2 and macrophages IL-6 production.(3)The rats are administrated with PI3K inhibitor LY294002 into cerebral ventricle continueously,it show the same result in accord with MCAO.What is more,the treatment of Emodin and PI3K inhibitor LY294002 have never shown the remarkable additive effects.(4)Astrocytes are administrated with PI3K inhibitor LY294002,PI3K inhibitor LY294002 can inhibit the expression of inflammatory cytokines mRNA and IL-6 production.Conclusion(1)Emodin which has a neuroprotective effect can alleviate the infarct volume,improve the neurological deficit,inhibit the neural apoptosis and reverse the hypoxia-reperfusion genetic change.(2)Emodin,a neuroprotective drug,can inhabite apoptosis,and have neuroprotection.(3)Emodin can alleviate the death of neurocyte by inhibiting PTEN/PI3K/AKT signaling pathway,inhibiting the expression of PTEN promoting PI3K/AKT,inhibiting inflammatory factor.