Propofol improved neurobehavioral outcome of cerebral ischemia–reperfusion rats by regulating Bcl-2 and Bax expression

Xi, Hongjie; Zhang, Tianhua; Tao, Tao; Song, Chun-yu; Lu, Shu-jun; Cui, Xiaoqian; Yue, Ziyong

doi:10.1016/j.brainres.2011.06.060

Cited by 46 publications

(21 citation statements)

References 23 publications

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“…PI3K/Akt pathway is a critical mediator of cell survival, which exerts anti-apoptotic function via inhibiting the pro-apoptotic Bax/Bcl-2 ratio (15)(16)(17). A large number of reports indicate that the suppression of PI3K/Akt pathway is strongly associated with the progression of cerebral ischemia/reperfusion (I/R) injury, increasing the infarct size and promoting cerebral cell death (18,19).…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture at the Quchi and Zusanli acupoints exerts neuroprotective role in cerebral ischemia-reperfusion injured rats via activation of the PI3K/Akt pathway

Chen

Lin

Lan

et al. 2012

International Journal of Molecular Medicine

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The PI3K/Akt pathway, a critical mediator of cell survival, is suppressed in cerebral ischemia/reperfusion (I/R) injury; therefore, it is a major focus in treatment of ischemic stroke. Acupuncture has long been used in China to clinically treat stroke. However, the precise mechanism of its neuroprotective activities remains largely unknown. Using a focal cerebral I/R injured rat model, in the present study we evaluated the in vivo therapeutic efficacy of electroacupuncture and investigated the underlying molecular mechanisms. We found that electroacupuncture at Quchi (LI11) and Zusanli (ST36) acupoints on the contralateral paralyzed limb significantly improved neurological deficits and cerebral infarction. In addition, electroacupuncture profoundly activated PI3K/Akt signaling in ischemic cerebral tissues. Consequently, the upregulatory effect of electroacupuncture on PI3K/Akt activation resulted in the inhibition of cerebral cell apoptosis. Moreover, electroacupuncture increased the serum secretion levels of the PI3K activators BDNF and GDNF, as well as upregulated the anti-apoptotic Bcl-2/Bax ratio in ischemic cerebrum. Our data suggest that electroacupuncture at Quchi and Zusanli acupoints exerts neuroprotective function in ischemic stroke via activation of the PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

Electroacupuncture at the Quchi and Zusanli acupoints exerts neuroprotective role in cerebral ischemia-reperfusion injured rats via activation of the PI3K/Akt pathway

Chen

Lin

Lan

et al. 2012

International Journal of Molecular Medicine

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“…On the contrary, up-regulation of Bax increased apoptosis 39 . Some neuroprotective drugs can exert anti-apoptotic effects via regulating Bcl-2 and Bax expression during ischemia–reperfusion pathology process 40 . Bcl-2 and Bax form heterodimers, which play an important role in apoptosis, such as transduction of apoptotic signals.…”

Section: Discussionmentioning

confidence: 99%

Hypertonic saline infusion suppresses apoptosis of hippocampal cells in a rat model of cardiopulmonary resuscitation

Zhou

Liu

Huang

et al. 2017

Sci Rep

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Hypertonic saline (HS) attenuates cerebral edema, improves microcirculation perfusion and alleviates inflammation. However, whether the beneficial effect of HS on neurological function after cardiopulmonary resuscitation (CPR) in rat model of asphyxial cardiac arrest (CA) is mediated via attenuating apoptosis of neurons is not known. We studied the neuroprotective effect of HS in rats after CA and CPR, and explored the likely underlying mechanisms. Animals were randomly assigned to 4 equal groups (n = 15 each) according to the different infusions administered during resuscitation: control (C), normal saline (NS), hypertonic saline (HS), and hydroxyethyl starch (HES) groups. NDS at 12, 24, 48 and 72 h post-ROSC in the HS group were significantly higher than those in the NS and HES groups. Western blot analysis demonstrated a significant increase in Bcl-2 expression in HS, as compared to that in the NS and HES groups. However, Bax and Caspase-3 expressions in HS were significantly lower than that in the NS and HES groups. The apoptosis rate in HS was significantly lower than that in the NS and HES groups, suggesting HS treatment during resuscitation could effectively suppress neuronal cell apoptosis in hippocampal CA1 post-ROSC and improve neuronal function.

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“…Moreover, the hippocampal expression of Bcl-2 was significantly higher, while the expression of Bax was significantly lower in propofol-treated rats compared to IRI-induced rats at 24 h after ischemia. Hence, this study suggests that the neuroprotective effects of propofol against neuronal apoptosis may be a consequence of the regulation of Bcl-2 and Bax [25]. …”

Section: Propofolmentioning

confidence: 99%

The Effect of Intravenous Anesthetics on Ischemia-Reperfusion Injury

Eroğlu

2014

BioMed Research International

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The effects of intravenous anesthetics on ischemia-reperfusion injury (IRI) have been investigated in both animals and clinical studies. The protective effects and the dosages of the intravenous anesthetics on IRI were discussed in this paper. The prevention of the tissue injury after the IRI was demonstrated with intravenous anesthetics in some studies. In the future, the studies should be focused on the dosage of the anesthetics related to diminishing the tissue injuries. Further studies might be required in order to investigate the effects of the anesthetics on molecular levels.

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Propofol improved neurobehavioral outcome of cerebral ischemia–reperfusion rats by regulating Bcl-2 and Bax expression

Cited by 46 publications

References 23 publications

Electroacupuncture at the Quchi and Zusanli acupoints exerts neuroprotective role in cerebral ischemia-reperfusion injured rats via activation of the PI3K/Akt pathway

Electroacupuncture at the Quchi and Zusanli acupoints exerts neuroprotective role in cerebral ischemia-reperfusion injured rats via activation of the PI3K/Akt pathway

Hypertonic saline infusion suppresses apoptosis of hippocampal cells in a rat model of cardiopulmonary resuscitation

The Effect of Intravenous Anesthetics on Ischemia-Reperfusion Injury

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