Protective effects of propofol against whole cerebral ischemia/reperfusion injury in rats through the inhibition of the apoptosis-inducing factor pathway
Authors: Hua Qian
Zi-Yong Yue
Tao Tao
Chun-Yu Song
Hong Dong
Wan-Chao Yang
Chun-Lei Li
Xian-Zhang Zeng
Journal: Brain Research (2016)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: AIF; Apoptosis; Brain rrotection; Ischemia/Reperfusion injury; Propofol.
Affiliations: Department of Anesthesiology, China and Heilongjiang Key Laboratory for Anesthesia and Critical Care, The Second Affiliated Hospital of Harbin Medical University, Harbin 150081, China., Department of Anesthesiology, China and Heilongjiang Key Laboratory for Anesthesia and Critical Care, The Second Affiliated Hospital of Harbin Medical University, Harbin 150081, China. Electronic address: .

Abstract:  Cerebral ischemia/reperfusion (I/R) injury could cause neural apoptosis that involved the signaling cascades. Cytochrome c release from the mitochondria and the followed activation of caspase 9 and caspase 3 are the important steps. Now, a new mitochondrial protein, apoptosis-inducing factor (AIF), has been shown to have relationship with the caspase-independent apoptotic pathway. In this study, we investigated the protective effects of propofol through inhibiting AIF-mediated apoptosis induced by whole cerebral I/R injury in rats. 120 Wistar rats that obtained the permission of the animal care committee of Harbin Medical University were randomly divided into three groups: sham group (S group), cerebral ischemia/reperfusion injury group (I/R group), and propofol treatment group (P group). Propofol (1.0mg/kg/min) was administered intravenously for 1h before the induction of ischemia in P group. The apoptotic rate in three groups was detected by flow cytometry after 24h of reperfusion. The mitochondrial membrane potential (MMP) changes were detected via microplate reader. The expressions of B-cell leukemia-2 (Bcl-2), Bcl-2 associated X protein (Bax) and AIF were evaluated using Western blot after 6h, 24h and 48h of reperfusion. The results of our study showed that apoptotic level was lower in P group compared with I/R group and propofol could protect MMP. The ratio of Bcl-2/Bax was significantly higher in P group compared with I/R group. The translocation of AIF from mitochondrial to nucleus was lower in P group than that in I/R group. Our findings suggested that the protective effects of propofol on cerebral I/R injury might be associated with inhibiting translocation of AIF from mitochondrial to the nucleus in hippocampal neurons. 

Retracted: No

PubPeer comments:
 Are the authors able to explain why figure 1A in this paper is identical to figure 4A in a previous paper in the same journal (doi:10.1016 j.brainres.2011.06.060). See also https: pubpeer.com publications 319E9189B5E1567C89A12160D00942   , 
 #1 In this study, I have only done a small part of the work, I do not know the cause of this problem. I have contacted Dr. Song and she will respond to this concern. Thank you. , 
 #1 Dear Editor: Firstly, thank you for error correction. Figure 1A in paper of 2016 and Figure 4A in a previous paper of 2011 were both sham group(untreated group). The protective effects of propofol were series studies in our team. So, we use the same picture in these two sham groups. I am so sorry for the mistake. Also, we can provide another picture for Figure 1A in 2016 paper in sham group(untreated group). Thank you very much for your correction again! , 
 In this study, I have only done a very small part of the work, I do not know the cause of this problem. I have contacted Dr. Song and she will respond to this concern. Thank you. ,