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Objective To explore whether hypertonic saline would partake in regulating Notch signaling in microglia in experimentally induced cerebral ischemic rats.Methods Male SD rats were randomly divided into sham group, cerebral ischemia group, normal saline group ( NS group ) , 10%hypertonic saline group (10%HS group) , the model of cerebral ischemia were established in all rats except the sham group by using middle cerebral artery occlusion ( MCAO) .After 2 hours of MCAO, the rats were through reperfusion for 24 h.In addition, rats in the normal saline group and 10% HS group were respectively treated with a continuous intravenous injection of normal saline (0.3 mL/h) and 10%HS (0.3 mL/h) by tail vein for 24 h.Immunofluorescence methods, RT-PCR and Western blot were used to detect the expression of Notch1 and intracellular Notch receptor domain ( NICD) .All data was analyzed by one-way analysis of variance ( ANOVA) , The intergroup comparisons were analyzed by the least-significant-difference (LSD) tests.Differences were considered statistically significant if P<0.05.Results Immunofluorescence showed that the expression of Notch1 and NICD were significantly increased in the microglia around peri-ischemia area in cerebral ischemia group and normal saline group compared to sham group;the expression of Notch1 and NICD in the microglia around peri-ischemia area were significantly reduced in 10% HS group compared to ischemia group and NS group.RT-PCR showed that the mRNA expression of Notch1 was significantly increased in ischemia group and NS group compared to sham group ( sham group: 1.000 ± 0.076; ischemia group: 2.203 ±0.283; NS group: 1.616 ±0.185; P <0.01 ); however, it was significantly reduced in 10% HS group compared to ischemia group and NS group ( ischemia group:2.203 ±0.283; NS group: 1.616 ±0.185; 10%HS group: 1.202 ±0.177; P <0.05 ) .Western blot showed that the protein expression of Notch1 was significantly increased in ischemia group and NS group compared to sham group ( sham group: 0.290 ±0.079; ischemia group: 0.750 ±0.029; NS group:0.765 ±0.182;P<0.01);but was significantly reduced in 10%HS group compared to ischemia group and NS group ( ischemia group:0.750 ±0.029; NS group:0.765 ±0.182;10%HS group:0.390 ±0.195;P<0.05 ) .The protein expression of NICD was significantly increased in ischemia group and NS group compared to sham group ( sham group: 0.401 ±0.196; ischemia group: 0.906 ±0.359; NS group:0.847 ±0.153;P<0.01);but was significantly reduced in 10%HS group compared to ischemia group and NS group ( ischemia group:0.906 ±0.359; NS group:0.847 ±0.153;10%HS group:0.561 ±0.165;P<0.05 ) .Conclusion Our results suggest that HS markedly suppresses Notch signaling in microglia around the ischemia tissue area in experimental induced cerebral ischemic rats.
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Objective To explore the clinical application value of early bundle therapy in patients with septic shock after per‐cutaneous nephrolithotomy(PCNL) .Methods The retrospective analysis was conducted patients with septic shock after PCNL ad‐mitted to the central ICU of the First Affiliated Hospital ,University of South China from January 1st ,2011 to september 30 ,2013 . The patients were divided into non‐bundle therapy group and bundle therapy group according to whether treated by early bundle therapy .the APACHE‐Ⅱscore and SOFA score in the before and 1 ,3 ,7 d after treatment ,mortality rate within 28 d and length of ICU were compared with both groups .Results 54 patients were enrolled in the study ,there were 28 and 26 patients in non‐bundle therapy group and bundle therapy group ,respectively .The clinical data of patients in both groups had no significant difference be‐tween the groups ,all P>0 .05 .Compared with the patients in non‐bundle therapy group ,the APACHE‐Ⅱscore and SOFA score in 1 ,3 ,7 d after treatment significantly decreased in bundle therapy group ,all P<0 .05 .mortality rate in bundle therapy group and non‐bundle therapy group were 15 .38% and 35 .71% ,respectively ,P<0 .05 ;and length of ICU were(9 .04 ± 4 .48)d and(7 .00 ± 2 .32)d ,respectively ,P<0 .05 .Conclusion Early bundle therapy can effectively alleviate the severity of the disease and reduce mor‐tality of patients with septic shock after PCNL .
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Objective To investigate the characteristic changes in cerebral infarction and brain edema. Method A total of 122 Healthy adult male Spraque-Dawley rats were randomly (random number) divided into three groups: normal group ( n = 12), sham operated group (n=12) and cerebral ischemia group ( n = 98). Cerebral infarction and brain edema were induced by a permanent occlusion of right middle cerebral artery (POM-CA) with ligature. According to the duration of POMCA, the rats of cerebral ischemia group were further divided into seven sub-groups, 2 h, 4 h, 6 h, 12 h, 18 h, 24 h and 30 hours. The hemispheric ratio was detected by staining with 2% 2,3,5-triphenyltetrazolium chloride solution, and brain water content was assayed by dry/wet ratio 2 h, 4 h, 6 h, 12 h, 18 h, 24 h and hours after POMCA. Results There was a focal cerebral infarction in the rats of cerebral ischemia group 4 hours after POMCA. There was no significant difference in hemispheric ratio between 4 hours and 6 hours after POMCA by One-way ANOVA (P = 0.091). Compared with 6 h sub-group, the hemispheric ratio increased significantly in 12 h, 18 h, 24 h and 30 h sub-groups (P < 0.01), and the peak was in the 24 h sub-group. The brain water content began to increase 4 hours after POMCA and aggravated 6 hours later, and reached the peak 24 hours after POMCA. The brain water content of the non-ischemic hemisphere increased 18 h,24 h and 30 hours after POMCA. Furthermore, there was a significant correlation between the hemispheric ratio and brain water content ( r = 0.834, P < 0.01). Conclusions The critical point of cerebral infarction and brain edema aggravated is 6 hours after POMCA. Both brain edema and cerebral infarction reach the most serious degree 24 hours after POMCA. It is an important experimental evidence for evaluating the milieu conducive to the pathogenesis, and choosing the suitable time window for the treatment of cerebral infarction and brain edema.