摘要
Background Danshen （Radix Salvia miltiorrhizae） has been used as a traditional medicine in Asia for treatment of various microcirculatory disturbance related diseases. Tanshinones are mainly hydrophobic active components, which have been isolated from Danshen and show various biological functions. In this study, we observed the neuroprotective effect of tanshinone I （Tsl） against ischemic damage in the gerbil hippocampal CA1 region （CA1） after transient cerebral ischemia and examined its neuroprotective mechanism. Methods The gerbils were divided into vehicle-treated-sham-group, vehicle-treated-ischemia-group, Tsl-treated-sham- group, and Tsl-treated-ischemia-group. Tsl was administrated intraperitoneally three times （once a day for three days） before ischemia-reperfusion. The neuroprotective affect of Tsl was examined using H＆E staining, neuronal nuclei （NeuN） immunohistochemistry and Fluoro-Jade B staining. To investigate the neuroprotective mechanism of Tsl after ischemia- reperfusion, immunohistochemical （IHC） and Western blotting analyses for Cu, Zn-superoxide dismutase （SOD1）, Mn- superoxide dismutase （SOD2）, brain-derived neurotrophic factor （BDNF） and insulin-like growth factor-I （IGF-I） were performed.Results Treatment with Tsl protected pyramidal neurons from ischemia-induced neuronal death in the CA1 after ischemia-reperfusion. In addition, treatment with Tsl maintained the levels of SOD1 and SOD2 as determined by IHC and Western blotting in the CA1 after ischemia- reperfusion compared with the vehicle-ischemia-group. In addition, treatment with Tsl increased the levels of BDNF and IGF-I determined by IHC and Westem blotting in the Tsl-treated-sham-group compared with the vehicle-treated- sham-group, and their levels were maintained in the stratum pyramidale of the ischemic CA1 in the Tsl-treated- ischemia-group. Conclusion Treatment with Tsl protects pyramidal neurons of the CA1 from ischemic damage induced by transient cerebral ischemia via the maintenance of antioxidants and the increase of neurotrophic factors.
Background Danshen （Radix Salvia miltiorrhizae） has been used as a traditional medicine in Asia for treatment of various microcirculatory disturbance related diseases. Tanshinones are mainly hydrophobic active components, which have been isolated from Danshen and show various biological functions. In this study, we observed the neuroprotective effect of tanshinone I （Tsl） against ischemic damage in the gerbil hippocampal CA1 region （CA1） after transient cerebral ischemia and examined its neuroprotective mechanism. Methods The gerbils were divided into vehicle-treated-sham-group, vehicle-treated-ischemia-group, Tsl-treated-sham- group, and Tsl-treated-ischemia-group. Tsl was administrated intraperitoneally three times （once a day for three days） before ischemia-reperfusion. The neuroprotective affect of Tsl was examined using H＆E staining, neuronal nuclei （NeuN） immunohistochemistry and Fluoro-Jade B staining. To investigate the neuroprotective mechanism of Tsl after ischemia- reperfusion, immunohistochemical （IHC） and Western blotting analyses for Cu, Zn-superoxide dismutase （SOD1）, Mn- superoxide dismutase （SOD2）, brain-derived neurotrophic factor （BDNF） and insulin-like growth factor-I （IGF-I） were performed.Results Treatment with Tsl protected pyramidal neurons from ischemia-induced neuronal death in the CA1 after ischemia-reperfusion. In addition, treatment with Tsl maintained the levels of SOD1 and SOD2 as determined by IHC and Western blotting in the CA1 after ischemia- reperfusion compared with the vehicle-ischemia-group. In addition, treatment with Tsl increased the levels of BDNF and IGF-I determined by IHC and Westem blotting in the Tsl-treated-sham-group compared with the vehicle-treated- sham-group, and their levels were maintained in the stratum pyramidale of the ischemic CA1 in the Tsl-treated- ischemia-group. Conclusion Treatment with Tsl protects pyramidal neurons of the CA1 from ischemic damage induced by transient cerebral ischemia via the maintenance of antioxidants and the increase of neurotrophic factors.
