ABSTRACT
Aim To investigate the effects of gastrodin on SH-SY5Y cell autophagy induced by methamphet-amine (METH) and the underlying mechanisms. Methods SY5Y cells were treated by METH with the concentration of 0.5,1.0,1.5,2.0,2.5,3.0 mmol·L-1for 24 h. The morphological changes were ob-served by microscopy,the expression of LC3-Ⅱ,Bec-lin-1,Akt,p-Akt,mTOR and p-mTOR were detected by Western blot. Gastrodin was added to the medium 1 h before METH treatment. Results The SY 5 Y cells were morphologically featured by shrinkage and den-drite disruption after exposed to METH(0~3 mmol· L-1),and autophagic vacuoles occurred in cytoplasm. The expression of LC3-Ⅱ increased over METH dose. Confocal results showed that LC3-Ⅱsignificantly in-creased in METH group as compared with control, while decreased in METH+ Gastrodin group. The ex-pression levels of LC3-Ⅱand Beclin-1 significantly in-creased (P<0.01) in METH group, p-mTOR and p-Akt decreased, and mTOR and Akt showed no signifi-cant difference as compared with control. However, the gastrodin could decrease the expression of LC3-Ⅱand Beclin-1 and increase the expression of mTOR,p-mTOR,Akt and p-Akt as compared with METH-trea-ted groups. Conclusions METH can induce SY5Y cells autophagy. The protective effect of gastrodin a-gainst METH-induced autophag may be related to gast-rodin regulation mTOR and Akt signaling pathway.
ABSTRACT
Amphetamines abuse is defined as a chronic recurrent encephalopathy, and it is a global public health problem which seriously threatens the health of human and the social stability. Long-term abuse and addiction of amphetamines leads to structural and functional changes of specific encephalic regions. Further researches on these encephalic regions, the network of brain and biological information may be helpful to understanding drug abuse mechanism and possible therapeutic measures. Recently, a series of functional imaging techniques, including magnetic resonance imaging (MRI), functional magnetic resonance imaging (f MRI), magnetic resonance spectroscopy (MRS), diffusion tensor imaging (DTI), and positron emission tomography (PET), were used to detect different brain structural changes of the volume and density of encephalic regions, functional changes of cerebral blood flow and brain cognition. The results showed functional imaging techniques play significant roles to detect different structural and functional changes of the brain. Based on these results, the researchers aim to clarify the mechanisms of drug abuse. That is the main focus of this review.
ABSTRACT
<p><b>AIM</b>To investigate the role of nuclear factor-kappaB in apoptosis pathway of HUVEC.</p><p><b>METHODS</b>The cell lines of HUVEC cultured in vitro were divided into three groups: normal control group, Ang II group, and Gliotoxin group. We investigated the effects of Ang II (0.01 micromol/L, 0.1 micromol/L, 1 micromol/L and 10 micromol/L) on the viability of HUVEC with modified MTT. Then agarose gel electrophoresis and flow cytometry were applied to detect the apoptosis of HUVEC. Finally, the nuclear translocation of NF-kappaB subunit p65 was evaluated by immunocytochemistry.</p><p><b>RESULTS</b>The viability of HUVEC decreased significantly after incubated with 10 micromol/L Ang II for 24 hours. The results of DNA agarose gel and flow cytometry showed that 10 micromol/L Ang II induced the apoptosis of HUVEC, and the apoptosis rate was significantlyhigher than normal control group (P < 0.05). 0.1 mg/L Gliotoxin antagonized this effect of Ang II. The results of immunocytochemistry suggested that NF-kappaB was activated in HUVEC induced by 10 micromol/L Ang II. In contrast, Gliotoxin inhibited the activation of NF-kappaB in HUVEC induced by Ang II.</p><p><b>CONCLUSION</b>(1) Ang II can induce the apoptosis of HUVEC, while the inhibitor of NF-kappaB, Gliotoxin, can antagonize the effect of Ang II. (2) NF-kappaB may play an important role in apoptosis pathway of HUVEC induced by Ang II.</p>