Rhubarb is a traditional Chinese medicines which possess laxative, lipid-lowering, and weight-loss activities, but the active compounds of lipid-lowering and underlying molecular mechanisms are not yet clear. This study aims to explore the effects of chrysophanol on the mRNA expressions of sterol regulatory element-binding proteins (SREBPs) and lipid metabolism in human liver carcinoma Huh-7 cells, which is one of the active compounds obtained from Rhubarb. A reporter gene assay was used to test the transcription of SREBP. The intracellular triglyceride and total cholesterol contents were measured by using commercially available test kits. The SREBPs target genes expressions were measured by Quantitative Real-Time PCR. Cell viability was evaluated by Cell Counting Kit-8. As the results shown, chrysophanol (40 μmol · L(-1), 16 h) could notably inhibited human SRE promoter activity in a dose-dependent manner and decrease intracellular cholesterol and triglyceride levels. Furthermore, the mRNA expressions of SREBPs target genes were significantly downregulated by chrysophanol treatment. However there are no significant differences on cell viability when compared with the control group. These results suggested that chrysophanol might improve lipid metabolism through suppressing the mRNA expressions of SREBPs target genes to attenuate intracellular lipid accumulation.

AIM: To investigate the effect of Ginkgo biloba extrac (GBE) on cerebral ischemia during early stage of subarachnoid hemorrhage (SAH). METHODS: Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group, SAH group and SAH+GBE group. Dynamic change of regional cerebral blood flow (rCBF) was detected. Brain endothelin-1(ET-1) and calcium contents were also determined at different time point during 24 hours after the operation. Pathological change of neurons of hippocampus CA1 region was observed. RESULTS: In SAH group, rCBF decreased immediately and persistently after induction of SAH. Values of brain ET-1 content and calcium content at 1 hour, 6 hours and 24 hours were significantly higher than those in sham-operated group. Neurons of hippocampus CA1 region were damaged severely 3 days after onset of SAH. Above abnormal changes in SAH+GBE group were much slighter than those in SAH group. CONCLUSION: GBE may relieve cerebral ischemic damage after SAH.

AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.

Objective To explore the effect of protein kinase C inhibitor on the level of phosphralated extracellular regulated protein kinases in the spinal trigeminal nucleus of migraine model rats.Methods Healthy adult male SD rats were randomly divided into four groups:normal group (group C),sham operation group (group C),migraine model group(group M),and H-7group(H-7group),with 18 rats in each group.Dural blood flow and the extracellular discharge frequency in the spinal trigeminal nucleus was recorded.ERK1/2 phosphorylation was tested.Results (1) Dural blood flow:compared with group C((3.8± 1.0)％),the dural blood flow in M group ((78.0±4.2) ％)increased obviously(P＜0.01) ; compared with M group((78.0±4.2)％),the dural blood flow in H-7 group((-24.8±4.9) ％) decreased obviously(P＜0.01).(2) The percentage of extracellular discharge frequency change:two hours after treatment,the percentage of extracellula discharge frequency change in group M ((325.9 ±47.3)％)was higher than that in group C((107.3±16.4)％).The percentage of discharge frequency change in group H-7((136.0±26.5)％) was lower than that in group M((325.9±47.3)％).There was no significant difference in the percentage of discharge frequency change between group H-7((136.0±26.5) ％) and group C((107.3 ± 16.4)％).(2) ERK1/2 phosphorylation:the ERK1/2 phosphorylation in group M was higher than that in group C.The ERK1/2 phosphorylation in group H-7 was lower than than that in group C and group M.Conclusion ERK1/2 is a downstream PKC signal path and PKC may have indirect activation of ERK1/2.

AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.

The MAPKs activation pathway consists of three protein kinases in activation sequence:MAPKs kinase kinases (MKKKs)→,MAPKs kinases (MKKs)→MAPKs and four pathways:extracellular signal-regulated kinase (MAPK~(ERK)),C-JUN N-terminal kinase (MAPK~(JNK)),MAPK~(P38) and MKKS/MAPK~(ERK5) activation pathways.It has been proved that MAPKs(ERK,JNK and P38) are acvtivated in the progress of morphine tolerance.Inhibitors of any element of MAPKs activation pathway may function as a potential clinical medicine for morphine tolerance.

