Objectives Study the expression of Heat shock protein 22 in the aortic hyperlipidemia rat and the effect of atorvastain intervention.
Methods 12 female SD rats were divided into normal group (n = 4) and model group (n = 8). Normal group was fed rodent chow and model group was fed high-fat diets. All of the rats in the model group were given intraperitoneal injections 0f vitamin D3 with total dose of 700000U/kg during the first three days. The serum lipids were detected after 10 weeks feeding in order to identify hyperlipidemia model. After the formation of hyperlipidemia,the model rats were divided into hyperlipidemia control (n = 4) and statins intervention (n = 4) two groups. Statins intervention group was given storvastain gavage with the dosage of 20mg/kg and fed the high-fat diets daily. Hyperlipidemia control group was still fed high-fat diets. After 21-weeks,all the rats were collected blood samples and aorta. The aorta morphology was observed by HE staining, the expression of HSP22 and TNF-α in the aortic vascular wall were detected by immunohistochemical.
High-fat diets fed for 10 weeks typical hypercholesterolemia was set up successfully.
After the experiment the thoracic and abdominal aorta of the hyperlipidemia control and statins intervention group were manifested exrensive calcification in the media. Chondroid cells proliferation were found in the tissue slice. No significant changes in the normal group.
The expression of HSP22 were negative in the normal group,while positive in the hyperlipidemia controlgroup and statins intervention group. The mean density of HSP22 postive particles was lower in the statins intervention group compared to hyperlipidemia control group (0.219 ± 0.090 vs 0.377 ± 0.094, P<0.05).
The expression of TNF-α were negative in the normal group, while positive in the hyperlipidemia control group and statins intervention group. There were no significant difference in the mean density of the hyperlipidemia control group and statins intervention group (P>0.05).
The high-fat diets combine vitamin D3 could slowly induce hyperlipidemia and arterosclerosis rat model.
Hyperlipidemia could increase the expression of HSP22 in the rat aorta. HSP22 may play a protective role in the hyperlipidemia induced artery lesion.
Atorvastain could decrease the expression of HSP22 and the mechanism may be partially related to the anti-inflammatory effect.