Key result
Irbesartan and emodin, alone or in combination, significantly inhibited myocardial remodeling and reduced TGF-β1 and CTGF expression compared to untreated hypertensive rats (P<0.05).
Why the study?
Does the combination of irbesartan and emodin improve myocardial remodeling in Goldblatt hypertensive rats?
RCT (n=60)
Randomized
Does the combination of irbesartan and emodin improve myocardial remodeling in Goldblatt hypertensive rats?
The combination of irbesartan and emodin synergistically inhibits myocardial remodeling in a rat model of renovascular hypertension by reducing TGF-β1 and CTGF expression.
Answers are grounded in this paper and cite their sources.
Supports preclinical testing of irbesartan-emodin synergy; leaves open translation to human myocardial remodeling.
OBJECTIVE: Interactions between the renin-angiotensin system and transforming growth factor-beta 1 (TGF-β1) have been well documented. The aim was to explore the effect of irbesartan combining with emodin on myocardial remodeling in Goldblatt (2K-1C) hypertensive rats. METHODS: All 60 Sprague-Dawley rats were randomly divided into 5 groups as follows: the sham-clipped without any drugs; 2K-1C without any drugs; the 2K-1C with irbesartan (50 mg/kg/day); the 2K-1C with emodin (80 mg/Kg/day); and the 2K-1C with irbesartan and emodin together for the last 8 weeks of a 12-week period of study. The outcome measures included left ventricular mass index, TGF-β1 and angiotensin II in the left ventricle, mRNA expression of TGF-β1, and connective tissue growth factor (CTGF). RESULTS: Compared with 2K1C group, the 2K1C/irbesartan group and 2K-1C/emodin plus irbesartan group had significantly lower systolic blood pressure and local angiotensin II (P < 0.05). The left ventricular mass index in each of the 3 treatment groups was significantly lower than that in the 2K1C group, especially in the combined group. The mRNA/protein TGF-β1 and the mRNA CTGF of 2K1C/irbesartan group, 2K1C/emodin group, and 2K-1C/emodin plus irbesartan group were significantly decreased compared with 2K-1C group (P < 0.05). CONCLUSIONS: Irbesartan or emodin or 2 drugs together can inhibit myocardial remodeling in renovascular hypertension rats probably by reducing TGF-β1 and CTGF expression. The combination of irbesartan and emodin is better than single drug application.
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Chen et al. (2012) conducted an RCT in Goldblatt (2K-1C) renovascular hypertension (n=60). Irbesartan and emodin vs. 2K-1C without drugs (untreated control) and sham-clipped was evaluated on Left ventricular mass index, TGF-β1, angiotensin II, mRNA expression of TGF-β1, and connective tissue growth factor (CTGF) (p=<0.05). Irbesartan and emodin, alone or in combination, significantly inhibited myocardial remodeling and reduced TGF-β1 and CTGF expression compared to untreated hypertensive rats (P<0.05).
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