YU Liang-zhu, SHI Chun-rong. Effects of Tetradrine on Cardiotrophin-1 and Its Receptor gp130/LIFR Expression in Left Ventricles of Hypertensive Rats[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(11): 151-155.
DOI:
YU Liang-zhu, SHI Chun-rong. Effects of Tetradrine on Cardiotrophin-1 and Its Receptor gp130/LIFR Expression in Left Ventricles of Hypertensive Rats[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(11): 151-155. DOI: 10.13422/j.cnki.syfjx.2014110151.
Effects of Tetradrine on Cardiotrophin-1 and Its Receptor gp130/LIFR Expression in Left Ventricles of Hypertensive Rats
Objective:To investigate the effects of tetradrine on cardiotrophin-1 (CT-1) and its receptor gp130/leukemia inhibitory factor receptor (LIFR) expression in hypertrophic left ventricles of renohypertensive rats. Method:Two-kidney-one-clip (2K1C) renohypertensive model was established in rats by partial constriction of left renal artery. All the rats were randomly divided into four groups (n=15 per group):① sham-operated group;② hypertensive model group;③-④ low-dose
high-dose tetradrine group
the hypertensive rats were treated with tetradrine (25
50 mg·kg-1·d-1) for 8 weeks. After drug treatment for 8 weeks
the rats were used to measure blood pressure by the standard tail-cuff method
the ratio of left ventricle weight to body weight (LVW/BW)
myocardial collagen content
and mRNA and protein expressions of CT-1
gp130 and LIFR. Result:Compared with sham-operated group
the hypertensive model group exhibited a marked increase in the mRNA and protein expression of CT-1 in hypertrophic myocardium (P<0.01)
but showed a significant decrease in LIFR mRNA and protein expression (P<0.01). Treatment with tetradrine inhibited the myocardial hypertrophy of hypertensive rats
decreased the expression of CT-1 mRNA and protein (P<0.01)
and increased the mRNA and protein expression of LIFR (P<0.01). Conclusion:Our findings suggested that treatment with tetradrine could inhibit myocardial structural remodeling in the left ventricles of renohypertensive rats
the mechanism of which might be related to its regulation of the signaling pathway involving cardiotrophin-1 and its receptor gp130/LIFR.
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