Objective To investigate the effects of astragalus membranaceus and angelica sinensis on grafted cochlea stem cells apoptosis in hearing imparied rats.Methods The hearing impaired rats were divided into 3 groups:cochlea stem cells group(45 rats),astragalus membranaceus and angelica sinensis group(45 rats),and the control group(35 rats).Cochlea stem cells only were grafted into the first group cochlea regions,mixture of stem cells and astragalus membranaceus and angelica sinensis were grafted into that of the second group.Saline was grafted into that of control rats.Observed was apoptosis at 1 day,3 days,5 days,10 days,15 days after the transplantation by CASPASE-3 and Bcl-2 immunofluorescence.Results After transplantationn 1 day,3 days,5 days,10 days,and 15 days of five time,for the cochlea stem cell group,the rates of apoptotic cells were 27.84%,49.37%,44.78%,39.37%,and 34.82%,respectively.The rates of astragalus membranaceus and angelica sinensis group were 18.35%,26.92%,23.18%,21.38%,and 18.19%,respectively.The percent of grafted cochlea stem cells apoptosis in astragalus membranaceus and angelica sinensis group was much lower than that in cochlea stem cells group and control group.The majority of apoptotic cells occurred within three to five days after transplantation.Conclusion The majority of apoptotic cells occur within three to five days after transplantation in the hearing impaired rats.The astragalus membranaceus and angelica sinensis could reduce the apoptotic rates of transplanted stem cells.

Objective To explore the differentiation of neural stem cells (NSCs) in hippocampus of rat model of Parkinson's disease (PD).Methods Rat models of PD were made by injection 6-hydroxydopamine (6-OHDA) into striatum. 5-bromodeoxyuridine (Brdu) was injected into the abdomens of PD rats for 14 days before they were killed. The expressions of Brdu/Glial fibrillary acidic protein (GFAP) and Brdu/ Neuronal nuclear antigen (Neun) were determined by immunocytochemistry. The distinctive marker for Brdu/GFAP and Brdu/Neun labeling method was used to determine the phenotype of the differentiated cells.Results After PD models were established, the Brdu/GFAP and Brdu/Neun positive cells appeared at 7 d, increased gradually at 14 d, and peaked at 28 d. In these double labelled cells, Brdu/GFAP positive cells were more than Brdu/Neun positive cells.Conclusions Direct injection of 6-OHDA into the striatum stimulates the proliferation of inherent NSCs in hippocampus of rats. Large amounts of NSCs differentiate into astrocytes and small amounts of them turn into neurons.

AIM: The objective of this study was to test the hypothesis that parthenolide suppresses ischemia-induced neuroinflammation in the MCAO model of adult rat. METHODS: MCAO rats were treated i.p. with parthenolide (500 μg/kg). Brain sections were analyzed for BrdU, BrdU-DCX, BrdU-Tuj-1, BrdU-MAP-2 and BrdU-GFAP staining. Total protein was extracted from ischemic striatum, and Western blot was used to determine TNF-α expression. RESULTS: Cerebral ischemia increases expression of TNF-α in the ischemic striatum. Parthenolide suppressed the expression of TNF-α and enhances the proliferation of newborn cells in the ischemic striatum. The cell number of BrdU~+-DCX~+, BrdU~+-Tuj-1~+, and BrdU~+-MAP-2~+ is increased in the ischemic striatum after parthenolide treatment at 3 d, 7 d or 28 d after MCAO. Furthermore, parthenolide depressed the cell number of BrdU~+-GFAP~+ in the ischemic striatum at 3 d, 7 d and 28 d after MCAO. CONCLUSION: Parthenolide inhibits neuroinflammation induced by cerebral ischemia and promotes neurogenesis in the ischemic striatum. Further study of the effects of parthenolide on inflammatory gene expression using model animal systems as described here are critical to elucidating their mechanisms of action.

Clinical neuroanatomy is a bridge between basic medicine and clinic. To resolve the deficiency existing in PBL teaching,we improved the basic teaching installation and teaching practice and evaluation system. The results indicated that we had gotten satisfactory effect by using teaching method of clinical neuroanatomy