Objective To investigate the roles of iron ion in the development of experimental hydrocephalus in rats. Methods Seventy-five Sprague-Dawley female rats were divided into 3 groups randomly,that is,the iron group,the semi-iron group and the artificial cerebrospinal fluid (CSF) control group. FeC13 of 5 ?l dissolved in artificial CSF with the concentration of 6.67 g/L and 3.33 g/L were slowly infused into the right lateral cerebral ventricle of the rats in the iron group and in the semis-iron group respectively. The rats in the artificial CSF control group were infused 5 ?l artificial CSF. The rats were sacrificed 1,14 and 28 d later to measure the transverse diameter of the lateral ventricle for the evaluation of hydrocephalus and the index of ventricle,and pathology of brain was also observed. Results There were significant difference of hydrocephalus between the iron group (9/10) and the semis-iron group(1/5) at 28 d (P

Objective To discuss the effect of deferoxamine in the treatment of chronic hydrocephalus (CH) after intraventricular hemorrhage (IVH) in rats. Methods A total of 184 female Sprague Dawley rats were randomly divided into normal saline group ( NS group), intracerebroventricular blood infusion group (Group A ) and deferoxamine plus intracerebroventricular blood infusion group ( Group B). The rat CH models were made by infusing autologous whole blood ( 130 μl) into the right lateral cerebral ventricle. The escape latency time was detected by Morris water maze at days 14 and 28.The rats were sacrificed 1,3, 7, 14, 28 days later, the transverse diameter of the lateral ventricle on the coronal slice of rat brain 0.4 mm posterior to the bregma was measured for evaluation of hydrocephalus and the index of ventricle. Pathological changes of the brain were observed. Results No CH was found in the NS group. The incidence of CH in the Group A was 73% (11/15), which was significantly higher than 27% (4/15) in Group B at day 28. The escape latency time in the NS group was (8.21 ± 2.00) s,which was significantly shorter than ( 16.36 ±5.93 ) s of the Group A ( P ＜0.01 ). There was no significant difference in the escape latency time between the NS group and Group B [(11.38 ± 2.57 )s] (P ＞0.05 ). The index of ventricle in the NS group was 1.05 ± 0.41, which was smaller than 4.53 ± 1.70 in Group A and 2.77 ± 1.53 in Group B (P ＜ 0.05 ). There were no obvious pathological changes in the NS group at different time points. There found edema of white matter surrounding the ventricle, twist and engorged callosum, proliferation of rhagiocrine cell as well as hemosiderin deposit in Group A. However, no hemosiderin deposit was found in Group B. Conclusions The content of iron in the cerebrospinal fluid may be correlated with hydrocephalus after IVH. Preventive use of deferoxamine can reduce incidence of hydrocephalus after ICH.

OBJECTIVE:To establish a method for the contents determination of phospholipid and γ-linolenic acid in Com-pound linolenic acid soft capsule. METHODS:HPLC was conducted to determine the content of soybean lecithin;the column was Agilent TC-C18 with mobile phase of methanol-water(84:16,V/V)at a flow rate of 1.0 ml/min,the detection wavelength was 219 nm,the column temperature was 30 ℃,and the injection volume was 10 μl.Gas chromatography was conducted to determine the content of γ-linolenic acid in the preparation;the column was DB WAX,injector temperature was 210 ℃ by temperature pro-grammed,carrier gas was helium at a flow rate of 1 ml/min by split injection(split ratio of 1:30),and the injection volume was 0.02μl. RESULTS:The linear range was 4.64-16.24μg/ml for phospholipid(r=0.999 6)and 0.093 44-0.327 04μg/ml forγ-linole-nic acid methy ester(r=0.999 6);RSDs of precision,stability and reproducibility tests were lower than 3%;recoveries were 97.44%-99.36%(RSD=0.93%,n=6) and 97.22%-99.07%(RSD=1.01%,n=6),respectively. CONCLUSIONS:The method is simple,stable with good separation,and can be use for the contents determination of phospholipid and γ-linolenic acid in Com-pound linolenic acid soft capsule.

Objective To establish the rat model of chronic hydrocephalus after intraventricular hemorrhage(IVH).Methods Totally 110 Sprague Dawley female rats were divided into 3 groups:IVH group(n=50),saline control group(n=50)and the normal group(n=10).The rats in IVH group were infused autologous whole blood(130 ?l)into the right lateral cerebral ventricle.All rats except the normal group were sacrificed on day 1,3,7,14,28 after operation,and the transverse diameter of the lateral ventricle was measured to evaluate hydrocephalus and the index of ventricle.The pathological changes of the brain were observed.Results Hydrocephalus occurred in 7 out of 10 rats in IVH group at 28 d.The index of ventricle in IVH group(4.51?1.94)was higher than that of saline control group(1.05?0.41)and the normal group(0.79?0.49)(P

