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Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion by Inhibiting Neuronal Apoptosis.
Med Sci Monit. 2018 Sep 19; 24:6587-6598.MS

Abstract

BACKGROUND

In this study, we investigated the potential neuroprotective effect of oleuropein (OLE) on apoptotic changes via modulating Akt/glycogen synthase kinase 3 beta (Akt/GSK-3b) signaling in a rat model of cerebral ischemia/reperfusion injury (IRI). MATERIAL AND

METHODS

Sprague-Dawley male rats (12 weeks, n=200) were randomly assigned to 5 groups: sham group, vehicle (IRI+ vehicle) group, OLE (IRI+OLE) group, OLE+LY294002 (IRI+OLE+LY294002) group, and LY294002(IRI+LY294002) group. The rats were subjected to cerebral ischemia/reperfusion injury (IRI) model and treated once daily for 5 days with vehicle and OLE (100 mg/kg via intraperitoneal injection) after IRI injury. LY294002 (0.3 mg/kg) was intraperitoneally injected once at 30 min after IRI injury. Brain edema, neurological deficit, rotarod latencies, and Morris water maze (MWM) performance were evaluated after IRI. The number of dead cells were assayed by TUNEL staining. Western blot was used to detect the expression of Bcl-2, Bax, cleaved caspase-3 (CC3), neurotrophic factors, and the phosphorylation levels of Akt and GSK-3β.

RESULTS

Compared with the vehicle group, brain water content, neurological deficits, rotarod latencies, and escape latency following IRI were reduced in the OLE group. Cell apoptosis and reduced neurotrophic factor caused by IRI was also attenuated by OLE. Furthermore, increased p-Akt and decreased p-GSK-3β were caused by OLE, which were associated with decrease of Bax/Bcl-2 ratio and the suppression of Caspase-3 activity after IRI. Importantly, all the beneficial effects of OLE in the vehicle group were abrogated by PI3K inhibitor LY294002.

CONCLUSIONS

Cerebral ischemia was protected by OLE via suppressing apoptosis through the Akt/GSK-3β pathway and upregulating neurotrophic factor after IRI.

Authors+Show Affiliations

Department of Nursing, Tangshan Gongren Hospital, Tangshan, Hebei, China (mainland).Department of Hepatobiliary Surgery, Tangshan Gongren Hospital, Tangshan, Hebei, China (mainland).Department of Nursing, Tangshan Gongren Hospital, Tangshan, Hebei, China (mainland).

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30230477

Citation

Zhang, Weijing, et al. "Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion By Inhibiting Neuronal Apoptosis." Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, vol. 24, 2018, pp. 6587-6598.
Zhang W, Liu X, Li Q. Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion by Inhibiting Neuronal Apoptosis. Med Sci Monit. 2018;24:6587-6598.
Zhang, W., Liu, X., & Li, Q. (2018). Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion by Inhibiting Neuronal Apoptosis. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, 24, 6587-6598. https://doi.org/10.12659/MSM.912336
Zhang W, Liu X, Li Q. Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion By Inhibiting Neuronal Apoptosis. Med Sci Monit. 2018 Sep 19;24:6587-6598. PubMed PMID: 30230477.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion by Inhibiting Neuronal Apoptosis. AU - Zhang,Weijing, AU - Liu,Xiaogang, AU - Li,Qiuyue, Y1 - 2018/09/19/ PY - 2018/9/20/entrez PY - 2018/9/20/pubmed PY - 2018/12/12/medline KW - Apoptosis KW - Brain Ischemia KW - Olea KW - Phosphatidylinositol 3-Kinases KW - Proto-Oncogene Proteins c-akt SP - 6587 EP - 6598 JF - Medical science monitor : international medical journal of experimental and clinical research JO - Med. Sci. Monit. VL - 24 N2 - BACKGROUND In this study, we investigated the potential neuroprotective effect of oleuropein (OLE) on apoptotic changes via modulating Akt/glycogen synthase kinase 3 beta (Akt/GSK-3b) signaling in a rat model of cerebral ischemia/reperfusion injury (IRI). MATERIAL AND METHODS Sprague-Dawley male rats (12 weeks, n=200) were randomly assigned to 5 groups: sham group, vehicle (IRI+ vehicle) group, OLE (IRI+OLE) group, OLE+LY294002 (IRI+OLE+LY294002) group, and LY294002(IRI+LY294002) group. The rats were subjected to cerebral ischemia/reperfusion injury (IRI) model and treated once daily for 5 days with vehicle and OLE (100 mg/kg via intraperitoneal injection) after IRI injury. LY294002 (0.3 mg/kg) was intraperitoneally injected once at 30 min after IRI injury. Brain edema, neurological deficit, rotarod latencies, and Morris water maze (MWM) performance were evaluated after IRI. The number of dead cells were assayed by TUNEL staining. Western blot was used to detect the expression of Bcl-2, Bax, cleaved caspase-3 (CC3), neurotrophic factors, and the phosphorylation levels of Akt and GSK-3β. RESULTS Compared with the vehicle group, brain water content, neurological deficits, rotarod latencies, and escape latency following IRI were reduced in the OLE group. Cell apoptosis and reduced neurotrophic factor caused by IRI was also attenuated by OLE. Furthermore, increased p-Akt and decreased p-GSK-3β were caused by OLE, which were associated with decrease of Bax/Bcl-2 ratio and the suppression of Caspase-3 activity after IRI. Importantly, all the beneficial effects of OLE in the vehicle group were abrogated by PI3K inhibitor LY294002. CONCLUSIONS Cerebral ischemia was protected by OLE via suppressing apoptosis through the Akt/GSK-3β pathway and upregulating neurotrophic factor after IRI. SN - 1643-3750 UR - https://www.unboundmedicine.com/medline/citation/30230477/Protective_Effects_of_Oleuropein_Against_Cerebral_Ischemia/Reperfusion_by_Inhibiting_Neuronal_Apoptosis_ L2 - https://www.medscimonit.com/download/index/idArt/912336 DB - PRIME DP - Unbound Medicine ER -