AIM: To observe morphological changes in transplanted intracerebral rat gliomas and rat survival time with gliomas under chemotherapy with angiotensin II-induced hypertension. METHODS: C6 glioma cells were cultured, and the effects of carmustine, nimodipine or/and teniposide on gliomas cells was observed. In addition, the brain tumor model was established in Wistar rats by stereotaxic inoculation of C6 glioma cells. The tumor-bearing rats were treated with carmustine, nimodipine lisplatin or/and teniposide during angiotensin II-induced hypertension, the pathological changes in gliomas was also examined. RESULTS: In vitro experiments showed chemotherapy resulted in morphologic changes in glioma cells, including cell enlargement, degeneration. In vivo experiments, the survival time of tumor-bearing rats was longer, the voume of gliomas was smaller in chemotherapy with hypertension group than those in chemotherapy alone, and pathological examination showed necrosis in the gliomas. CONCLUSION: Chemotherapy with angiotensin II-induced hypertension has a better inhibitory effect on rat intracerebral gliomas than chemotherapy alone.

AIM: To explore the role of calcineurin i n th e expression of NF-?B and the neurotoxicity in cultured cortical neurons treate d with interleukin-1? (IL-1?) and NMDA. METHODS: The cultured rat cortical neurons were used in the expe riment, damage of neurons was induced by interleukin-1?(IL-1?) or excitator y amino acid (NMDA). The degree of neuron damage was examined with the methods o f MTT assay and LDH releasing rate assay, as well as the Annexin V and PI immuno fluorescence. The expression of NF-?B p65 on the neurons was tested by the West ern blot analysis. RESULTS: Viability of neurons was obviously lower in the IL-1? group and NMDA group respectively than that in control group (P0.05). Annexin V and PI immunofluoresc ence showed that IL-1? mainly induced the neuron apoptosis, and NMDA induced th e neuron necrosis. CONCLUSIONS: The calcineurin mediates the higher expression of N F -?B p65 and neuron damage induced by IL-1?, but not play a critical role in th e necrosis induced by NMDA in the cultured cortical neurons. These results indic ate that calcineurin is the key molecule in the apoptotic signaling pathway.

AIM:To study the protection and mechanism of Asclepiadaceae against the damage of neuron by free radical. METHODS:The model of ischemia and damaged neuron induced by H 2O 2 was made respectively. The protection of Asclepiadaceae was observed with the measurement of contents of MDA in brain and cultured neuron, transudatory rate of LDH, breaking rate of DNA and clearance rate of?OH in cultured neuron. RESULTS:Asclepiadaceae decreased the raising of MDA in brain induced by ischemia. The raising of transudatory rate of LDH,breaking rate of DNA and content of MDA inducing by H 2O 2 in cultured neuron were also observed. The clearance rate of?OH in cultured neuron increased as the contents of Asclepiadaceae raised. CONCLUSION: The mechanism of Asclepiadaceae protecting the neuron is related to its ability to clean up free radical.

AIM: To investigate the activity of interleukin-1? converting enzyme in transplanted intracerebral rat gliomas under angiotensin II-induced hypertension chemotherapy. METHODS: The brain tumor model was produced in Wistar rats by stereotaxic inoculation of C6 glioma cells (1?10 12 /L). Tumor-bearing rats were treated with carmustine, teniposide and lisplatin (chemotherapy) during angiotensin II-induced hypertension. Then, the survival time of tumor-bearing rats, tumor blood flow, the concentration of drug, volume of gliomas and the activity of interleukin-1? converting enzyme in glioma were examined.RESULTS: The survival time of tumor-bearing rats was significantly longer in chemotherapy with angiotensin II-induced hypertension group than that of chemotherapy alone. In addition, regional tumor blood flow, the concentration of chemotherapeutic drug and the activity of interleukin-1? converting enzyme in transplanted rat gliomas were increased, while the volume of gliomas was decreased in hypertention chemotherapy group compared with chemotherapy alone. CONCLUSION: Chemotherapy with angiotensin II-induced hypertension has a enhancing effect on chemotherapy for improving the drug delivery to tumor tissue by a increased tumor blood flow and enhancing activity of interleukin-1? converting enzyme.