OBJECTIVE To observe the effect of 32P intertissue injection on advanced head and neck cancer. METHODS Eight patients with advanced head and neck cancer were treated with 32P injection into the tumors according to the size of the cancer as determined by CT scan. RESULTS Local tumors were controlled evidently and the pain of the patients were alleviated. The survival periods of the 8 cases ranged from 3 to 18 months (average 14.2 months). CONCLUSION 32P intertissue injection offer an useful method for patients with advanced head and neck cancer .

AIM: To investigate the role of nitric oxide in neuronal damage induced by cerebral vasospasm (CVS) following subarachnoid he morrhage (SAH) in rats. METHODS: Noncraniotomy models of SAH by a endovascular puncture method in Wistar rats were used and animals were divided i nto sham-operated group, SAH group and SAH+L-arginine group. Dynamic changes of regional cerebral blood flow (rCBF) within 24 hours were monitored. Diameters of basilar artery (BA) were measured. Serum NO(NO - 2/NO - 3) and plasma endo thelin-1 content at different time points within 24 hours were also detected. RESULTS: Sham operation did not affect all of above parameters. In SAH group, rCBF reduced immediately after induction of SAH, reaching its lowe st at 1 h, persisting within 24 h. Diameter of BA significantly decreased after S AH. Serum NO - 2/NO - 3 decreased and plasma endothlin-1 increased statisti cally after SAH. In SAH+L-arginine group, decline of rCBF was not as rapid and s evere as that in SAH group. L-arginine also effectively antagonized vasospasm of BA and damage of hippocampal neurons. Decrease of serum NO - 2/NO - 3 and increase of plasma endothlin-1 were not so obvious in SAH+L-arginine group comp ared to SAH group. CONCLUSION: Decrease in NO is involved in the development of CVS- induced neuronal damage following SAH, and L-arginine partly increases serum NO and thus protectes ischemic brain neurons.

AIM: To investigate the role of nitric oxide in the development of brain edema after subarachnoid hemorrhage(SAH), and the influence of L-arginine on them. METHODS: Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group, SAH group and SAH plus L-arginine group. Dynamic changes of regional cerebral blood flow within 24 hours were measured. Serum nitric oxide level, brain water and sodium content at different time points within 24 hours were also detected. RESULTS: Regional cerebral blood flow and serum nitric oxide level at every time point after operation in SAH group were lower than those in sham-operated group, while brain water content and sodium content in the former group were higher than those in the latter group. Above pathological alterations in SAH plus L-arginine group were not so obvious as in SAH group. CONCLUSION: Decrease in serum nitric oxide plays a role in the development of brain edema after SAH, which may be partly reversed by administration of L-arginine.

Aim: To investigate the pathological changes in NTBC[2-(2-nitro-4-trifluoro-methyl-benzoyl) -1,3 cy-clohexanedione]-induced hepatic injury in mice and in the repopulation of adult hepatocytes in Fah~(-/-) mouse. Methods: Autogenous hepatic injuries in Fah~(-/-) mice were induced by the treatment of NTBC. Injection of hepatocytes obtained from wild-type mice to spleen were transplanted into the Fah~(-/-) mice. Then, changes to body weight and the likelihood of the transplanted Fah~(-/-) mice, and hepatic immunohistochemistry were ob-served. In addition, pathological changes to liver damage induced by NTBC treatment were analyzed under HE-staining microscopy and electron microscopy. Results: The surviving Fah~(-/-) mice subjected to hepatocyte trans-plantation were found to be healthy and in stable body weight. liver repopulation reached to 90% in the 8th week. Repopulating hepatocytes caused no alteration to histological structure of the recipient liver, and subacute hepatic injury occurred in the Fah~(-/-) mice after NTBC treatment. Electronic microscopy observations indicated that necrosis in the hepatocytes occurred at early stage and that apoptosis gradually appeared. It was also shown both necrosis and apoptosis co-existed in the same samples of interest at the following stages of the induced liver injury. Conclusion: Transplanted hepatocytes proliferated in Fah~(-/-) mice allow 90% of the hepatocytic repopula- tion. Repopulation renders normal hepatic function and structure in the recipient Fah~(-/-) mice, as a model of liver repopulation, could be applicable in study of stem cell derived hepatic cells in transplantation assay.