Abstract:
OBJECTIVE To study the protective effects of Compound Rhodiola extract on acute cerebral ischemia in mice and focal cerebral ischemia in rats.
METHODS KM mice were randomly divided into sham group, model group, nimodiping positive control group, and Compound Rhodiola extract high, medium and low dose groups(2.18, 1.09, 0.55 g·kg
-1). The acute cerebral ischemia model in mice was induced by ligaturing the bilateral carotid arteries and vagus nerve after 7 d of intragastric administration, and survival time was observed. SD rats were randomly divided into sham group, model group, nimodiping positive control group, and Compound Rhodiola extract high, medium and low dose groups(1.45, 0.73, 0.36 g·kg
-1). Middle cerebral artery occlusion(MCAO) models in rats were made with thread blocking method. Drugs were given to the rats 7 d before preparation of the models, ig for consecutive 10 d. The scores of nerve function and cerebral infarction proportion were measured. TUNEL method was used to evaluate the apoptosis of neurons. Western bolt method was used to detect the quantitative expression level of caspase-3.
RESULTS The high and medium dose groups of Compound Rhodiola extract could prolong the survival time in mice with acute cerebral ischemia, and had significant difference compared with model group (
P<0.01 or
P<0.05). Compared with model group, the high and medium dose groups of Compound Rhodiola extract significantly reduced the scores of nerve function (
P<0.01 or
P<0.05); Each dose group of Compound Rhodiola extract significantly reduced the proportion of cerebral infarction, inhibited the apoptosis of cortex neurons in rats and down-regulated the caspase-3 expression (
P<0.01 or
P<0.05).
CONCLUSION Compound Rhodiola extract has good protective effects on cerebral ischemia models in mice and rats. It can prolong the survival time in mice with acute cerebral ischemia, alleviate the nerve function damage, reduce the proportion of cerebral infarction and inhibite the apoptosis of neurons in MCAO rats. The mechanism is related to the down-regulation of the expression of caspase-3.