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The Protective Effect of 11‐Keto‐β‐Boswellic Acid a selective 5‐LOX Inhibitor on Myocardial ischemia Reperfusion Injury in Rats
Author(s) -
Nassar Noha N,
El Shazly Shimaa M,
El Motteleb Dalia M Abd
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.652.3
Subject(s) - pharmacology , myeloperoxidase , glutathione peroxidase , reperfusion injury , ischemia , in vivo , medicine , glutathione , leukotriene b4 , cyclooxygenase , chemistry , inflammation , enzyme , biochemistry , biology , microbiology and biotechnology
Myocardial ischemia induces 5‐lipoxygenase (LOX) translocation and leukotriene production in the heart. Leukotrienes increase inflammatory responses and could thereby aggravate ischemic injury. This study aimed to investigate whether 11‐Keto‐β‐boswellic (a selective 5‐LOX inhibitor) in three different dose levels exert protective effect on myocardial ischemia reperfusion injury in an in vivo rat heart model. In the current study, forty rats were randomly assigned into 5 groups. GP1: sham operated, Gp 2: ischemic reperfusion (I/R) model while Gps 3,4,5 received 11‐ Keto‐boswellic acid in doses 250, 500, 1000 mg/kg respectively via an oral gavage for 7 days, then subjected to I/R which was induced by ligation of left anterior descending coronary artery for 45 minutes followed by 4 hours reperfusion. At the end of the experiments hearts were excised for analysis. There were significant elevation in the expression of nuclear factor (erythroid‐derived 2)‐like 2, heneoxygenease‐1 and restoration of glutathione peroxidase in a dose dependent manner. Furthermore, there were significant and dose dependent reduction in elevated myeloperoxidase, reduction in the expression of nuclear factor kappa B, tumor necrosis factor ‐α, 5‐LOX, cyclooxygenase‐2 and intercellular adhesion molecule 1 in the heart tissues. We concluded that 11‐Keto‐boswellic acid exerts a protective effect in myocardial I/R injury through mechanisms related to enhancement of antioxidant capacity and prevention of inflammatory cascades.