Objective To study the therapeutic effect of IGF?1R inhibitor TAE226 on malignant pleural effusion ( MPE) in nude mice. Methods Human lung carcinoma A549 cells were injected into the pleural cavity of nude mice to establish MPE model. The mice were randomly divided into model group and treatment group, and were orally administered with distilled water and TAE226 ( 20 mg/kg ) in the same volume, respectively. The volume of pleural effusion and tumor weight of the two groups were observed. HE staining was used to reveal the histological changes and enzyme?linked immunosorbent assay ( ELISA) was used to detect the IGF?1R protein expression. IGF?1R mRNA level in the tumor tissue was determined by RT?PCR. Microvessel density (MVD) and cell proliferation index (PI) were assessed by immunohistochemical analysis. The protein expression levels of IGF?1R, p?IGF?1R, PI3K and p?PI3K in the tumor tissue were determined by Western blotting. Results The volumes of pleural effusion were ( 241. 4 ± 89. 7 ) μl and (121.7±78.8) μl in the model and treatment groups, respectively (P<0.05). The tumor weight of treatment group was (316.7±186.3) mg, significantly lower than that of the model group (671.4±281.4) mg (P<0.05) . RT?PCR analysis showed that IGF?1R mRNA level was 0. 914 ± 0. 029 in the treatment group, significantly lower than that of the model group (1.152±0.037, P<0.01). The ELISA data revealed that IGF?1R protein expression level of the model group was significantly higher than that of the treatment group [(41.0±4.7) μg/L vs. (24.0±3.1) μg/L, P<0.01]. Immunohistochemical analysis showed that there were significant differences between MVD and PI in the model and treatment groups [ MVD, 34. 75 ± 3. 49 vs. 22.25±3.63;PI, (75.25±7.15)% vs. (45.75±5.12)%;P<0.01 for both). Western blot data showed that IGF?1R and PI3K protein expression levels were not significantly different between the model and treatment groups (1.03±0.33 vs. 0.98±0.37 and 1.05±0.28 vs. 0.98±0.19), respectively (P>0.05), but p?IGF?1R and p?PI3K protein expression levels had significant differences between the two groups (1.08±0.10 vs. 0.51± 0.08 and 1.12±0.09 vs. 0.86±0.09), respectively (P<0.01 for both). Conclusions The IGF?1R inhibitor can effectively inhibit the formation of malignant pleural effusion. Its mechanism may be related to the suppression of tumor cell proliferation, invasion and angiogenesis through inhibition of PI3K signaling. TAE226 treatment may be a potential therapeutic regimen of treating malignant pleural effusion.

Objective To study the therapeutic effect of IGF?1R inhibitor TAE226 on malignant pleural effusion ( MPE) in nude mice. Methods Human lung carcinoma A549 cells were injected into the pleural cavity of nude mice to establish MPE model. The mice were randomly divided into model group and treatment group, and were orally administered with distilled water and TAE226 ( 20 mg/kg ) in the same volume, respectively. The volume of pleural effusion and tumor weight of the two groups were observed. HE staining was used to reveal the histological changes and enzyme?linked immunosorbent assay ( ELISA) was used to detect the IGF?1R protein expression. IGF?1R mRNA level in the tumor tissue was determined by RT?PCR. Microvessel density (MVD) and cell proliferation index (PI) were assessed by immunohistochemical analysis. The protein expression levels of IGF?1R, p?IGF?1R, PI3K and p?PI3K in the tumor tissue were determined by Western blotting. Results The volumes of pleural effusion were ( 241. 4 ± 89. 7 ) μl and (121.7±78.8) μl in the model and treatment groups, respectively (P<0.05). The tumor weight of treatment group was (316.7±186.3) mg, significantly lower than that of the model group (671.4±281.4) mg (P<0.05) . RT?PCR analysis showed that IGF?1R mRNA level was 0. 914 ± 0. 029 in the treatment group, significantly lower than that of the model group (1.152±0.037, P<0.01). The ELISA data revealed that IGF?1R protein expression level of the model group was significantly higher than that of the treatment group [(41.0±4.7) μg/L vs. (24.0±3.1) μg/L, P<0.01]. Immunohistochemical analysis showed that there were significant differences between MVD and PI in the model and treatment groups [ MVD, 34. 75 ± 3. 49 vs. 22.25±3.63;PI, (75.25±7.15)% vs. (45.75±5.12)%;P<0.01 for both). Western blot data showed that IGF?1R and PI3K protein expression levels were not significantly different between the model and treatment groups (1.03±0.33 vs. 0.98±0.37 and 1.05±0.28 vs. 0.98±0.19), respectively (P>0.05), but p?IGF?1R and p?PI3K protein expression levels had significant differences between the two groups (1.08±0.10 vs. 0.51± 0.08 and 1.12±0.09 vs. 0.86±0.09), respectively (P<0.01 for both). Conclusions The IGF?1R inhibitor can effectively inhibit the formation of malignant pleural effusion. Its mechanism may be related to the suppression of tumor cell proliferation, invasion and angiogenesis through inhibition of PI3K signaling. TAE226 treatment may be a potential therapeutic regimen of treating malignant pleural effusion.