| Objective:To establish a rat hyperlipidemia model for studying the expression of Heatshock protein22(HSP22) and the effect of atorvastatin intervention.Methods:Male Wistar rats (n=30) were selected in the current study. All rats were fed7days to adapt the environment before collecting the blood samples from orbitalvenous plexus. Total cholesterol (TC), triglyceride (TG), low-density lipoproteincholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) in rats serumwere measured to get the baseline levels. The rats were randomly divided into normalcontrol group (n=10) and hyperlipidemia model group (n=20). Normal control grouprats were fed with regular chow and hyperlipidemia model group rats were kept on ahigh-fat diet. In the hyperlipidemia model group, the rats were given intraperitonealinjections of vitaminD3during the first three days. The serum lipids concentrationswere dynamically monitored in the two groups after10weeks’ feeding. Thehyperlipidemia model was achieved according to the TC standard. Afterwards, twosubgroups were established the hyperlipidemia control (n=9) and statins intervention(n=9) group. Statins intervention group rats received high-fat diets and atorvastatingavage at the dosage of20mg/kg. Hyperlipidemia control group and normal controlgroup received high-fat diets and normal rodent chow respectively,whereas all of therats in two groups received saline gavage with the same volume of atorvastatin. Theblood lipids of all the rats were tested again after21weeks treatment. The rats aorticmorphology were performed by HE staining, whereas the expression of HSP22, TNF-α and NF-κB in the aortic vascular wall were assessed by immune-histochemicalassay. Results:1. Changes of blood lipids in the hyperlipidemia rat modelThe serum levels of TC and LDL-C in the hyperlipidemia model group onhigh-fat diets fed for10weeks were1.6(P＜0.05) and1.9(P＜0.05) times higherthen the normal control group respectively. However, TG and HDL-C did not changesignificantly among these groups. Therefore, hypercholesterolemia was establishedsuccessfully.When fed on the high-fat diet for21weeks, the levels of TC and LDL-C in thehyperlipidemia control group rats were5.2(P＜0.01) and8.0(P＜0.01) times higherthen the normal control group. The levels of TC and LDL-C in the statins interventiongroup rats were3.6(P＜0.01) and5.8(P＜0.01) times higher than the normal controlgroup with21-week atorvastatin intervention. Therefore, TC and LDL-C weresignificantly down-regulated with the statins intervention in the hyperlipidemia ratmodel.2. Pathological changes in the rats aorticThere was no obvious pathological change in the thoracic and abdominal aortaof the rats in normal control group. In contrast, the lumen of the thoracic andabdominal aorta was shown irregular under the microscope in the hyperlipidemiagroup, and the media layer were arranged in disorder and accompanied by extensivecalcification lesions. The foam cell and lipidosis were not observed in the tissue slices,but chondroid cells proliferation was seen. In the statins intervention group, thelumen of the thoracic and abdominal aorta was irregular. Moreover, the media layerwas disordered, accompanied by extensive calcification lesions. No Foam cellsaccumulation or lipidosis was seen, but chondroid cells proliferation was observed inthe tissue slice.3. The expression of HSP22No detectable expression of HSP22was found in the normal control group.However, the expression of HSP22was positive in the thoracic aorta wall of thehyperlipidemia control group and the statins intervention group rats. Positive stainingmostly distributed in the media and partly diffused in the intima. The mean density ofHSP22positive particles was significant lower in the statins intervention group whencompared to the hyperlipidemia control group (0.211±0.014vs0.345±0.042，P＜ 0.05).4. The changes of TNF-α and NF-κBNo masculine brown-yellow positive staining was seen in the intima and mediaof rats thoracic aorta in the normal control group. However, the expression of TNF-αand NF-κB were positive in the hyperlipidemia control group and statins interventiongroup. The mean density of TNF-α was significantly lower in the statins interventiongroup compared to the hyperlipidemia control group (0.218±0.09vs0.377±0.094，P＜0.05). The mean density of NF-κB was significant lower in the statins interventiongroup compared to the hyperlipidemia control group(0.200±0.032vs0.363±0.090，P＜0.05).Conclusion:The expression of HSP22in the rat aorta was increased in the hyperlipidemia ratmodel. This effect can be restored by atorvastatin treatment. |
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