Objective To analyze changes in lactic acid level in patients with late-onset intracranial hematoma after craniocerebral injury and investigate their relativity.Methods Forty-eight patients with late-onset intracranial hematoma after craniocerebral injury treated in our hospital between May 2009 and December 2012 were enrolled as observation group.There were 32 males and 16 females.Moreover,50 cases checked up in our hospital during the same period were studied as health population controls,including 35 males and 15 females.Level of lactic acid was measured on admission,at the time of definite diagnosis as well as at days 7 and 14 after treatment and compared between groups.Results Level of lactic acid was (1.77 ±0.21) mmol/L in control group and (1.82 ± 0.25) mmol/L in observation group respectively on admission (t =1.070,P ＞ 0.05) ; Level of lactic acid was (3.32 ± 0.89) mmol/L in observation group at the time of definite diagnosis,which increased to (3.74 ± 1.16) mmol/L at days 7 after treatment and decreased to (1.89 ±0.75) mmol/L at days 14 after treatment.When diagnosed and treated for 7 days,level of lactic acid differed significantly between the two groups (P ＜ 0.05).Level of lactic acid related to craniocerebral injury at each time point,but higher correlation coefficient was observed at the time of definite diagnosis and 7 days after treatment with 0.986 and 0.989 respectively.Conclusion Level of lactic acid relates to late-onset intracranial hematoma after craniocerebral injury,which can be used as reference for progression of the disease.

Objective To investigate the correlation of angiotensin Ⅱ type 1 receptor (AT1R) gene polymorphism with AT1R expression levels and brain edema after hypertensive intracerebral hemorrhage .Methods 45 operative patients with hypertensive intracerebral hemorrhage in the Affiliated Yongchuan Hospital of Chongqing Medical Univercity from December 2011 to August 2012 were collected as the experimental group and 45 operative patients with refractory epilepsy weres selected as the control group .The venous blood in the two groups were collected for detecting the AT 1R gene polymorphism ;The brain tissue was taken from lesions in operation ,then AT1R mRNA concentration was determined by RT-PCR and the AT1R protein level was determined by Western blot ;Head CT was performed on postoperative 1 ,3 ,5 d;the degree of cerebral edema was reflected by CT value . Results The levels of two kinds of genotype AT1R mRNA in the experimental group had no statistically significant difference(P>0 .05);the operative area CT value of AC genotype was significantly lower than that of AA genotype with statistical difference (P<0 .05);the ATIRmRNA of various genotypes ,protein level and cerebral edema in the control group had no statistical differences . Conclusion The AT 1R gene polymorphism has no obvious correlation with the concentration expression of AT 1R mRNA in the brain tis-sue;there is correlation between AT 1R protein level and AT 1R protein level and the cerebral edema degree in the brain tissue .

Objective To study the effects of methylprednisolone on the permeability of blood-spinal cord barrier (BSCB) and claudin-5 expression after spinal cord injury in rats. Methods The rat model of spinal cord injury was estab?lished using modified Allen method. SD rats were randomly divided into sham-operated group, spinal cord injury group and methylprednisolone pretreatment group. The permeability of BSCB and expression of claudin–5 were assessed at 12 h, 1, 3, 5, and 7 d after the onset of spinal cord injury (five animals per each time point). RT-PCR and Western blot were used to detect the expression of claudin-5. Results The success rate of the model was 84.0%. EB content was sig?nificantly higher in spinal cord injury group than in sham-operated group at each time point (F value 27.732,P<0.05). EB content was lower in methylprednisolone pretreatment group than in spinal cord injury group (F value 48.149,P<0.05). The mRNA expression of claudin-5 was lower in spinal cord injury group than sham-operated group at each time point (F value 12.248,P<0.05). The mRNA expression of claudin–5 was higher in methylprednisolone pretreatment group than in spinal cord injury group at each time point (Fvalue 15.316,P<0.05). The protein expression of claudin-5 was lower in spinal cord injury group than in sham operated group at each time point (Fvalue 18.108,P<0.05). The pro?tein expression of Claudin-5 was higher in methylprednisolone pretreatment group than spinal cord injury group at each time point (F value 20.247,P<0.05). Conclusions Methylprednisolone improves permeability of BSCB after spinal cord injury probably through enhancing claudin-5 expression in rats.
was lower in spinal cord injury group than in sham operated group at each time point (Fvalue 18.108,P<0.05). The pro?tein expression of Claudin-5 was higher in methylprednisolone pretreatment group than spinal cord injury group at each time point (F value 20.247,P<0.05). Conclusions Methylprednisolone improves permeability of BSCB after spinal cord injury probably through enhancing claudin-5 expression in rats.

