动物造模,非酒精性脂肪肝 z-bio 2021-07-19 279

　　Objective: To explore the mechanism of the trace element strontium in improving non-alcoholic fatty liver in rats.

　　Method: 50 SD rats were randomly divided into control group, model group, 18 mg/L strontium group, 36 mg/L strontium group, and simvastatin group. The control group was given a normal diet, and the other 4 groups were given a high-fat diet. From the 6th week, 18mg/L and 36mg/L strontium were given 18mg/L and 36mg/L strontium. I was drinking water. Start drinking water containing strontium from the 11th week. Water containing 18 mg/L and 36 mg/L strontium was injected at 3 mL/kg body weight of 18 mg/L and 36 mg/L, respectively. The body weight of the Symvasstat group was 10 mg/kg. The control group and the model group were given 3 mL/kg body weight of normal saline. The rats were sacrificed at the end of the 14th week. Detect serum TG, TC, LDL-C and liver tissue TG, TC content. The liver tissue was stained with Oil Red O and fatty degeneration was observed. Use immunohistochemistry to detect liver tissue GRP78. , SREBP2, HMGCR and LDLr protein expression levels.

　　Result: The serum TC, LDL-C, liver TC and TG of the model group were higher than those of the control group (P u003c0.05).

　　Conclusion: Long-term intake of high concentrations of strontium can improve lipid metabolism and reduce NAFLD. Its mechanism of action may be related to the regulation of endoplasmic reticulum stress, HMGCR activity and LDLr function.