| abstract |
The present invention finds that under the condition of high-fat diet, anistrisulfide (H 2 S donor) can significantly reduce the expression of ACC1, FAS and SCD1, up-regulate FADS1 and FADS2, and inhibit the de novo synthesis of toxic saturated fatty acid (palmitic acid); Oleic acid synthesis, promotes fatty acid desaturation, and adjusts the ratio of n‑3/n‑6 polyunsaturated fatty acids. At the same time, inhibition of PAQR3 promotes lipid peroxisomal oxidation and LDL degradation; and can reduce the expression of RTN3, thereby downregulating the overexpression of SREPB1c, reducing the formation of fat droplets in hepatocytes; it can also reduce FATP2 , FATP4, FATP5, and L-FABP were up-regulated, indicating that the drug enhanced the uptake of fatty acids in hepatocytes and promoted their transport; it is particularly noteworthy that anisole can significantly increase the expression of Mitofusin 1, Mitofusin 2, and CPT1a, which promotes mitochondrial Fusion enhances the β-oxidation of fatty acids, and is widely used in the damage of toxic fatty acids to organs such as the heart, brain, liver, and kidney. |