The influence of the aqueous extract of ephedra sinica treating in brain damage after subarachnoid hemorrhage in rats / 重庆医学

Objective To observe the therapeutic effect and mechanism of the aqueous extract of ephedra sinica on brain damage after subarachnoid hemorrhage(SAH)in rats.Methods Totally 50 rats of Sprague-Dawley were randomly divided into control group,model group and three groups treated with different concentrations(4,12,36 mg/kg).The changes of the cerebral water content,malondialdehyde(MDA),glutathione peroxidase(GSH-Px)and hydroxy radical of brain tissue were recorded,and he-matoxylin-eosin(HE)staining was used to test the subarachnoid haemorrhagia and oedema,and immunohistochemistry and western blot were carried out to assay the expression of complement C3 in brains of different animal in different group 3d after operation. Results On the postoperative 3 days,compared with the model group,the content of MDA、GSH-Px activity and hydroxyl radical of 12、36 mg/kg treatment groups significantly reduced(P 0.05),but GSH-Px activity and inhibition of hydroxyl radical significantly reduced(P <0.01),and the cerebral water content of 12,36 mg/kg groups were obviously lower compared with model group.The expression of complement C3 was significantly lower on 36 mg/kg treatment group and edema reduced.Conclusion The aqueous extract of ephedra could significantly inhibit the activity of complement C3,prevent the production of MDA、GSH-Px and hydroxyl radical,reduce the severity of cerebral edema and the in-flammatory response,which has a better therapeutic effect SAH animals.

Effect of splenectomy on mortality and brain water content of rats with brain injury / 中华创伤杂志

Objective To observe the effect of splenectomy on mortality and brain water content of rats with brain injury so as to explore novel way for better clinical management of patients with severe traumatic brain injury. Methods Adult male SD rats were randomly divided into three groups, ie, sham operation on brain and spleen (Group A, n = 23), experimental brain trauma & sham operation on spleen (Group B, n =48) and experimental brain injury & splenectomy (Group C, n = 47). Modified Feeney' s method was used to create the animal model of experimental brain trauma, Longa' s scale was applied to evaluate the neurologic defect. Mortality within seven days following brain injury was calculat-ed. In the meantime, the brain water content was detected at days 1 (n = 8), 2 (n = 8), 3 (n = 8) and 7 (n = 7) after brain injury in each group, Results No statistical difference of Longs' s scale was found between Group B and Group C (P > 0.05). The mortalities within seven days after brain injury were 0%, 35.42 and 14.89% in Groups A, B and C respectively, with statistical difference between groups (P<0.05). The brain water content of Groups B and C at days 1, 2, 3 and 7 were (81.98±0.35)% & (81.78±0.41)%, (82.58±0.63)% & (81.81±0.48)% (P<0.05),(82.54±0.54)% & (81.52±0.84)% (P<0.05) and (81.50±0.41)% & (81.21±0.36)% (P>0.05) respectively. Conclusion Splenectomy can effectively reduce brain water content and significantly decrease mortality in rata with brain injury.

The significance of the expression of endothelial ICAM-1 induced by LPS / 中华烧伤杂志

<p><b>OBJECTIVE</b>To investigate the significance of the expression pattern and its signal modulating mechanism of endothelial ICAM-1 induced by LPS.</p><p><b>METHODS</b>(1) The expression pattern of the ICAM-1 was observed at mRNA level in cultured human umbilical vascular endothelial cells (HUVECs) strain ECV-304 after being stimulated by different LPS concentrations at different time points. (2) The modulating effects of different signal pathways on the ICAM-1 expression of the HUVECs were observed at mRNA and protein levels under the stimulation of LPS after the cells were primed by signal pathway blocking agents for 30 mins.</p><p><b>RESULTS</b>(1) The ICAM-1 mRNA expression could be induced by LPS (100 pg/ml) for 6 hours, and the expression was enhanced along with the increase of LPS concentration. The expression peaked when LPS was at concentrations of 100 approximately 1 000 ng/ml. Temporally, the mRNA expression reached the top level at 6 approximately 8 hours and remained high 12 hours after the stimulation. (2) The expressions of ICAM-1 mRNA and protein could be significantly inhibited by PSI, the NF-kappaB inhibitor. Moreover, the expression of ICAM-1 could all be partially inhibited at mRNA and protein levels by PD98059, the ERK1/2MAPK inhibitor, as well as SB203580, the p38MAPK inhibitor.</p><p><b>CONCLUSION</b>The ICAM-1 mRNA expression of HUVECs could be induced by LPS in both dose and time dependent manner. NF-kappaB might be the major signal pathway of modulating ICAM-1 expression, and p38 and ERK1/2 could possibly be signal pathways of minor importance.</p>

