Objective

2

To explore the mechanism and pathological basis of phlegm syndrome in metabolic syndrome （MS）.

Methods

2

Fifty rats were randomly divided into blank group （12 rats） and modeling group （38 rats）. The rat model of MS with phlegm syndrome was established by feeding high sugar， high fat and high salt diet. Twenty-four successfully modeled rats were randomly divided into a model group and a

Erchen Decoction

（二陈汤） group， with 12 rats in each group. The

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group was given 5.3 g/kg of

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by gavage， while the other groups were administered with 10 ml/kg of normal saline by gavage， once daily for four weeks. Plasma lactic acid levels in the blank group and the model group were detected by spectrophotometry at 0， 4， 8 and 12 weeks， respectively. Adenosine triphosphate （ATP） levels in serum and liver tissues of the three groups were detected by ELISA. Citric acid synthase （CS）， carnitine palmitoyltransferase I （CPT-1）， lactate dehydrogenase （LDH）， hypoxia indu-cible factor-1α（HIF-1） levels and mRNA expression in liver tissue were detected by ELISA and real-time PCR.

Results

2

During the modeling period， the difference of lactic acid level between the blank group and the model group was statistically significant. At 8 and 12 weeks of modeling， the lactic acid level of the model group was higher than that of the blank group （

P

＜0.05）. At the end of the 16th week during the experiment， compared with those of the blank group， the ATP content in serum and liver tissue of the model group and the

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group increased （

P

＜0.05）， and the levels of LDH， CS， CPT-1 and HIF-1α in the liver tissue of the model group increased （

P

＜0.05）. Compared with those of the model group， the contents of ATP in serum and liver tissue， the expression of CPT-1 mRNA in liver and the levels of LDH， CPT-1 and HIF-1α in liver tissue of the

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group significantly decreased （

P

＜0.05）.

Conclusion

2

The energy imbalance promotes the development of MS phlegm syndrome， and the change in the energy metabolic pathway is the pathological basis.