动物造模,大鼠非酒精性脂肪肝 z-bio 2021-01-29 300

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

　　Method: 50 SD rats were randomly divided into control group, model group, 18mg/L strontium group, 36mg/L strontium group and simvastatin group. The control group was given a normal diet, and the remaining 4 groups were given a high-fat diet. From the 6th week, the 18 mg/L and 36 mg/L strontium groups contained 18 mg/L and 36 mg/L strontium, respectively. I give him water. Gavage started from the 11th week. 18 mg/L and 36 mg/L strontium-containing water 3 mL/kg body weight were injected into the 18 mg/L group and 36 mg/L group, respectively. The simvastatin group was given 10 mg/kg. kg body weight. 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. GRP78, SREBP2, HMGCR and LDLr proteins in liver tissue were detected by immunohistochemistry.

　　Result: The serum TC, LDL-C, liver TC and TG of the model group were all higher than those of the control group (P0.05).

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