Objective:

2

To research the effect of traditional Chinese medicine compound Chaijie Yiganxian (CJYGX) on the hepatic fibrosis in rats and explore the mechanism.

Method:

2

Totally 60 SD rats were randomly divided into normal group

model group

positive group (Biejia Jianwan)

and low

medium and high-dose CJYGX groups. Except for the normal group

the remaining five groups were involved in establishing the hepatic fibrosis model through the intraperitoneal injection of thioacetamide (TAA). Fourth weeks after modeling

the positive group was given Biejiajian pill (1 g·kg

-1

·d

-1

)

and high

medium and low-dose CJYGX groups were given CJYGX(7.96

3.98

1.99 g·kg

-1

·d

-1

)

respectively. The model group was given normal saline once a day for 5 weeks. 24 h after the last intragastric administration with chloral hydrate

the rats were anesthetized slightly. Serum and liver tissues were collected. The liver wet weight was weighed electronically

and the liver index was calculated. Liver function indexes [alanine transaminase (ALT)

aspartate aminotransferase (AST)

alkaline phosphatase (ALP)] and serum markers [laminin (LN)

hyaluronidase (HA)

Ⅳ collagen (CⅣ)

procollagen Ⅲ (PCⅢ)]

of hepatic fibrosis were detected by enzyme linked immunosorbent assay (ELISA). The degree of hepatic fibrosis by Masson stain

mRNA expressions of transforming growth factor-

β

1

(TGF-

β

1

)

Smad2

Smad3

Smad4

Smad7 were detected by Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR)

and protein expression levels of platelet derived growth factor (PDGF)

TGF-

β

1

and

α

-smooth muscle actin (

α

-SMA) were detected by immunohistochemical or Western blot.

Result:

2

Compared with the blank group

the model group liver index was significantly increased; the contents of ALP

AST and ALT were significantly increased; the liver fibrosis indexes LN

HA

Ⅳ-C

PCⅢ and HYP were significantly increased; the degree of liver fibrosis was significantly increased in Masson tissue; the mRNA expressions of TGF-

β

1

Smad2

Smad3

Smad4 were significantly increased; and the Smad7 mRNA expression was significantly decreased. The protein expressions of TGF-

β

1

PDGF and

α

-SMA increased significantly (

P

<

0.01). Compared with model group

different doses of CJYGX can reduce the concentrations of ALP

AST

ALT

and the hepatic fibrosis indexes (LN and HA

Ⅳ-C

PCⅢ) and HYP also were significantly lower. Masson staining show that CJYGX can significantly reduce the degree of hepatic fibrosis. Real-time PCR show that CJYGX can significantly down-regulate mRNA expressions of TGF-

β

1

Smad2

Smad3

Smad4 and up-regulate mRNA expression of Smad7.Immunohistochemical and Western blot analysis show that

compared with model group

CJYGX could significantly reduce the protein expressions of TGF-

β

1

PDGF and

α

-SMA (

P

<

0.05

P

<

0.01).

Conclusion:

2

Traditional Chinese medicine compound CJYGX may protect TAA-induced hepatic fibrosis injury by interfering with TGF-

β

1

/Smad signaling pathway.