Objective To investigate the effect of naringin on hyperlipidemia in mice and to elucidate its mechanism.Methods C57BL/6 mice were randomly divided into control group,hyperlipidemia group and naringin group.Mice in hyperlipidemia group and naringin group were fed high-fat diet for 4 weeks,and hyperlipidemia model was established.The control group was fed normal diet.After successful modeling,naringin group mice were intragastric with 200 mg·kg-1 naringin per day,and mice in control group and hyperlipemia group were intragastric with 0.9％NaCl per day for 5 weeks.The blood of mice was collected for lipid detection.The activities of superoxide dismutase(SOD)and catalase(CAT)and the contents of malondialdehyde(MDA)and glutathione(GSH)were detected by biochemical method.Western blot was used to detect the protein expression.Results The activity of SOD in liver tissue of mice in control group,hyperlipidemia group and naringin group were(58.43±6.27),(37.16±4.10)and(51.23±4.81)U·mg prot-1,respectively;CAT activities were(176.11±13.59),(112.65±10.02)and(158.46±14.37)U·mg prot-1,respectively;the contents of MDA were(3.15±0.74),(12.62±2.07)and(5.76±1.83)U·mg prot-1;the contents of GSH were(91.52±11.47),(34.16±4.62)and(71.64±8.79)U·mg prot-1,respectively;the relative protein expression levels of induced nitric oxide synthase(iNOS)were 0.28±0.05,4.26±1.13 and 0.94±0.19;the relative protein expression levels of adenosine 5'-monophosphate activated protein kinase(AMPK)were 1.32±0.18,0.84±0.11 and 1.49±0.16,respectively;the relative protein expression levels of cholesterol regulatory element binding protein(SREBP)were 1.76±0.24,5.78±1.21 and 2.93±0.42;the relative protein expression levels of 3-hydroxy-3-methyl glutaryl coenzyme A reductase(HMGCR)were 1.69±0.18,6.13±1.38 and 3.26±0.43,respectively.The above indexes in the control group and the naringin group were significantly different from those in the hyperlipidemia group(P＜0.05,P＜0.01,P＜0.001).Conclusion Naringin can effectively regulate the level of blood lipids,inhibit oxidative stress and apoptosis in hyperlipidemia mice,and its mechanism may be related to the regulation of AMPK/HMGCR/SREBP signaling pathway.
naringinadenosine 5'-monophosphate activated protein kinase/3-hydroxy-3-methyl glutaryl coenzyme A reductase/sterol-regulatory element binding proteins signaling pathwayhyperlipidemiaoxidative stress
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