Kinetics of nuclear factor ?B in LPS stimulated rat alveolar macrophages and its regulative effect on tumor necrosis factor ? expression / 中华创伤杂志

Objective To investigate the activation of nuclear factor ?B (NF-?B) induced by lipopolysaccharides (LPS) in rat alveolar macrophages (AM) and its regulative role in tumor necrosis factor (TNF-?) expression. Methods The dynamic activity changes of NF-?B DNA induced by LPS (E.coli 026:B6) were determined with electrophoretic mobility shift assay (EMSA). The phosphorothioate oligodeoxynucleotides (S-ODN) decoy was transfected into AM 12 hours prior to LPS stimulation. The effect of NF-?B S-ODN decoy on expression of TNF-? in AM stimulated by LPS were measured with enzyme-linked immunosorbent assay (ELISA) kit. Results NF-?B could be activated remarkably after 0.5 hour of LPS stimulation at concentration of 100 ng/ml, reached the highest level 1 hour after LPS stimulation and gradually decreased. But the activation of NF-?B could last at least 8 hours. The dose for LPS stimulation was related to activation of NF-?B in a dose-dependent fashion, ie, the activation of NF-?B gradually strengthened with dose increase of LPS. Supershift assays proved that p50 and p65 were involved in the activation of NF-?B. NF-?B S-ODN decoy could markedly (not completely) inhibit LPS-induced TNF-? production. Conclusions NF-?B plays an important role in LPS induced inflammatory response. However, entire inhibition of the activity of NF-?B can not completely prevent TNF-? expression induced by LPS in rat AM, which implies that other nuclear factors may participate in TNF-? expression.

KINETICS OF AP-1 IN LPS-STIMULATED RAT ALVEOLAR MACROPHAGES AND ITS REGULATION ON TNF-? EXPRESSION / 解放军医学杂志

To investigate the kinetics of activation of the activator protein-1(AP-1) and elucidate its role in TNF-? expression induced by lipopolysaccharide(LPS) in rat alveolar macrophages(AM), dynamic changes of the activity of AP-1 were detected with electrophoretic mobility shift assay(EMSA). The phosphorothioate oligodeoxynucleotide (S-ODN) decoy was transfected into AM prior to LPS stimulation. The level of TNF-? in culture supernatants was measured with an ELISA kit. The results showed that after LPS stimulation for 0.5 hour, remarkable activation of AP-1 could be detected and reached the highest level. The activation of AP-1 rapidly decreased at 1 hour, then increased at 3 hours again and reduced at 5 and 8 hours after LPS stimulation. The activation of AP-1 could persist at least 8 hours and showed a dose-dependent manner to LPS within 1000ng/ml. AP-1 S-ODN decoys could markedly inhibit the LPS-induced TNF-? production by rat AM, but it could not completely inhibit the production of TNF-? induced by LPS in rat AM. It is suggested that LPS could induce activation of AP-1 in rat AM; AP-1 played an important role in LPS-induced inflammatory response. It is also suggested that AP-1 involved in the regulation on LPS-induced TNF-? production by rat AM, however, entirely inhibition of the activity of AP-1 could not completely prevent TNF-? production by rat AM. It is also implied that other nuclear factors might also play an important role in the regulation on LPS-induced TNF-? expression by rat AM.