Abstract: Fifteen novel ligustrazine-tetrahydroisoquinoline derivatives were designed and synthesized according to the association principle of pharmaceutical chemistry. The structures were identified by IR, NMR and ESI-MS. The inhibitory activities of platelet aggregation induced by ADP and AA have been measured by Bron method. Preliminary pharmacological results showed that compounds 7g, 7h and 7n had potent inhibitory activity against platelet aggregation induced by AA, and the compound 7o showed significant inhibitory activity against platelet aggregation induced by ADP.

Objective: To investigate the effects of a Chinese herbal formula for calming liver and suppressing yang on the protein expressions of vascular tissues in spontaneously hypertensive rats (SHRs), and to explore the mechanism of efficacy. Methods: Twenty SHRs were randomly divided into model group and treatment group. Another 10 Wistar-Kyoto rats were selected as a normal control. SHRs in the treatment group were administered with the formula for calming liver and suppressing Yang for 4 weeks. During the course of treatment, blood pressure and heart rates were monitored every week and the ethology of rats, including irritability and rotation endurance was also evaluated. After treatment, thoracic aorta was obtained and its proteins were separated by 2-dimensional gel electrophoresis (2-DE). The differentially expressed proteins were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and database query. Results: The formula for calming liver and suppressing yang not only decreased the systolic blood pressure and heart rate, but also improved irritability degree and rotation endurance time of SHRs. This experiment had established the 2-DE graph of protein expressions of vascular tissues in SHRs. Compared with the normal group, the expressions of 15 proteins were down-regulated, and 12 proteins were up-regulated in vascular tissues of the model group. The formula for calming liver and suppressing yang treatment up-regulated expressions of 10 proteins in the 15 down-regulated proteins, and down-regulated 8 proteins in the 12 up-regulated proteins in vascular tissues of SHRs. After analysis, 16 obviously differentially expressed proteins were found, and 13 of them were identified. Conclusion: The formula for calming liver and suppressing yang can improve the ethology of SHRs. The mechanism is probably concerned with regulating the protein expressions of vascular tissues.

Aim To investigate the Yiqi Yangyin Qingre Oral Liquid(YYQ) on insulin resistance in hyperglycemic fatty rats.Methods The model of hyperglycemic fatty rats was induced by intravenous injection with a low dose of streptozotocin(STZ) and a fed high fat and high caloric diet.The YYQ was given via gavage for a period of 4 weeks.The fasting blood glucose(FBG),oral glucose tolerance(OGT),serum insulin(INS),triglyceride(TG),total cholesterol(TC),free fatty acid(FFA)levels,glucose infusion rate(GIR) by euglycemic hyperinsulinemic clamp technique as well as erythrocyte insulin receptors(INSR)of rats were tested when the experiment was finished.The weight of the epididymal fat pads and the perirenal fat pads were measured.The IR,IRS-1mRNA expressions in liver tissue were measured by RT-PCR technology.Results YYQ treatment decreased the levels of FBG,TC,TG,LDL-C,FFA and increased the level of HDL-C in hyperglycemic fatty rats.As compared with the model rats,glucose tolerance was improved and body weight was reduced in hyperglycemic fatty rats treated with YYQ.Moreover,YYQ treatment upregulated IR,IRS-1mRNA expressions in liver tissue and increased insulin receptor amounts on the erythrocytes surface as well as GIR in the hyperinsulinemic euglycemic clamp experiment.Conclusions YYQ ameliorated insulin resistance in hyperglycemic fatty rats,and its mechanism might be related to increment of INSR and stimulation of insulin pathway.

A series of valproic acid salicylanilide esters were designed and synthesized based on the principle of prodrug. The structures of the target compounds were confirmed by MS, 1H NMR and 13C NMR. Anti-tumor activities of these compounds against K562, A549, A431 cells in vitro were investigated by MTT assay and SRB assay. The results indicated that the compounds 6h-6j were found to have stronger cell growth inhibitory action than gefitinib, and comparable to niclosamide, which are worth to be intensively studied further.

