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Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation.
J Biomed Sci. 2006 Jan; 13(1):127-41.JB

Abstract

Infarction in adult rat brain was induced by middle cerebral arterial occlusion (MCAO) followed by reperfusion to examine whether taxifolin could reduce cerebral ischemic reperfusion (CI/R) injury. Taxifolin administration (0.1 and 1.0 microg/kg, i.v.) 60 min after MCAO ameliorated infarction (by 42%+/-7% and 62%+/-6%, respectively), which was accompanied by a dramatic reduction in malondialdehyde and nitrotyrosine adduct formation, two markers for oxidative tissue damage. Overproduction of reactive oxygen species (ROS) and nitric oxide (NO) via oxidative enzymes (e.g., COX-2 and iNOS) was responsible for this oxidative damage. Taxifolin inhibited leukocyte infiltration, and COX-2 and iNOS expressions in CI/R-injured brain. Taxifolin also prevented Mac-1 and ICAM-1 expression, two key counter-receptors involved in firm adhesion/transmigration of leukocytes to the endothelium, which partially accounted for the limited leukocyte infiltration. ROS, generated by leukocytes and microglial cells, activated nuclear factor-kappa B (NF-kappaB) that in turn signaled up-regulation of inflammatory proteins. NF-kappaB activity in CI/R was enhanced 2.5-fold over that of sham group and was inhibited by taxifolin. Production of both ROS and NO by leukocytes and microglial cells was significantly antagonized by taxifolin. These data suggest that amelioration of CI/R injury by taxifolin may be attributed to its anti-oxidative effect, which in turn modulates NF-kappaB activation that mediates CI/R injury.

Authors+Show Affiliations

Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16283433

Citation

Wang, Yea-Hwey, et al. "Taxifolin Ameliorates Cerebral Ischemia-reperfusion Injury in Rats Through Its Anti-oxidative Effect and Modulation of NF-kappa B Activation." Journal of Biomedical Science, vol. 13, no. 1, 2006, pp. 127-41.
Wang YH, Wang WY, Chang CC, et al. Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation. J Biomed Sci. 2006;13(1):127-41.
Wang, Y. H., Wang, W. Y., Chang, C. C., Liou, K. T., Sung, Y. J., Liao, J. F., Chen, C. F., Chang, S., Hou, Y. C., Chou, Y. C., & Shen, Y. C. (2006). Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation. Journal of Biomedical Science, 13(1), 127-41.
Wang YH, et al. Taxifolin Ameliorates Cerebral Ischemia-reperfusion Injury in Rats Through Its Anti-oxidative Effect and Modulation of NF-kappa B Activation. J Biomed Sci. 2006;13(1):127-41. PubMed PMID: 16283433.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation. AU - Wang,Yea-Hwey, AU - Wang,Wen-Yen, AU - Chang,Chia-Che, AU - Liou,Kuo-Tong, AU - Sung,Yen-Jen, AU - Liao,Jyh-Fei, AU - Chen,Chieh-Fu, AU - Chang,Shiou, AU - Hou,Yu-Chang, AU - Chou,Yueh-Ching, AU - Shen,Yuh-Chiang, Y1 - 2005/11/09/ PY - 2005/06/20/received PY - 2005/09/08/accepted PY - 2005/11/12/pubmed PY - 2006/9/26/medline PY - 2005/11/12/entrez SP - 127 EP - 41 JF - Journal of biomedical science JO - J Biomed Sci VL - 13 IS - 1 N2 - Infarction in adult rat brain was induced by middle cerebral arterial occlusion (MCAO) followed by reperfusion to examine whether taxifolin could reduce cerebral ischemic reperfusion (CI/R) injury. Taxifolin administration (0.1 and 1.0 microg/kg, i.v.) 60 min after MCAO ameliorated infarction (by 42%+/-7% and 62%+/-6%, respectively), which was accompanied by a dramatic reduction in malondialdehyde and nitrotyrosine adduct formation, two markers for oxidative tissue damage. Overproduction of reactive oxygen species (ROS) and nitric oxide (NO) via oxidative enzymes (e.g., COX-2 and iNOS) was responsible for this oxidative damage. Taxifolin inhibited leukocyte infiltration, and COX-2 and iNOS expressions in CI/R-injured brain. Taxifolin also prevented Mac-1 and ICAM-1 expression, two key counter-receptors involved in firm adhesion/transmigration of leukocytes to the endothelium, which partially accounted for the limited leukocyte infiltration. ROS, generated by leukocytes and microglial cells, activated nuclear factor-kappa B (NF-kappaB) that in turn signaled up-regulation of inflammatory proteins. NF-kappaB activity in CI/R was enhanced 2.5-fold over that of sham group and was inhibited by taxifolin. Production of both ROS and NO by leukocytes and microglial cells was significantly antagonized by taxifolin. These data suggest that amelioration of CI/R injury by taxifolin may be attributed to its anti-oxidative effect, which in turn modulates NF-kappaB activation that mediates CI/R injury. SN - 1021-7770 UR - https://www.unboundmedicine.com/medline/citation/16283433/Taxifolin_ameliorates_cerebral_ischemia_reperfusion_injury_in_rats_through_its_anti_oxidative_effect_and_modulation_of_NF_kappa_B_activation_ L2 - https://dx.doi.org/10.1007/s11373-005-9031-0 DB - PRIME DP - Unbound Medicine ER -