Objective:

2

To study the antimalarial effects and mechanisms of artemisinin (Qinghaosu in Chinese

QHS) on mitochondria in mice infected with

Plasmodium berghei

.

Methods:

2

A total of 108 C57 mice infected with

Plasmodium berghei

were randomly divided into 3 groups by weight: the control group

200 and 400 mg/kg QHS groups. The two QHS treatment groups were further divided into 4 sub-groups with 12 animals each time according to the treatment time

0.5

1

2

and 4 h. Normal saline was intragastrically (i.g.) administered to the control group. The other two groups received different doses of QHS by i.g. administration. Animals were treated once with QHS for different detection time as follows: 0.5

1

2

and 4 h. The mitochondrial energy metabolism

oxidative damage

membrane potential

and membrane permeability and other indexes were detected.

Results:

2

After administration of 200 and 400 mg/kg QHS

adenosine triphosphate (ATP) levels in

Plasmodium

and its mitochondria were reduced (

P

<

0.05)

the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) were increased (

P

<

0.05)

and the activity of superoxide dismutase (SOD) was also increased (

P

<

0.05). At the same time

the membrane potential of the mitochondria was reduced and the degree to which the membrane permeability transition pore was opened was irreversibly increased (

P

<

0.05).

Conclusions:

2

Mitochondria in

Plasmodium

were the targets of QHS

which can adversely affect mitochondrial energy metabolism

oxidative damage

membrane potential

and membrane opening

and ultimately exert an antimalarial effect.