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[Effects of propofol on PI3K/Akt signaling pathway and endoplasmic reticulum stress pathway of apoptosis induced by ischemia-reperfusion in isolated rat hearts].
Zhonghua Yi Xue Za Zhi. 2012 Oct 09; 92(37):2611-4.ZY

Abstract

OBJECTIVE

To explore the effects of propofol on the PI3K/Akt signaling pathway and the endoplasmic reticulum stress pathway of apoptosis induced by ischemia-reperfusion in isolated rat hearts.

METHODS

Forty isolated rat hearts were completely randomly assigned into 5 different groups: control (C), ischemia/reperfusion (I/R), propofol (P), propofol plus Wortmannin (P + Wort) and Wortmannin (W). The isolated hearts were perfused on a Langendorff apparatus. Except for group C, all hearts were subjected to 30 min global ischemia and 120 min reperfusion. In the P, P + W and W groups, 50 µmol/L propofol or 50 µmol/L propofol + 100 nmol/L Wortmannin or 100 nmol/L Wortmannin were respectively added in the K-H buffer to perfuse for 10 min at pre-ischemia and 20 min at the beginning of reperfusion. The parameters of cardiac function were recorded at pre-ischemia and at the 120 min of reperfusion. The apoptotic index was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (Tunel). The expressions of caspase-12 and CCAAT/C/EBP homologous protein (chop) were measured by immunohistochemistry while those of Akt and p-Akt (Ser473) detected by Western blot.

RESULTS

Compared with the I/R group, LVEDP significantly deceased and +dp/dtmax significantly increased, the apoptotic index [(27.89 ± 1.04)% vs (33.70 ± 2.20)%], the expressions of caspase-12 [(0.1728 ± 0.0096) vs (0.2332 ± 0.0114)] and chop [(0.1889 ± 0.0078) vs (0.2407 ± 0.0123)] significantly deceased while that of p-Akt (Ser473) significantly increased in Group P (P < 0.05). Wortmannin abolished the partial protective effects of propofol postconditioning (P < 0.05).

CONCLUSION

Propofol perfusion may attenuate the endoplasmic reticulum stress pathway of apoptosis induced by ischemia/reperfusion in isolated rat hearts partly through the PI3K/Akt signal pathway.

Authors+Show Affiliations

Liu L
Department of Anesthesiology, First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China.
Pang Y
No affiliation info available
He DW
No affiliation info available
Liu XW
No affiliation info available

MeSH

AnimalsApoptosisEndoplasmic Reticulum StressHeartIn Vitro TechniquesMalePhosphatidylinositol 3-KinasesPropofolProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyReperfusion InjurySignal Transduction

Pub Type(s)

English Abstract
Journal Article

Language

chi

PubMed ID

23290061

Citation

Liu, Liu, et al. "[Effects of Propofol On PI3K/Akt Signaling Pathway and Endoplasmic Reticulum Stress Pathway of Apoptosis Induced By Ischemia-reperfusion in Isolated Rat Hearts]." Zhonghua Yi Xue Za Zhi, vol. 92, no. 37, 2012, pp. 2611-4.
Liu L, Pang Y, He DW, et al. [Effects of propofol on PI3K/Akt signaling pathway and endoplasmic reticulum stress pathway of apoptosis induced by ischemia-reperfusion in isolated rat hearts]. Zhonghua Yi Xue Za Zhi. 2012;92(37):2611-4.
Liu, L., Pang, Y., He, D. W., & Liu, X. W. (2012). [Effects of propofol on PI3K/Akt signaling pathway and endoplasmic reticulum stress pathway of apoptosis induced by ischemia-reperfusion in isolated rat hearts]. Zhonghua Yi Xue Za Zhi, 92(37), 2611-4.
Liu L, et al. [Effects of Propofol On PI3K/Akt Signaling Pathway and Endoplasmic Reticulum Stress Pathway of Apoptosis Induced By Ischemia-reperfusion in Isolated Rat Hearts]. Zhonghua Yi Xue Za Zhi. 2012 Oct 9;92(37):2611-4. PubMed PMID: 23290061.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Effects of propofol on PI3K/Akt signaling pathway and endoplasmic reticulum stress pathway of apoptosis induced by ischemia-reperfusion in isolated rat hearts]. AU - Liu,Liu, AU - Pang,Yong, AU - He,Dong-wei, AU - Liu,Xin-wei, PY - 2013/1/8/entrez PY - 2013/1/8/pubmed PY - 2013/9/10/medline SP - 2611 EP - 4 JF - Zhonghua yi xue za zhi JO - Zhonghua Yi Xue Za Zhi VL - 92 IS - 37 N2 - OBJECTIVE: To explore the effects of propofol on the PI3K/Akt signaling pathway and the endoplasmic reticulum stress pathway of apoptosis induced by ischemia-reperfusion in isolated rat hearts. METHODS: Forty isolated rat hearts were completely randomly assigned into 5 different groups: control (C), ischemia/reperfusion (I/R), propofol (P), propofol plus Wortmannin (P + Wort) and Wortmannin (W). The isolated hearts were perfused on a Langendorff apparatus. Except for group C, all hearts were subjected to 30 min global ischemia and 120 min reperfusion. In the P, P + W and W groups, 50 µmol/L propofol or 50 µmol/L propofol + 100 nmol/L Wortmannin or 100 nmol/L Wortmannin were respectively added in the K-H buffer to perfuse for 10 min at pre-ischemia and 20 min at the beginning of reperfusion. The parameters of cardiac function were recorded at pre-ischemia and at the 120 min of reperfusion. The apoptotic index was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (Tunel). The expressions of caspase-12 and CCAAT/C/EBP homologous protein (chop) were measured by immunohistochemistry while those of Akt and p-Akt (Ser473) detected by Western blot. RESULTS: Compared with the I/R group, LVEDP significantly deceased and +dp/dtmax significantly increased, the apoptotic index [(27.89 ± 1.04)% vs (33.70 ± 2.20)%], the expressions of caspase-12 [(0.1728 ± 0.0096) vs (0.2332 ± 0.0114)] and chop [(0.1889 ± 0.0078) vs (0.2407 ± 0.0123)] significantly deceased while that of p-Akt (Ser473) significantly increased in Group P (P < 0.05). Wortmannin abolished the partial protective effects of propofol postconditioning (P < 0.05). CONCLUSION: Propofol perfusion may attenuate the endoplasmic reticulum stress pathway of apoptosis induced by ischemia/reperfusion in isolated rat hearts partly through the PI3K/Akt signal pathway. SN - 0376-2491 UR - https://www.unboundmedicine.com/medline/citation/23290061/[Effects_of_propofol_on_PI3K/Akt_signaling_pathway_and_endoplasmic_reticulum_stress_pathway_of_apoptosis_induced_by_ischemia_reperfusion_in_isolated_rat_hearts]_ DB - PRIME DP - Unbound Medicine ER -
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