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[Effect of propofol on the activation of nuclear factor-kappa B and expression of inflammatory cytokines in cerebral cortex during transient focal cerebral ischemia-reperfusion: experiment with rats].
Zhonghua Yi Xue Za Zhi. 2004 Dec 17; 84(24):2110-4.ZY

Abstract

OBJECTIVE

To investigate the effect of propofol on the activation of nuclear factor-kappa B (NF-kappa B) and the expression of inflammatory cytokines, such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule-1 (ICAM-1) in cerebral cortex during transient focal cerebral ischemia-reperfusion, and to discuss the probable mechanism of its protective effect.

METHODS

Ninety male Wistar rats were randomly divided into 3 equal groups: sham operation group undergoing sham operation; ischemia/reperfusion (I/R) group undergoing thread embolism of the left middle cerebral artery occlusion (MCAO) to cause focal ischemia for 2 hours and then undergoing reperfusion; and propofol group undergoing peritoneal injection of propofol 2 hours before the ischemia-reperfusion of MCAO. Then the rats in the 3 groups were re-divided into subgroups of 5 rats, totally 18 subgroups, to be decapitated 2, 3, 6, 12, 24, and 72 hours after reperfusion for the latter 2 groups, and their brains were taken out and fixed. Immunohistochemistry was used to detect the translocation of NF-kappaB in the neurons and the expression of IL-1, TNF-alpha, and ICAM-1 in the brain. Western blotting was used to detect the expression of NF-kappa B. The opposite non-ischemic cortexes were used as controls.

RESULTS

Two to 24 hours after the reperfusion NF-kappaB was significantly translocated from the cytoplasm into the nucleus; however, NF-kappa B remained in the cytoplasm of bilateral cortexes in the sham operation groups, and the nonischemic cortexes in the I/R and protofol groups. The translocation of NF-kappa B from cytoplasm into nucleus was significantly inhibited in the ischemic cortex of the propofol group. The expression values of NF-kappa B in the nuclei of ischemic cortexes in the I/R group 2 to 24 hours after reperfusion were significantly higher than those in the sham operation group and the nonischemic cortexes of the I/R and propofol groups (all P < 0.01). The expression values of NF-kappa B in the ischemic cortex of the propofol group 2 to 24 hours after reperfusion was significantly lower than that of the I/R group (all P < 0.05). The expression values of IL-1, TNF-alpha, and ICAM-1 in the ischemic cortexes were significantly higher than that in the cortex of the sham operation group and those in the nonischemic cortexes of the I/R group and propofol group (P < 0.01 or P < 0.05) and the expression values of IL-1, TNF-alpha, and ICAM-1 in the propofol group were all significantly lower than those in the I/R group (all P < 0.05).

CONCLUSION

Propofol inhibits the inflammatory reaction by inhibiting the NF-kappa B activation during focal ischemia-reperfusion which may be one of the mechanisms of its neuroprotective function.

Authors+Show Affiliations

Department of Anesthesiology, Beijing Chaoyang Hospital Affiliated to Capital University of Medical Sciences, Beijing 100020, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

