Key result
Low-dose emodin lowers LDL-C and improves aortic vasorelaxation in rats via enhanced nitric oxide.
Why the study?
Few studies have investigated the mechanism of emodin's anti-hypercholesterolemic effect in a high-cholesterol diet model.
Does emodin improve lipid profiles and endothelial function in a rat model of hypercholesterolemia?
Does emodin improve lipid profiles and endothelial function in a rat model of hypercholesterolemia?
Low-dose emodin improves lipid profiles, endothelial function, and antioxidant capacity in a rat model of hypercholesterolemia.
Emodin shows lipid-lowering effects in hypercholesterolemic rats; hypothesis-generating and leaves open human translation pending clinical trials.
BACKGROUND Emodin has been widely used in traditional Chinese medicine, but few studies have tried to understand the mechanism of its anti-hypercholesterolemic effect. MATERIAL AND METHODS To delineate the underlying pathways, high-cholesterol diet (HCD)-fed Sprague-Dawley rats were orally administrated emodin or the lipid-lowering medicine simvastatin. Emodin was administered at 10, 30, or 100 mg/kg, while simvastatin was administered at 10 mg/kg. Parameters measured included lipid profiles (serum total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol, aorta endothelium-dependent vasorelaxation in response to acetylcholine, and nitric oxide (NO) production. RT-qPCR and western blotting were performed to evaluate aortic endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS), and hepatic LDL receptor (LDLR). Indices of liver and serum oxidation were also measured. RESULTS The atherogenic index was increased by the HCD but significantly reduced in all treatment groups. The HCD-fed experimental group treated with emodin at 10 mg/kg had significantly lower serum total-C and LDL-C and improved aorta vasorelaxation and enhanced NO production. Also, emodin significantly attenuated the lipid profiles and restored endothelial function, as reflected by upregulated expression of hepatic LDLR and p-eNOS, respectively. Furthermore, emodin at 10 mg/kg significantly enhanced superoxide dismutase activity, lowered the malondialdehyde level in both liver and serum, and enhanced catalase activity in serum. CONCLUSIONS The ability of emodin to inhibit hypercholesterolemia in HCD-fed rats was associated with lower serum total-C and LDL-C, restoration of aortic endothelial function, and improved antioxidant capacity. Low-dose emodin showed better protection of aortic endothelium and better antioxidant activity than did higher doses.
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Lv et al. (2021) studied Hypercholesterolemia. Emodin vs. Simvastatin (10 mg/kg) and HCD alone was evaluated on Lipid profiles, aorta endothelium-dependent vasorelaxation, and nitric oxide production. In high-cholesterol diet-fed rats, low-dose emodin (10 mg/kg) significantly lowered serum total cholesterol and LDL-C, improved aorta vasorelaxation, and enhanced nitric oxide production.
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