动物实验,非酒精性脂肪肝 z-bo 2020-08-28 412

　　Objective: To explore the mechanism of trace element strontium to improve 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 received normal feed, and the other 4 groups received high-fat feed. From the 6th week, the 18 mg/L and 36 mg/L strontium groups were given 18 mg/L and 36 mg/L strontium-containing drinking water, respectively. The 11th week Gave the stomach, the 18 mg/L and 36 mg/L strontium groups were given 18 mg/L and 36 mg/L strontium-containing water 3 mL/kg body weight, respectively, and the simvastatin group was given simvastatin 10 mg/kg Body weight, the control group and the model group were infused with normal saline 3 mL/kg body weight. Rats were sacrificed at the end of the 14th week. Serum TG, TC, LDL-C and liver tissue TG, TC content were detected, and liver tissue oil red O staining was performed to observe steatosis. Immunohistochemistry was used to detect liver tissue GRP78, SREBP2, HMGCR and LDLr protein The expression level.

　　Results: Compared with the control group, the serum TC, LDL-C, liver TC and TG of the model group were all increased (P<0.05). Compared with the model group, the serum TC, LDL-C and liver TC of the 36 mg/L strontium group Both TG and TG decreased (P<0.05). Oil red O staining showed that the liver tissue of the model group contained a large number of red-stained lipid particles. The red-stained particles in the 18 mg/L strontium group, 36 mg/L strontium group and simvastatin group were all reduced to varying degrees compared with the model group (P<0.05) ). The results of immunohistochemistry showed that the protein expression levels of GRP78, SREBP2, HMGCR and LDLr in the liver tissue of the model group, the protein expression levels of GRP78, SREBP2 and LDLr in the liver tissue of the 18 mg/L strontium group, and the liver tissue of the 36 mg/L strontium group The expression level of LDLr protein in tissues and the expression levels of SREBP2 and LDLr protein in liver tissues of rats in the simvastatin group were significantly higher than those in the control group (P<0.05). The expression levels of GRP78, SREBP2 and HMGCR protein in the liver tissue of the 36 mg/L strontium group were significantly lower than the model group, while the expression level of LDLr protein was significantly higher than that of the model group; the expression level of GRP78 and HMGCR protein in the liver tissue of the simvastatin group was obvious Lower than the model group (P<0.05); 18="" and="" p="">0.05).

　　Conclusion: Long-term intake of higher concentrations of strontium can 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.