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Xu, F., Dai, C.L., Peng, S.L., Zhao, Y., Jia, C.J., Xu, Y.Q. and Zhao, C. (2014) Polymyxin B Protects against Hepatic Ischemia/Reperfusion Injury in a Rat Model of Obstructive Jaundice. Inflammation, 37, 1015-1021.
http://dx.doi.org/10.1007/s10753-014-9822-4

has been cited by the following article:

  • TITLE: Polymyxin B Alleviates Angiotensin II-Induced Stress Fiber Formation and Cellular Hypertrophy

    AUTHORS: Kwang-Seok Oh, Jeong Hyun Lee, Byung Koo Oh, Jihye Mun, Byung Kil Park, Byung Ho Lee

    KEYWORDS: Polymyxin B, GRK5, Angiotensin II, Actin Stress Fiber, Cellular Hypertrophy

    JOURNAL NAME: Pharmacology & Pharmacy, Vol.5 No.9, August 21, 2014

    ABSTRACT: Polymyxin B is widely used antibiotic in the clinic for resistant Gram-negative infections. In addition, polymyxin B-immobilized hemoperfusion cartridge has been used for endotoxin removal therapy in patients with septic shock. The aim of this study was to investigate the anti-fibrotic and anti-cellular hypertrophic effects of polymyxin B, and further to explore its possible mechanism. Polymyxin B (3, 10 μM) significantly inhibited stress fiber formation induced by angiotensin II (Ang II) in rat heart-derived H9c2 cells. Furthermore, polymyxin B (1 - 10 μM) showed a potent inhibitory effect on Ang II-induced cellular hypertrophy in H9c2 cells. Under the mechanism study, the inhibitory activities of polymyxin B against kinases involved in cellular hypertrophy such as AKT1, CAMK, GRK5, GSK3β, MLCK, PKC, PKD2, AMPK, ROCK2, p70S6K, SGK1were evaluated. Polymyxin B possesses a potent G protein related kinase 5 (GKR5) inhibitory activity with IC50 value of 1.1 μM, and has an ATP non-competitive inhibitory mode. Taken together, these results indicate that polymyxin B alleviates Ang II-induced stress fiber formation and cellular hypertrophy, and propose that one mechanism underlying these effects involves inhibition of the GRK5 pathway.