AIM: To verify the neuroprotective effect and optimize the therapeutic dose and time window of picroside Ⅱon cerebral ischemic injury in rats .METHODS:The forebrain ischemia model was established by the method of bilateral common carotid artery occlusion ( BCCAO ) .The successful model rats were randomly divided into 16 groups according to orthogonal design and treated by intraperitoneal injection of picroside Ⅱat different ischemic time poinis and different doses .The changes of the nerve fiber myelin were observed by fast green staining .The immunohistochemical assay and Western blotting were used to quantitatively and qualitatively determine the expression of myelin basic protein (MBP). The mRNA level of MBP in the brain tissues was tested by reverse transcription polymerase chain reaction (RT-PCR).RE-SULTS:Picroside Ⅱ increased the expression of MBP and decreased demyelination after cerebral ischemic injury .The best therapeutic time window and dose were:(1) ischemia for 2.0 h with picrosideⅡat dose of 10 mg/kg according to the results of fast green staining;(2) ischemia for 2.0 h with the dose of 10 mg/kg according to the results of immunohisto-chemical assay;(3) ischemia for 2.0 h with the dose of 10 mg/kg according to the analysis of Western blotting;(4) is-chemia for 1.5 h with the dose of 20 mg/kg according to the detection of RT-PCR.CONCLUSION:Given the principle of the lowest therapeutic dose with the longest time window , the optimized therapeutic dose and time window for rat cerebral ischemic injury is intraperitoneal injection of picroside Ⅱat the doses of 10~20 mg/kg and the time window of ischemia for 1.5~2.0 h.

Objective To study the expressions and prognostic significance of high mobility group protein A1 (HMGA1) and high mobility group protein A.2 (HMGA2) in pancreatic carcinoma.Methods The expressions of HMGA1 and HMGA2 were examined by immunohistochemical SP method in 60 cases of pancreatic carcinoma and 30 cases of normal pancreatic tissues.The relationship between the expression and prognosis was also analyzed.Results The expressions of HMGA1 and HMGA2 in pancreatic carcinoma were significantly higher than those in normal tissues,and the positive expression rates were 70.0％ vs.6.7％ (x2 =32.105,P =0.000) and 73.3％ vs.3.3％ (x2 =39.200,P =0.000).The expression of HMGA1 in pancreatic carcinoma was correlated with histological grade (x2 =6.774,P =0.034),TNM stage (x2 =4.776,P =0.029) and lymphatic metastasis (x2 =12.614,P =0.000).The expression of HMGA2 in pancreatic carcinoma was correlated with histological grade (x2 =8.200,P =0.017) and TNM stage (x2 =7.253,P =0.007).The expression of HMGA1 was positively associated with HMGA2 expression (r =0.393,P =0.001).Kaplan-Meier analysis showed that the median survival time of HMGA1 and HMGA2 positive patients were shorter than those patients with HMGA1 negative and HMGA2 negative (14.0 months vs.24.0 months,x2 =14.568,P =0.000;15.0 months vs.21.0 months,x2 =7.270,P =0.007).Conclusion HMGA1 and HMGA2 are highly expressed in pancreatic carcinoma,and play synergistic roles in the generation and progress of pancreatic carcinoma.There is certain value of combined detection of HMGA1 and HMGA2 to predict the prognosis of pancreatic carcinoma.

Objective To explore the neuroprotective effect and mechanism of picroside II on ERK1/2 signal transduction pathway after cerebral ischemia injury in rats.Methods The focal cerebral is-chemic models were established by inserting a monofilament threads into middle cerebral artery occlusion (MCAO) in 100 Wistar rats and treated by injecting picroside II (20 mg/kg) intraperitoneally.The neu-robehavioral function was evaluated by modified neurological severity score points ( mNSS) test.The cerebral infarct volume was measured by tetrazolium chloride ( TTC) staining.The apoptotic cells were counted by terminal deoxynucleotidyl transferase dUTP nick end labeling ( TUNEL) assay.The expression of pERK1/2 in cortex was determined by the immunohistochemistry ( IHC) and Western Blot ( WB) .Results mNSS test showed that severe neurological dysfunction was found in model and LPS groups,and the scores of mNSS were significantly increased;meanwhile the scores of mNSS in treatment group and U0126 group were signifi-cantly lower than that in model and LPS groups (P<0.05).TUNEL assay showed that the apoptotic cell inde-xes (ACI) in different groups were (0.06±0.02),(0.27±0.03),(0.07±0.02),(0.26±0.03)and(0.09± 0.05) ,and the ACI in treatment and U0126 groups was obviously lower than that in model and LPS groups (P<0.05) .With IHC and WB,pERK1/2 level in model group was the highest,which was slightly higher than that of LPS group,and pERK1/2 expression in treatment and U0126 groups was significantly decreased com-pared with that in model and LPS groups (P<0.05) .Conclusion The activation of ERK1/2 by cerebral is-chemia could induce the cell apoptosis.Picroside II might reduce cell apoptosis by inhibiting the activation of ERK1/2 in ischemic brain injury.

