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Thymoquinone enhances coronary flow and reduces infarct size in Langendorff‐perfused rat hearts through attenuation of inflammatory responce and apoptosis
Author(s) -
Ismail Raed S,
ElSayed ElSayed M,
Mansour Ahmed M,
ElMahdy Mohamed A,
Zweier Jay L
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.652.7
Subject(s) - thymoquinone , pharmacology , oxidative stress , apoptosis , ischemia , chemistry , reperfusion injury , nigella sativa , antioxidant , medicine , biochemistry , traditional medicine
The use of natural compounds to protect against a variety of cardiovascular diseases has been established. Thymoquinone (TQ), a constituent of the volatile oil derived from Nigella sativa seeds , possesses antioxidant, anti‐inflammatory, and vasodilating properties. TQ has demonstrated promising effects against ischemia‐reperfusion (IR) injury in different organs. However, the effect of TQ on myocardial IR injury (m‐IRI) has not been delineated. We show the efficacy and provide a mechanism of TQ effect on m‐IRI. Langendorff‐perfused rat hearts were subjected to 30 min of global ischemia followed by 120 min of reperfusion. TQ was infused for 20 min either pre‐or post‐ischemia. Isolated hearts of TQ‐treated rats were also subjected to the same IR protocols. TQ significantly enhanced coronary flow and markedly reduced the infarct size. IR‐induced increase of TNF‐α, myocardial NF‐kB protein expression, and apoptosis of cardiac muscle cells were attenuated following TQ treatment. Moreover, TQ modulated the expression of myocardial Bcl2, and Bax proteins and also markedly reduced oxidative stress markers and LDH release. This study indicates that TQ induced inhibition of the pro‐inflammatory cytokines and oxidative stress modulated myocardial NF‐kB, Bcl2, and Bax expression, protecting the heart against IR injury. We provide mechanistic insight for understanding the molecular basis and efficacy of TQ on m‐IRI. (NIH # HL63744 to JLZ; Egyptian government)