[Syndrome identification of CCl4 induced liver fibrosis model rats based on syndrome detecting from recipe used].

Objective: To further demonstrate the cognition upon the prominent effect of Yiguanjian and Xiayuxue Decoction on the CCI4 induced rat model of chronic liver fibrosis which have been verified in the previous studies. From the viewpoint of detecting TCM syndrome by recipe used, through this cognition the pathological features of the liver injury model manifesting a syndrome of "Gan-yin deficiency with blood stasis obstructing collaterals" were further explored.

Methods: Wistar rats were randomly divided into the normal group, the model group, and the three medicated groups. All rats, except those in the normal group, were made into chronic liver injury model by subcutaneously injecting CCI4 for 12 weeks. Medication for the three medicated groups began from the 9th week after modeling, with oral administering of Yiguanjian (YGJ, a recipe has been verified to be effective for liver injury and fibrosis), Liuwei Dihuang Decoction (LWDH, a recipe with effects similar to YGJ) and Yinchenhao Decoction (YCHD, a recipe functioned differently) respectively for four weeks. Rats were sacrificed at the end of the experiment, changes of hepatic function, liver pathology and hydroxyproline (Hyp) content in the liver tissue were detected, and contents of Afamin and mRNA expression of alpha-smooth muscle actin (alpha-SMA) in the liver tissue were assayed as well with Real-time PCR.

Results: As compared with the normal group, the pathological figures of the chronic liver injury and fibrosis and hepatic function deterioration obviously appeared in the model rats, with the liver content of Hyp and alpha-SMA mRNA expression increased, and Afamin mRNA expression decreased significantly. In the YGJ treated group, the hepatic collagen hyperplasia and deteriorated hepatic function alleviated significantly after treatment, with content of Hyp significantly lowered, and mRNA expressions of alpha-SMA and Afamin restored to some extent (P < 0.05); the same effects on mRNA expressions of alpha-SMA and Afamin were shown in the LWDH treated group, also a decreasing trend of Hyp content (0.05 < P < 0.1), and a significant decreasing of alanine transaminase (ALT) activity was found; while in the YCHD treated group these pharmacological effects mentioned above were not observed at all.

Conclusion: The pharmacological effects of LWDH and YGJ were similar to some degree, which gives support to the cognition that the feature of chronic liver injury model rat induced by CCI4 is attributable to yin-deficiency sydrome.