Objective To evaluate the effect of the autogenous split-thickness cranial bone grafts on treatment of deformity of oral and maxillofacial regions. Methods The split-thickness cranial bone was harvested through the coronal incisions or the parietotemporal region incisions. The bone graft was then fashioned to the appropriate size and configuration and fixed to the regions of defects and deformities. The cranial bone was used to reconstruct facial bone framework or as sustaining bone graft for facial augmentation. Results 31 patients with the oral and maxillofacial deformities or bone defects were repaired with the cranial bone grafts, including 17 cases of orbital floor defects, 6 cases of malunion of the zygoma fractures, 5 cases of secondary deformity after ankylosis of temporomandibular joint, 2 cases of bone reconstruction after tumor resection and 1 case of cleft palate deformity. The followed-up period ranged from 6 months to 7 years, averaging 11 months. There were no complications of infection and extrusion, no obvious bone resorption was observed, and the facial appearance were greatly improved. Only one patient had a small ectropion which persisted three months. After six-month, the ectropion was not obvious. Conclusion Autogenous bone grafts used to reconstruct the defect and deformity of oral and maxillofacial regions can reduce the risks of infection and extrusion, and there is less visible scar and less bone resorption. Skull bone is an ideal source of bone graft material in the oral and maxillofacial deformity.

Objective: To study the therapeutic effects of Xuesaitong injections on senile coronary heart disease ( CHD) . Methods: Retired veteran cadres and their relations in our unit were enrolled in this study. They were divied into Xuesaitong treatment group (58 cases) and control group ( Salvia Miltiorrhi-za Compound Injections and Venoruton, 34 cases). Follow-up time was 10 days per period of treatment. The symptoms, ECG, serum cholesterol and triglyceride before and after treatment were compared. Results :ECG and serum lipids were significantly improved in Xuesaitong treatment group (P 0.05). Conclusion: Xuesaitong injections have therapeutic effects on senile CHD.

Objective To investigate the regulating effects and mechanism of Laminaria japonica (L.japonica) on serum lipid of hyperlipidemia rats.Methods Forty healthy female Wistar rats were used to establish hyperlipidemia models by feeding fat-rich forage,and the powder of L.japonica was applied as a supplement in forage for test groups.The levels of serum lipid including the triglyceride(TG),total cholesterol(TC),low-density lipoprotein (LDL),high-density lipoprotein(HDL) and the activities of lipoproteinesterase(LPL) and hepatic lipase(HL) were detected by biochemical assay.Results The levels of serum TG and TC in test group decreased significantly than those in pre-treated and model group (P

Aim To explore the effect of picrodideⅡ on the expressions of Caspase-3 and poly ADP-ribose polymerase (PARP) in brain tissue following cerebral ischemic reperfusion injury in rats.Methods The middle cerebral artery occlusion reperfusion models were established with intraluminal thread methods in rats. PicrodideⅡ (10 mg·kg~(-1)) and salvianic acid A sodium (10 mg·kg~(-1)) were injected from tail vein for treatment. The neurological function was evaluated with Bederson's test and the cerebral infarction volume was observed with tetrazolium chloride (TTC) staining.The brain structure was observed by hematoxylin-eosin (HE) staining and the apoptosis was counted by TUNEL immunofluorescence assay. The expressions of Caspase-3 and PARP were detected with immunohistochemical and enzyme linked immunosorbent assay.Results After ischemia 2 h and reperfusion 22 h, the rats showed neurological function deficit and cerebral infarction in ischemic hemisphere. The expressions of Caspase-3 and PARP and the number of apoptotic cells in brain tissue increased compared with those in the sham operative group (P <0.05). In picroside and salvianic acid A sodium groups, the Bederson's scores and cerebral infarction volume, the expressions of Caspase-3 and PARP and the number of apoptosis cells were lower than those in the negative control group (P <0.05). While there was no significant difference in five indexes metioned above between picroside group and salvianic acid A sodium group (P >0.05).Conclusion PicrosideⅡ might reduce the expressions of Caspase-3 and PARP to inhibit the neuronal apoptosis induced by cerebral ischemia reperfusion injury and improve the neurological function of rats.

