Ethanol extract of Oenanthe javanica increases cell proliferation and neuroblast differentiation in the adolescent rat dentate gyrus

Oenanthe javanica is an aquatic perennial herb that belongs to theOenanthe genus in Apiaceae family, and it displays well-known medicinal properties such as protective effects against glu-tamate-induced neurotoxicity. However, few studies regarding effects ofOenanthe javanica on neurogenesis in the brain have been reported. In this study, we examined the effects of a normal diet and a diet containing ethanol extract ofOenanthe javanica on cell proliferation and neu-roblast differentiation in the subgranular zone of the hippocampal dentate gyrus of adolescent rats using Ki-67 （an endogenous marker for cell proliferation） and doublecortin （a marker for neuroblast）. Our results showed thatOenanthe javanica extract signiifcantly increased the number of Ki-67-immunoreactive cells and doublecortin-immunoreactive neuroblasts in the subgranular zone of the dentate gyrus in the adolescent rats. In addition, the immunoreactivity of brain-derived neurotrophic factor was signiifcantly increased in the dentate gyrus of the Oenanthe javanica extract-treated group compared with the control group. However, we did not ifnd that vascular endothelial growth factor expression was increased in theOenanthe javanica extract-treated group compared with the control group. These results indicate thatOenanthe javanica extract improves cell proliferation and neuroblast differentiation by increasing brain-de-rived neurotrophic factor immunoreactivity in the rat dentate gyrus.

Long-term administration of scopolamine interferes with nerve cell proliferation, differentiation and migration in adult mouse hippocampal dentate gyrus, but it does not induce cell death

Long-term administration of scopolamine, a muscarinic receptor antagonist, can inhibit the survival of newly generated cells, but its effect on the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus remain poorly understood. In this study, we used immunohistochemistry and western blot methods to weekly detect the biological behaviors of nerve cells in the hippocampal dentate gyrus of adult mice that received intraperito- neal administration of scopolamine for 4 weeks. Expression of neuronal nuclear antigen （NeuN; a neuronal marker） and Fluoro-]ade B （a marker for the localization of neuronal degeneration） was also detected. After scopolamine treatment, mouse hippocampal neurons did not die, and Ki-67 （a marker for proliferating cells）-immunoreactive cells were reduced in number and reac hed the lowest level at 4 weeks. Doublecortin （DCX; a marker for newly generated neurons）-im- munoreactive cells were gradually shortened in length and reduced in number with time. After scopolamine treatment for 4 weeks, nearly all of the 5-bromo-2＇-deoxyuridine （BrdU）-labeled newly generated cells were located in the subgranular zone of the dentate gyrus, but they did not migrate into the granule cell layer. Few mature BrdU/NeuN double-labeled cells were seen in the subgranular zone of the dentate gyrus. These findings suggest that long-term administration of scopolamine interferes with the proliferation, differentiation and migration of nerve cells in the adult mouse hippocampal dentate gyrus, but it does not induce cell death.

Neuroprotection via maintenance or increase of antioxidants and neurotrophic factors in ischemic gerbil hippocampus treated with tanshinone I

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.