Objective:To observe the influence of Dedu Honghua Qiwei powder (DHQP) on liver mitochondrial energy metabolism in rats with chronic liver injury induced by Carbon tetrachloride(CCl4). Method: Male Wistar rats were randomly divided into blank control group

model group

colchicine positive control group

DHQP low and high dose groups based on body weight

8 rats in each group. Except the blank control group

other groups were injected intraperitoneally 30% of CCl4 olive oil solution 20 mL·kg-1

twice a week

continued for 7 weeks. Blank control group and model group were given distilled water orally; colchicine group was given 0.4 mg·kg-1

DHQP low-dose group and high-dose group were given 0.62

1.04 g·kg-1 respectively

20 mL·kg-1

bid

continued for 7 weeks. Forty-eight hours after last administration

the rats were fasted 12 hours

and then anesthetized by 10% of chloral hydrate 0.3 mL·kg-1

blood was collected. Liver was taken out immediately

and the left lobe of liver was used to make liver homogenates

then sodium potassium adenosine triphosphatase(Na+-K+-ATPase)activity of liver mitochondrial and superoxide dismutase (SOD)

malondialdehyde (MDA) content of liver tissue were measured. High performance liquid chromatography (HPLC) was used to measure the liver mitochondrial adenosine triphosphate (ATP)

adenosine diphosphate (ADP)

adenosine monophosphate (AMP) and the energy charge was calculated. Result: Compared with blank control group

model group's SOD

Na+-K+-ATPase activity were decreased significantly

MDA contents was increased

colchicine group's Na+-K+-ATPase activity was decreased significantly (P<0.05). Compared with model group

the colchicine group

DHQP high

low dose group's liver mitochondrial Na+-K+-ATPase activity was significantly increased (P<0.05). Compared with blank control group

modeling group's ATP

ADP contents and ED decreased significantly(P<0.05). Compared with model group

DHQP high

low dose group and colchicine group's ATP

ADP contents and ED were significantly increased (P<0.05). Conclusion: DHQP may act an anti-lipid peroxidation role to protect the liver mitochondrial energy metabolism

and act a role as protecting the chronic liver injury.