Effects of ginsenoside Rb1 on spinal cord ischemia-reperfusion injury in rats.

BACKGROUND: The aim of this study was to evaluate the effects of different doses of ginsenoside Rb1 (GRb1) pretreatment on spinal cord ischemia-reperfusion (SCII) in rats and explore the potential mechanisms about the expression of survivin protein after the intervention. METHODS: A total of 90 healthy adult Sprague-Dawley (SD) rats were randomly divided into six groups: sham-operated (n = 15), SCII model (n = 15), and GRb1-treated groups (n = 60). The GRb1-treated group was divided into four subgroups: 10 mg/kg, 20 mg/kg, 40 mg/kg, and 80 mg/kg (n = 15). The corresponding dose of GRb1 was injected intraperitoneally 30 min before operation and every day after operation. Forty-eight hours after model establishment, the neurological function of hind limbs was measured with Basso, Beattie, and Bresnahan (BBB) scale. The superoxide dismutase (SOD) and malondialdehyde (MDA) levels in serum and spinal cord tissue were detected respectively. The expression of survivin protein was observed by immunofluorescence staining. HE and TUNEL staining were used to observe neural cell injury and apoptosis, respectively, in the spinal cord of rats with SCII. RESULTS: The intervention of different doses of GRb1 could increase SOD activity and decrease MDA content in serum and spinal cord tissue, increase survivin protein expression, and decrease neuronal apoptosis. It was dose-dependent, but there was no significant change between 40 mg/kg and 80 mg/kg. CONCLUSIONS: GRb1 could reduce the cell apoptosis induced by SCII through inhibiting oxidative stress. It can also inhibit apoptosis by promoting the expression of Survivin protein. Ginsenoside Rb1 had a dose-dependent protective effect on SCII in the dose range of 10 mg/kg-40 mg/kg.

[Changes of mitochondrial apoptosis in spinal cord ischemia-reperfusion injury and the effects of Herba Erigerontis Breviscapi Injection preconditioning intervention in rabbits].

OBJECTIVE: To investigate the mechanisms of mitochondrial apoptosis in spinal cord ischemia-reperfusion injury and the effects of Herba Erigerontis Breviscapi Injection preconditioning intervention. METHODS: Sixty Japanese rabbits were divided into sham-operated group, ischemia group, ischemia-reperfusion group (1, 6, 24 and 48 h), and Herba Erigerontis Breviscapi Injection group (1, 6, 24 and 48 h). Clamping the abdominal aorta was used to construct the rabbit model of spinal cord ischemia-reperfusion injury. The rabbits in the ischemia-reperfusion group and the Herba Erigerontis Breviscapi Injection group underwent reperfusion for 1, 6, 24, 48 h respectively after fifty-minute ischemia. The rabbits in the Herba Erigerontis Breviscapi Injection group were administered with Herba Erigerontis Breviscapi Injection at 9 mg/kg 30 minutes before ischemia. Rate of apoptotic cells was measured by flow cytometry; contents of caspase-9 and apoptosis-inducing factor (AIF) in cytoplasm and serum were measured by enzyme-linked immunosorbent assay. RESULTS: Compared with the sham-operated group and the ischemia group, the rates of apoptotic cells, the contents of caspase-9 and AIF in cytoplasm were increased at all time points after reperfusion, and the contents of caspase-9 and AIF in serum were decreased after 1 h and 6 h reperfusion, and increased after 24 h and 48 h reperfusion in the ischemia-reperfusion group. Herba Erigerontis Breviscapi Injection intervention could decrease the rate of apoptotic cells and the contents of caspase-9 and AIF in cytoplasm and serum as compared with those in the ischemia-reperfusion group, and the effects appeared after 1 h reperfusion. CONCLUSION: The apoptosis of nerve cells after spinal cord ischemia-reperfusion is related to the mitochondrial pathways. Herba Erigerontis Breviscapi Injection can inhibit nerve cell apoptosis by decreasing the contents of caspase-9 and AIF in cytoplasm and serum.