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. Author manuscript; available in PMC: 2012 Dec 12.
Published in final edited form as: Prostaglandins Other Lipid Mediat. 2012 Oct 2;99(0):68–78. doi: 10.1016/j.prostaglandins.2012.09.004

Figure 3.

Figure 3

Figure 3

Tie2-CYP2J2-Tr mice have altered levels of Bcl-2, Bcl-xl, Bax and caspase-3 after BCCAO. Immunoblots of brain homogenates show that CYP2J2 overexpression increases levels of Bcl-2 and Bcl-xl (panels A) compared to WT after ischemia. Ischemia results in increased expression of Bax (panels A) and caspase-3 (panels C), an effect that is attenuated in Tie2-CYP2J2-Tr (2J2-Tr) mice. Ratios of Bcl-2/Bax and Bcl-xl/Bax (panel B) are reduced in WT mice after ischemia, but significantly higher in Tie2-CYP2J2-Tr mice. The above effects of CYP2J2 were inhibited by C26, the increased level of Bcl-2 and Bcl-xl (panels A) were decreased with the level of Bax up regulated in Tie2-CYP2J2 Tr mice applied C26 compared to Tie2-CYP2J2-Tr mice alone. Ratios of Bcl-2/Bax and Bcl-xl/Bax (panel B) are reversed when Tie2-CYP2J2-Tr mice administrated C26. Blots were scanned and relative protein levels normalized to β-actin were determined from three independent experiments. *p<0.05 vs. WT ischemic; #p<0.05 vs. Tie2-CYP2J2 ischemia.