Objective To examine the expression of tight junction protein claudin-5 in blood-spinal cord barrier (BSCB) after spinal cord injury about rat. Methods One hundred-twenty adult male SD rats were randomly divided into blank group (60) and injured group (60). The animal model of spinal cord injury was established using modified Allen method. The expression of claudin-5 in BSCB was examined at 6 h, 12 h, 1 d, 3 d, 5 d and 7 d (five rats per time point). Western blot and RT_PCR were used to detect protein and mRNA expression levels of claudin-5, respectively. Results The success rate of spinal cord injury molding was 81.7%. In injured group, EB content increased gradually over time, reached the peak at the third day(0.9435 ± 0.0813)μg/g and then reduced gradually (P<0.05), EB content was signifi-cantly higher in injured group than in blank group. Claudin-5 mRNA expression in injured group reduced gradually over time and reached the lowest point at the third day(2.871 ± 0.527)and then increased gradually(P<0.05). Claudin-5 mRNA expression was significantly lower in injured group than in blank group(P<0.05). Claudin-5 protein expression in injured group reduced gradually over time, reached the lowest at the third day(0.072 ±0.008)and then increased gradually (P<0.05). Claudin- 5 protein expression was significantly lower in injured group than in blank group(P<0.05). Con-clusions The alteration of claudin-5 expression after SCI may lead to the permeability of BSCB, which may in turn con-tribute to the secondary spinal cord injury.

Background and purpose: The previous work of this study has showed that the treatment of liver cancer cells with emodin could induce endoplasmic reticulum (ER) stress and apoptosis. Given the cross-talk between ER stress and autophagy, this study aimed to investigate whether blockage of autophagy, a defense mechanism against environmental stress, could improve the killing effect of emodin on liver cancer cells. Methods: The CYTO-ID auto-phagy detection kit and Western blot were used to determine autophagy in liver cancer cells. After combined treatment with chloroquine (CQ) and emodin, cancer cell survival was analyzed by ATPlite assay and clonogenic assay. Apoptosis was detected by both flow cytometry analysis and Western blot. Results: Autophagy could be induced in liver cancer cells after treatment with emodin. Inhibition of autophagy significantly increased growth-inhibitory effect of emodin on both HepG2 and Huh7 cancer cells. The combination treatment with CQ and emodin promoted remarkable apoptosis in liver cancer cells, evidenced by the increase in the percentage of cells in sub-G1 phase and the higher expression lever of cleaved caspase-3. Conclusion: Therapeutically targeting autophagy is capable of enhancing cytotoxicity of emodin in liver cancer cell lines.

Aim To make a research of rats with focal cerebral ischemia/reperfusion injury on pathological changes in brain and the changes of AQP4 and related proteins, in order to explore the relationship between AQP4 and brain edema. Methods Adult male SD rats, weighting 250~300 g, were randomly divided in-to Sham group and cerebral ischemia/reperfusion ( I/R) injury model group. The I/R model group was di-vided into the I/R-6 h, 12 h, 24 h, 48 h-four time point groups. The animal model of the right MCA is-chemia/reperfusion was established by suture method in mature SD rats. The nerve symptom score was con-ducted in the corresponding time points. Then, the permeability of brain tissue was detected by EB stai-ning;TTC staining was conducted to observe the cere-bral infarction volume;the dry wet weight method was used to detect the changes of brain water content; im-munohistochemical( IHC) , WB and RT-PCR were ap-plied to detect the expression of AQP4 , and the related factors at different time points of the model rats after is-chemia-reperfusion around infarcts. Results Com-pared with the Sham group, then ever function score of the rats in I/R model groups were much higher. With the increase of the reperfusion time, the cerebral in-farction volume, brain tissue permeability and the brain water content were also increased. IHC results showed that AQP4 expression gradually rose with widen distribution. WB and RT-PCR results verified the in-creasing level of AQP4 expression. The detection of the related proteins expression showed apparent changes. The expression of MMP-9 was increased, while the Oc-cludin and JAM-1 expression showed a decreasing trend. The I/R-48 h model group showed the most ob-vious differences in the expression of the related pro-teins and mRNA ( P <0. 01 vs Sham, respectively ) . Conclusion Accompanied with the aggravating cere-bral injury after cerebral ischemia/reperfusion, the ex-pression of AQP4 and MMP-9 level were activated, while the degradation of TJPs, Occludin and JAM-1, was increased. These factors are combined to make the formation of brain edema. This study makes a further research on the formation mechanism of the early stage for cerebral edema on I/R model and offers a potential for intervention in the filed of looking for a reliable drug therapy on cerebral edema.