Objective To investigate the neuroprotective effects of picrodideⅡ on cerebral ischemic reperfusion injury in rats. Methods Intraluminal thread methods were applied to establish the left middle cerebral artery occlusion reperfusion models (MCAO/R) in rats. PicrodideⅡ (10mg/kg) and salvianic acid A sodium (10mg/kg) were injected from tail vein for treatment. The neurological behavioral function was evaluated with Bederson's test. The cerebral infarction volume was observed with tetrazolium chloride (TTC) staining. The structure of cells was observed with histopathology. The apoptosis positive cells were counted by terminal deoxynucleotidyl transferase midiated dUTP nick end labeling (TUNEL). Results The neurological behavioral malfunction appeared in all rats with MCAO/R. The infarction focus showed in the ischemic hemisphere following cerebral ischemia reperfusion injury. In the picrodideⅡ and salvianic acid A sodium treatment groups, the number of apoptosis positive cells decreased and the cerebral infarction volume reduced, while the neurological behavioral function was significantly improved than those in the model control group (P<0.05). The cerebral infarction volume in the picrodideⅡ group was smaller than that in the salvianic acid A sodium group (P<0.05).Conclusion PicrodideⅡ might reduce cerebral infarction volume and improve the neurological behavioral function through inhibiting the neuronal apoptosis induced by ischemia reperfusion injury.

Aim To study the interfering effects of picroside Ⅱ on the expressions of nuclear transcription factor kappaB(NF-?B)and inhibitor of NF-?B(I-?B) after cerebral ischemic reperfusion in rats. Methods Intraluminal thread methods were applied to establish the middle cerebral artery occlusion reperfusion models in rats. PicrosideⅡ(10 mg?kg-1) and salvianic acid A sodium(10 mg?kg-1 ) were injected from the tail vein for treatment. TUNEL positive cells were counted by immunofluorescence assay. The expressions of NF-?B and I-?B were determined by immunohistochemical assay,and the concentration of NF-?B and I-?B in brain tissue was determined by ELISA. Results The exprssions of NF-?B and I-?B were weakly and the apoptotic cells were scattering at cortex,striatum and hip-pocampus in the sham operative group. In the negative control group,the number of TUNEL positive cells and the expressions of NF-?B and I-?B increased,the absorption(A) values and the concentration were significantly higher than those in the sham operative group(P0.05 ). Conclusion Picroside Ⅱ might downregulate the expressions of NF-?B and I-?B to inhibit neuronal apoptosis induced by inflammation after cerebral ischemia reperfusion injury in rats.

Objective To observe endothelial cells secreting and expressing nitric oxide by using red laser irradiation ( RLI) on cultured endothelial cells. Methods Cultured endothelial cells were irradiated with a red laser for 10, 20, and 30 minutes, respectively, and the concentration of nitric oxide in the cell supernatant was measured after 15 min,30 min.1 h,3 h and 6 h. In addition, the expression of inducible nitric oxide synthetase (iNOS) and endotlielial nitric oxide synthetase (eNOS) was measured through immunohistochemical staining. Results Compared with that in the control group, the expression of eNOS by the endothelial cells and the concentration of NO were stimulated by 2 mW RLI for 10 min, 20 min and 30 min, and reached a peak at 1 h, then declined gradually. The expression of iNOS, however, showed no significant difference. Conclusion RLI can increase NO concentrations in endothelial cells by stimulating the expression of eNOS rather than iNOS.