chi

PubMed ID

15730629

Citation

Feng, Chun-sheng, et al. "[Effect of Propofol On the Activation of Nuclear Factor-kappa B and Expression of Inflammatory Cytokines in Cerebral Cortex During Transient Focal Cerebral Ischemia-reperfusion: Experiment With Rats]." Zhonghua Yi Xue Za Zhi, vol. 84, no. 24, 2004, pp. 2110-4.
Feng CS, Ma HC, Yue Y, et al. [Effect of propofol on the activation of nuclear factor-kappa B and expression of inflammatory cytokines in cerebral cortex during transient focal cerebral ischemia-reperfusion: experiment with rats]. Zhonghua Yi Xue Za Zhi. 2004;84(24):2110-4.
Feng, C. S., Ma, H. C., Yue, Y., Zhang, Y. Q., & Qu, X. D. (2004). [Effect of propofol on the activation of nuclear factor-kappa B and expression of inflammatory cytokines in cerebral cortex during transient focal cerebral ischemia-reperfusion: experiment with rats]. Zhonghua Yi Xue Za Zhi, 84(24), 2110-4.
Feng CS, et al. [Effect of Propofol On the Activation of Nuclear Factor-kappa B and Expression of Inflammatory Cytokines in Cerebral Cortex During Transient Focal Cerebral Ischemia-reperfusion: Experiment With Rats]. Zhonghua Yi Xue Za Zhi. 2004 Dec 17;84(24):2110-4. PubMed PMID: 15730629.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Effect of propofol on the activation of nuclear factor-kappa B and expression of inflammatory cytokines in cerebral cortex during transient focal cerebral ischemia-reperfusion: experiment with rats]. AU - Feng,Chun-sheng, AU - Ma,Hai-chun, AU - Yue,Yun, AU - Zhang,Yong-qian, AU - Qu,Xiang-dong, PY - 2005/2/26/pubmed PY - 2006/5/10/medline PY - 2005/2/26/entrez SP - 2110 EP - 4 JF - Zhonghua yi xue za zhi JO - Zhonghua Yi Xue Za Zhi VL - 84 IS - 24 N2 - OBJECTIVE: To investigate the effect of propofol on the activation of nuclear factor-kappa B (NF-kappa B) and the expression of inflammatory cytokines, such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule-1 (ICAM-1) in cerebral cortex during transient focal cerebral ischemia-reperfusion, and to discuss the probable mechanism of its protective effect. METHODS: Ninety male Wistar rats were randomly divided into 3 equal groups: sham operation group undergoing sham operation; ischemia/reperfusion (I/R) group undergoing thread embolism of the left middle cerebral artery occlusion (MCAO) to cause focal ischemia for 2 hours and then undergoing reperfusion; and propofol group undergoing peritoneal injection of propofol 2 hours before the ischemia-reperfusion of MCAO. Then the rats in the 3 groups were re-divided into subgroups of 5 rats, totally 18 subgroups, to be decapitated 2, 3, 6, 12, 24, and 72 hours after reperfusion for the latter 2 groups, and their brains were taken out and fixed. Immunohistochemistry was used to detect the translocation of NF-kappaB in the neurons and the expression of IL-1, TNF-alpha, and ICAM-1 in the brain. Western blotting was used to detect the expression of NF-kappa B. The opposite non-ischemic cortexes were used as controls. RESULTS: Two to 24 hours after the reperfusion NF-kappaB was significantly translocated from the cytoplasm into the nucleus; however, NF-kappa B remained in the cytoplasm of bilateral cortexes in the sham operation groups, and the nonischemic cortexes in the I/R and protofol groups. The translocation of NF-kappa B from cytoplasm into nucleus was significantly inhibited in the ischemic cortex of the propofol group. The expression values of NF-kappa B in the nuclei of ischemic cortexes in the I/R group 2 to 24 hours after reperfusion were significantly higher than those in the sham operation group and the nonischemic cortexes of the I/R and propofol groups (all P < 0.01). The expression values of NF-kappa B in the ischemic cortex of the propofol group 2 to 24 hours after reperfusion was significantly lower than that of the I/R group (all P < 0.05). The expression values of IL-1, TNF-alpha, and ICAM-1 in the ischemic cortexes were significantly higher than that in the cortex of the sham operation group and those in the nonischemic cortexes of the I/R group and propofol group (P < 0.01 or P < 0.05) and the expression values of IL-1, TNF-alpha, and ICAM-1 in the propofol group were all significantly lower than those in the I/R group (all P < 0.05). CONCLUSION: Propofol inhibits the inflammatory reaction by inhibiting the NF-kappa B activation during focal ischemia-reperfusion which may be one of the mechanisms of its neuroprotective function. SN - 0376-2491 UR - https://www.unboundmedicine.com/medline/citation/15730629/[Effect_of_propofol_on_the_activation_of_nuclear_factor_kappa_B_and_expression_of_inflammatory_cytokines_in_cerebral_cortex_during_transient_focal_cerebral_ischemia_reperfusion:_experiment_with_rats]_ L2 - http://journal.yiigle.com/LinkIn.do?linkin_type=pubmed&amp;issn=0376-2491&amp;year=2004&amp;vol=84&amp;issue=24&amp;fpage=2110 DB - PRIME DP - Unbound Medicine ER -