Abstract
Oxidative stress is a common pathological process in stress-stimulated heart failure. Klotho, known as an anti-aging protein, has been shown to play important pleiotropic roles. This study characterized the effect of klotho on the mechanism of pathological alternations in isoproterenol-treated cardiomyocytes. Cardiac injury was induced for 9 days by isoproterenol (subcutaneous injection, 5mg/kg) in BALB/c mice. Klotho (intraperitoneal injection, 0.01 mg/kg) was administered every other day for 4 days, to detect its effects on isoproterenol-induced cardiac alternations. Mouse hearts were harvested at day 9 after isoproterenol injection. Isoproterenol increased the heart weight/body weight (HW/BW) ratio representing abnormal hypertrophic growth, induced disarranged myocardial fibers, and altered cardiomyocyte morphology. However, klotho partly reversed the above pathological alternations. The same effects were also observed in cultured H9c2 cardiomyocytes. Klotho significantly reduced production of isoproterenol-induced reactive oxygen species. However, oxidative stress inhibited the transcriptional activity of the klotho gene promoter. The results suggested that the cardioprotective effects of klotho were related to the attenuation of oxidative stress, and oxidative stress suppressed the transcription of klotho. The results provided a rational basis for the treatment of clinical heart failure.
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