Processed Rehmanniae radix can Improve Cold Syndrome Damage of Rats by Regulating Glycolipid Metabolism

Objectives: The present study intended to assess the drug property of Rehmanniae Radix Praeparata (PRR), called Shudihuang in traditional Chinese medicine and to discover its mechanism of cold syndrome in rats. Materials and Methods: Through the creation of a typical cold syndrome animal model, the appearance score, body weight, rectal temperatures, and survival rate of the animals treated were evaluated at different time points. Several indices in vivo correlated with glycolipid metabolism (glucose transporters (GLUT- 4), fructose phosphate kinase (PFK- 2), glycogen synthetase (GS), acetyl- CoA carboxylase 1 (ACC1), acetyl- CoA carboxylase 2 (ACC2), hydroxy methylglutaryl coenzyme A (HMG CoA) and hormone- sensitive lipase (HSL) were determined; Western blot is used to analyze of phosphorylated amp- dependent protein kinase (p- AMPK) appearance in liver tissues. Results: Compared with the normal group, the levels of GLUT- 4, PFK- 2, GS, ACC1, ACC2, HMG- CoA, and HSL in the model group all reduced significantly and p- AMPK protein expression diminished. Compared with the model group, PRR can significantly relapse to GLUT- 4, PFK- 2, GS, ACC1, ACC2, HMG- CoA, and HSL (P < 0.01 or P < 0.05) and rise the expression of p- AMPK. RR could suggestively diminution the level of these indices (P < 0.01 or P < 0.05). Conclusion: Drug property of PRR was inferred as trending to “heat and warm,” which still essential for further study. PRR may recover the metabolic function of the cold syndrome model rats by distressing the process of glycolipid metabolism which is by triggering the AMPK signaling pathway.