ABSTRACT
Objective: To observe the effects of ginsenoside Rg1 pretreatment on the expression of survivin protein and apoptosis after spinal cord ischemia-reperfusion injury (SCII) in rats so as to explore the possible mechanism of ginsenoside Rg1 on motor function recovery after SCII in rats. Methods: We selected 120 adult healthy SD rats to construct the model of SCII and randomly divided them into four groups: sham operation group, ischemia group, ischemia-reperfusion group, and drug group. Basso Beattie and Bresnahan score (BBB score) was used to evaluate the motor function of the hind limbs of the rats. The expressions of survivin protein and apoptosis-inducing factor (AIF) was observed by immunohistochemistry. The expression and activity of survivin protein and Caspase-9 in each group were observed and analyzed by Western blot and RT-PCR. Results: The intervention of ginsenoside Rg1 could increase the score of the motor function of the rat hind limbs. It could decrease the number of AIF positive cells, but increase the number of survivin protein positive cells. Ginsenoside Rg1 could decrease the expressions of survivin and Caspase-9, and decrease the apoptosis of nerve cells in SCII. Conclusion: Ginsenoside Rg1 could inhibit the expression of Caspase-9 by promoting the expression of survivin protein and decrease the apoptosis of rat SCII induced by the level of cytoplasmic AIF.
ABSTRACT
@#Objective To observe the effects of ginsenoside Rb1 pretreatment on spinal cord ischemia-reperfusion injury in rats, and to explore the possible mitochondrial mechanism of ginsenoside Rb1 against ischemia-reperfusion injury. Methods The spinal cord ischemia-reperfusion injury model was established. The rats were randomly divided into sham operation group (n=12), ischemia-reperfusion group (n=12) and drug group (n=12). The drug group received gin-senoside Rb1 peritoneal injection with 10 mg/kg, 20 mg/kg, 40 mg/kg and 80 mg/kg, respectively, 30 minutes be-fore modeling and once a day after modeling. After 48 hours of reperfusion, the BBB score was tested, the levels of superoxide dismutase (SOD) and malonaldehyde (MDA) in the serum and spinal cord tissue, and the cyto-chrome C oxidase (COX) activity in spinal cord tissue were detected. Results Compared with the ischemia-reperfusion group, the BBB score increased (P<0.05), the SOD level increased, and the MDA level decreased both in serum and spinal cord tissue, the activity of COX increased in the spinal cord tissue (P<0.05). All the indexes were dose-dependent, however, no difference was found between 40 mg/kg and 80 mg/kg. Conclusion Ginsenoside Rb1 can inhibit oxidative stress induced by spinal cord ischemia-reperfusion injury in rats by inhibiting mitochondrial damage. The protective effect of ginsenoside Rb1 on the spinal cord ischemia-reperfu- sion injury is dose-dependent during 10 to 40 mg/kg dose.