Astragaloside Ⅳ Regulates Blood Lipid and Inflammatory Factors Through NLRP3 Inflammasome in Early Diabetic Atherosclerosis Rats
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Graphical Abstract
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Abstract
OBJECTIVE To investigate the effect and mechanism of astragaloside Ⅳ in regulating blood lipid and inflammatory factors in early diabetic atherosclerosis rats.METHODS Forty-eight GK rats were randomly divided into model group, positive drugs (gliquantel positive drug combined with benazepril hydrochloride tablets) group, astragaloside Ⅳ low-dose and high-dose groups, 12 rats in each group were fed with high-fat diet. 12 Wistar rats were used as blank control. The administration groups were intragastrically administrated Gliquanone tablets (10 mg/kg), combined with Benazepril hydrochloride tablets (10 mg/kg), astragaloside Ⅳ (20, 40 mg/kg), respectively. The control group and model group were intragastrically given normal saline once a day for 6 weeks. The rat body weight and blood sugar were monitored. The contents of total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL) and low density lipoprotein (LDL) in serum of rats were determined by biochemical method. The pathological morphology of abdominal aorta of rats was observed by HE staining. The contents of IL-6, IL-10, CRP and TNF-α in rat abdominal aorta were determined by ELISA. The protein expression levels of NLRP3, ASC and Caspase-1 in rat abdominal aorta were detected by Western blot.RESULTS Compared with model group, astragaloside Ⅳ high and low dose groups significantly improved atherosclerosis, decreased blood glucose, levels of serum TC, TG, LDL, increased HDL level, decreased the levels of IL-6, CRP, TNF-α in abdominal aorta, increased IL-10 level, and down-regulated the protein expressions of NLRP3, ASC and Caspase-1 (P < 0.05, P < 0.01, P < 0.001, P < 0.000 1).CONCLUSION Astragaloside Ⅳ can regulate blood lipid and inflammatory status in early diabetic atherosclerosis rats, and the mechanism is closely related to the regulation of NLRP3 inflammasome related protein expression.
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