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. 2007 Mar;12(1):83–95. doi: 10.1379/CSC-231R.1

Fig 6.

Fig 6.

Hsp70 overexpression mitigates stress-induced cardiomyocytes injury. (A) Protection of Hsp70 on cardiac function of stressed rats. The elevated Hsp70 correlated with significantly decreased frequency of abnormal electrocardiographies (ECGs) of rats after 3 and 4 weeks of stress, to 67 and 50%, respectively, less than controls that were not preconditioned. (B) Hsp70 lessens the severity of injury of stressed rat myocardium. a: control; b–d: stress for 2, 3, and 4 weeks, respectively; e: preconditioned control; f–h: stress for 2, 3, and 4 weeks following preconditioned for 1 week, respectively. The pathological slice viewed with routine light microscopy showed acid fuchsin–positive cells decreased in the myocardium of preheated rats, such that the specific staining grade became lighter and the stain area became smaller. (C) Hsp70 augments cell viability in cardiomyocytes treated with corticosterone (CORT). Upregulation of Hsp70 was accompanied by a significant increase in cell viability in cardiomyocytes treated with CORT for 6 hours, and increased 13, 33, and 16% in response to 10−7, 10−6, and 10−5 mol/L CORT stress, respectively. * P < 0.05 vs control