Background: Left ventricular (LV) hypertrophy is a natural adaption of the heart to pressure overloading and
results in life-threatening heart failure. Matrix metalloproteinase (MMP) activity is upregulated in hearts with LV hypertrophy
and its activation is the main cause of change in the LV wall. Clarithromycin (CAM), a major macrolide antibiotic,
has various biologic effects including MMP regulation. However, little is known about the effect of CAM on LV hypertrophy.
Methods and Results: To clarify the role of CAM on LV hypertrophy, we used the transverse aortic constriction (TAC)
model. The mice were randomly assigned into three groups; (a) CAM administration with TAC (CAM-treated group,
n=10); (b) vehicle administration with TAC (non-treated group, n=10); (c) vehicle administration with sham-operation
(control group, n=10). M-mode echocardiograms showed that LV end-diastolic posterior wall (LVPWd) thickness increased
progressively from week 1 to 3 after TAC in the non-treated group. However, it was attenuated in the CAMtreated
group. Furthermore, heart to body weight ratio increased in the non-treated group (15.8±1.7%); this increase was
negated by CAM administration (10.2±1.4%). Histpathologically, LV wall thickness increased in the non-treated group
(18.0±4.0%); this increase was also negated in the CAM-treated group (-8.5±3.5%). Real-time RT-PCR demonstrated that
CAM treatment tended to suppress MMP-9 and elevate TIMP-2 mRNA levels compared to the non-treated group.
Conclusion: CAM attenuates the progression of LV hypertrophy via MMP suppression after pressure overload in mice. It
might be a basic solution for LV hypertrophy.
Keywords: Clarithromycin, clarithromycin, extracellular matrix, echocardiograms, heart, fibrosis, macrolide antibiotic, matrix
metalloproteinase, mice, pressure overload, pathology, polymerase chain reaction, transverse aortic constriction, ventricular
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