Objective To observe the change of neuron-specific enolase (NSE) an d glial fibrillary acidic protein (GFAP) in neonatal rats' cerebral cortex with hypoxic-ischemic brain damage (HIBD). Methods The 7 day- old SD rats were subjected to the ligation of right carotid artery, then were pu t into a hypoxic box to establish a HIBD model. The immunohistochemical method w as used to detect the expression of NSE and GFAP in rats' cerebral cortex. Results ① The NSE decreased in damaged cerebral cortex in HIBD 24 h group, after 7 days it gradually increased but was still lower than that of the controls. ② The expression of GFAP was limited and scarce in control and it did not change in HIBD 24 h group, while in HIBD 7 d group GFAP expression was increased and spread widely in the damaged cerebral cortex. Conclu sion ① The NSE decreases in damaged cerebral cortex in early stage of neonatal rat HIBD, suggesting that NSE is a specific marker for neuron damage . ② The GFAP increases in damaged cerebral cortex in the recovery stage of neon atal rat HIBD, suggesting that GFAP participates the repair of lesion region.

Chlorides ; metabolism ; Diarrhea ; congenital ; Humans

AIM: To investigate whether grafting neural stem cells (NSCs) improves the impaired cognitive deficits and spatial recognition after ischemic-hypoxic brain damage (HIBD) in neonatal rats. METHODS: Non-immunosuppressed 7-day-old SD rats were used as research subject and randomly divided into 3 groups: (1) sham group (n=10); (2) HIBD group (n=11); (3) transplant group (n=13). (2) and (3) were anesthetized and subjected to a hypoxic/ischemic injury obtained by combination of left carotid ligation and exposure to 8% oxygen for 2 h. At 3 days post injury, hypoxic-ischemic brain damaged animals were re-anesthetized and randomized to receive stereotactic injection of NSCs prelabeling with BrdU or control media into the hippocampus in the ipsilateral hemisphere. Cognitive (i.e., learning) deficits were assessed at 2 to 4 weeks after transplantation. At the end of the behavioral tests, the animals were killed and evaluated for NSC survival and histopathological analysis. RESULTS: Transplant group showed significantly improved cognitive function in selected tests as compared with HIBD group during the 4-week observation period. They took less time than HIBD group in finding the 3 arms baited with water and had a decreased number of working and reference memory errors in radial maze acquisition tests. Histological analysis showed that transplanted NSCs attenuated CA1 cell loss after HIBD, and NSCs survived for as long as 4 weeks after transplantation and were detected in the hippocampus. CONCLUSION: These data suggest that transplanted NSCs attenuate brain damage and cognitive dysfunction after hypoxic-ischemic brain damage. This approach warrants continued investigation in light of potential therapeutic uses.

AIM: To discuss the mechanism of hyperbaric oxygen(HBO) therapy by assessing the changes of neural stem cells(NSCs),after hypoxic-ischemic brain damage(HIBD) in neonatal rats.METHODS: Seven-day-old SD rat pups were randomly divided into 4 groups: control group(CON,n=16),HIBD group(n=16),hyperbaric air group(HBA,n=16),and HBO group(n=16).The HIBD model was produced by permanent occlusion of left common carotid artery and was exposed to a mixture of 8% oxygen and 92% nitrogen for 2 h(at 37 ℃).HBA and HBO treatment was administered by placing pups in a chamber(2 ATA for 1 h) 1 h after hypoxia exposure and performed once daily for 7 days.BrdU immunohistochemistry was used to assess how the insult had affected NSCs in the SVZ of the lateral ventricle and DG of the hippocampus.The NSCs from the ipsilateral SVZs were isolated at 3 weeks recovery from hypoxia-ischemia(HI).The number of spheres was then counted as an index of the number of NSCs residing within the SVZ.RESULTS: At 3 week survival,the SVZ of HIBD group was smaller and markedly less cellular than control group.BrdU-positive cells were dramatically decreased in the SVZ and DG of the affected hemisphere(P

Hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC) is one of the most frequently occurring cancers. Hepadnaviral DNA integrations are considered to be essential agents which can promote the process of the hepatocarcinogenesis. More and more researches were designed to find the relationship of the two. In this study, we investigated whether HBV DNA integration occurred at sites of DNA double-strand breaks (DSBs), one of the most detrimental DNA damage. An 18-bp I-SceI homing endonuclease recognition site was introduced into the DNA of HepG2 cell line by stable DNA transfection, then cells were incubated in patients' serum with high HBV DNA copies and at the same time, DSBs were induced by transient expression of I-SceI after transfection of an I-SceI expression vector. By using nest PCR, the viral DNA was detected at the sites of the break. It appeared that integration occurred between part of HBV x gene and the I-SceI induced breaks. The results suggested that DSBs, as the DNA damages, may serve as potential targets for hepadnaviral DNA insertion and the integrants would lead to widespread host genome changes necessarily. It provided a new site to investigate the integration.

