Objective: To observe the effect of Huangqisan and its disassembled recipes on insulin resistance and mRNA and protein expression levels of 11 beta-hydroxysteroid dehydrogenase typem 1(11β-HSD1)

phosphoenolpyruvate carboxykinase (PEPCK) in type 2 diabetic rats induced by glucocorticoid and high fat diet. Method: The study was performed after the rats received adaptive feeding for 1 week. Rats were randomly divided into normal control group(CD)

glucocorticoid group(GC)

high fat diet group(HFD) and combined model group(HFD+GC)

rosiglitazone group(Ros)

Huangqisan prescription 1 group(HQS-1

2.91 g·kg-1)

 Huangqisan prescription 2 group(HQS-2

3.85 g·kg-1)

and Huangqisan original prescription group(HQS

2.96 g·kg-1)

8 rats in each group. The rats in CD and GC groups were fed with basic diet

and other groups were fed with high-fat diet. The rats in CD and HFD groups were given with the same volume of normal saline

and the rats in other groups were given with prednisolone acetate (3.5 mg·kg-1) by intragasic administration once a day

and then the corresponding testing drugs were given one hour later by intragasic administration. After intervention by drugs for 10 weeks

fasting blood glucose(FBG)

insulin levels and insulin sensitivity index (ISI) of all rats were measured. The liver pathological changes were observed by HE staining; and the mRNA and protein expression levels of 11β-HSD1 and PEPCK in liver issues were detected by Real-time PCR and Western blot methods. Result: As compared with CD group

the rats in HFD+GC model group showed hyperglycemia

hyperinsulinemia

hepatocyte degeneration

and increased expression of 11β-HSD1 and PEPCK(P<0.01)

and pathological examination showed that the pathological changes of liver tissues were obvious. As compared with HFD+GC model group

each treatment group could decrease FPG and insulin levels

increase ISI to some degree

and also improve pathological morphology to some degree. The effect of HQS original prescription on insulin level and pathological morphology was superior to other groups. In addition

HQS and its disassembled recipes could reduce 11β-HSD1 and PEPCK mRNA and protein expression levels to different degrees(P<0.05

P<0.01)

and the effect of Huangqisan original prescription was still superior to other groups. Conclusion: HQS could enhance insulin sensitivity and improve liver pathology

and its mechanism for preventing and treating diabetes and improving insulin resistance was probably related to reducing 11β-HSD1 mRNA and proteins expression levels.