Aim Neural injury in the central nervous system following is chemic insult is believed to result from oxygen and glucose deprivation.In this study,baicalin was investigated for its neuroprotective effects against oxygen and glucose deprivation(OGD) in Neuro2A cells.Methods Mitochondrial activity was assessed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) reduction activity assay.Apoptosis was monitored with flow cytometry.It was found that baicalin increased MTT reduction activity and decreased percentage of apoptosis of the cultured Neuro2A cells.Results Baicalin showed significant protective effects on the OGD-induced apoptosis in cultured Neuro2A cells.Conclusion These results suggest that baicalin is an effective compound in preventing neurotoxicity induced by OGD and therefore deserves further scrutiny.

Hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC) is one of the most frequently occurring cancers. Hepadnaviral DNA integrations are considered to be essential agents which can promote the process of the hepatocarcinogenesis. More and more researches were designed to find the relationship of the two. In this study, we investigated whether HBV DNA integration occurred at sites of DNA double-strand breaks (DSBs), one of the most detrimental DNA damage. An 18-bp I-SceI homing endonuclease recognition site was introduced into the DNA of HepG2 cell line by stable DNA transfection, then cells were incubated in patients' serum with high HBV DNA copies and at the same time, DSBs were induced by transient expression of I-SceI after transfection of an I-SceI expression vector. By using nest PCR, the viral DNA was detected at the sites of the break. It appeared that integration occurred between part of HBV x gene and the I-Scel induced breaks. The results suggested that DSBs, as the DNA damages, may serve as potential targets for bepadnaviral DNA insertion and the integrants would lead to widespread host genome changes necessarily. It provided a new site to investigate the integration.

Objective:To study the effect of baicalein on the expression of glutamate receptor related protein in PC12 cells injured by Aβ 25-35. Methods:PC12 cells were divided into control group, model group, estradiol group and baicalein group with different concentrations. The survival condition of PC12 cells in each group were detected by thiazole blue (MTT). PC12 cells were divided into control group, model group, estradiol group and baicalein group. The control group and model group were cultured with DMEM medium, and the estradiol group was added with 1×10 -3 μmol/L estradiol DMEM medium, baicalein group was added with 1 μmol/L baicalein DMEM medium. After 2 hours of intervention, 20 μmol/L Aβ 25-35 was added to the model group, estradiol group and baicalein group with induced PC12 cell injury. After 22 hours of intervention, flow cytometry was used to detect the apoptosis of PC12 cells. The expression of estrogen receptor β (ER β), phosphorylated c-Jun N-terminal kinase (p-JNK/JNK) and ionic receptor N-methyl-D-aspartate receptor 1 (NMDAR1), glutamate receptor 2 (GluR2) and calcium/calmodulin dependent protein kinase Ⅱ (CaMK Ⅱ) were detected by Western blot. Results:Compared with model group, 1 μmol/L baicalein significantly increased the proliferation rate [(95.80±2.47)% vs. (64.34±3.84)%]. The apoptosis rate of PC12 cells[(7.83±0.67)% vs. (12.84±0.91)%] was significantly decreased in baicalein group ( P<0.01). The expression of NMDAR1 (0.582±0.012 vs. 0.352±0.012), GluR2(0.538±0.017 vs. 0.355±0.006), ER β (0.362±0.015 vs. 0.262±0.018) in baicalein group were significantly increased ( P<0.01), the expression of p-JNK/JNK (0.476±0.013 vs. 0.752±0.014) and CaMK Ⅱ(0.499±0.019 vs. 0.670±0.016) in baicalein group were significantly decreased ( P<0.01). Conclusions:Baicalein has a protective effect on PC12 cells injured by Aβ 25-35. Its mechanism may be related to the inhibition of p-JNK/JNK activity by activating ERβ and regulating the expression of glutamate receptor related protein.