Objective To explore the relationships between the expression of PECAM-1 and the degree of ALI in Paraquat induced lung injury model of rabbits. Method Thirty six adult New Zealand rabbits were randomly divided into three groups: 8 mg/kg (Group A), 16 mg/kg (Group B) and 32 mg/kg ( Group C) according to the dose of Paraquat which were infusion into stomach. After poisoned, the animals were monitored for seven days, and then sacrificed. The upper lobe of lung were removed for HE,Masson staining and immunohistochemisty. The ALl score, fibrosis of lung and expression of PECAM-1 were semiquantitative analyzed. Results Each group has 12 animals suffered from poisoning. The survival time of animals in Group C was (6. 47 ± 0. 99 ) days, shorter than (6. 09 + 1.04) days ( P = 0. 031 ) in Group B and (4. 77 + 2. 04) days ( P = 0. 0 07) in Group A. The ALI score were ( 8. 33 ± 1.03) points in Group A, superior to (9. 83 ± 1.17) points ( P = 0. 047 ) in Group B and ( 11.50 + 1.38) points ( P ＜ 0. 01 ) in group C, Group B vs Group C, P=-0.03o The fibrosis degree of lung was (31.09 +2.05)% in Group A,not severe as (34. 37 ±1.62)% (P=0. 002) in Group B and (36. 54 ±0. 44)% (P ＜0. 01 ) in Group C, Group B vs Group C, P = 0. 026. The Pearson correlation analysis showed the expression of PECAM-1 was negative correlated to ALI score (Coe = -0. 732, P =0. 001 ) and fibrosis degree of lung (Coe = -0. 779, P ＜ 0. 001 ) . Conclusions The expressions of PECAM-1 were significantly decreased in New Zealand after Paraquat poisoned, which were dose dependent, correlated to ALI scored and fibrosis degree of lung, so it may play an important role in the development of lung injured induced by Paraquat.

AIM: To study the role of p38 mitogen-activated protein kinase (p38MAPK) activation in high glucose-induced collagen Ⅲ synthesis in NRK52E cells. METHODS: Normal rat tubular epithelial cell line NRK52E was cultured in D-glucose of different concentrations, pretreated with SB203580 and collected at different time points. The levels of phospho-p38MAPK and extracellular matrix collagen Ⅲ were examined by Western blotting. RESULTS: The activation of p38MAPK was shown to be dependent upon D-glucose concentration and the time-course. Pretreatment with SB203580 blocked p38MAPK activation induced by high concentration of D-glucose in NRK52E cells. CONCLUSIONS: The activation of p38MAPK induced by high concentration of glucose may play a role in diabetic interstital renal fibrosis. SB203580 has a potential value of clinical applications in the prevention and treatment of diabetic nephropathy.

Objective To investigate the incidence of systemic inflammatory response syndrome(SIRS) after cardiopulmonary resuscitation(CPR) and to observe the effect of Ulinastain in inhibition of inflammatory mediator.Methods Forty patients surviving more than 48 hours after CPR were divided into Ulinastain and control groups randomly. Activity of nuclear factor kappa B(NF-?B), IL-6,TNF-? of the patients was detected .All patients were evaluated by SIRS diagnosis standard and their general organ function was examined. All data were compared between two groups.Results Activities of NF-?B, IL-6,TNF-? of patients after CPR was significantly higher than that of normal people (P

AIM:To observe the characterization in neural cells derived from the hippocampus of embryonic rats and to examine the effect of myelin-associated glycoprotein(MAG) on the proliferation,differentiation and neurite growth of neural stem cells(NSCs).METHODS:The hippocampus cells of embryonic rats were isolated and cultured in vitro.The expressions of nestin and doublecortin,the marks of NSCs,were observed by immunocytochemical method.The rate of proliferating cells was examined by BrdU immunocytochemistry.The average neuronal neurite length and the percentage of differentiated neurons were detected by immunocytochemistry staining.RESULTS:The hippocampus cells of 16 days old embryonic rats had the characteristics of NSCs.The percentage of differentiated neurons(?-tubulin Ⅲ-positive cells) was 18.17%?2.79% and the average neuronal neurite length was(136.27?33.66)?m,seven days after the differentiation initiated in vitro in control group.After NSCs were treated with MAG-Fc(200 ?g/L),the percentage of differentiated neurons and the average neurite length were decreased,respectively,to 10.05%?3.42%(P0.05).CONCLUSION:MAG-Fc inhibits the differentiation and neurite growth of the NSCs,but has no effect on the proliferation.

Objective To establish the cardiac arrest-cardiopulmonary resuscitation model in rats, and to observe the effect of mild hypothermia on autophagy in hippocampal CA1 neurons after ROSC.Methods A total of 36 Wistar rats were randomly divided into two groups: normal temperature treatment group(NT group) and mild hypothermia treatment group(HT group).To establish the cardiac arrest-cardiopulmonary resuscitation(CA-CPR) model in rats by epicardial electrical stimulation induced ventricular fibrillation, and to sacrifice 3 animals in each group to obtain the brain cortex in 2nd and 4th hours after ROSC in order to observe the expression of p-AMPK by electron microscope and LC3 granules through Western blot.The neurological deficit score(NDS) was assessed in 24、48、72 hours respectively after ROSC.To sacrifice the animals so as to take the cerebrum in 72 hours after ROSC, then calculate the apoptotic index of the hippocampal CA1 neurons, which were dyed through TUNEL method.Results The expression of p-AMPK、Beclin-1 and LC3-Ⅱ/LC3-Ⅰratio in Normothermia group were all lower than the Mild hypothermia group(P<0.05), the neurons plasma of hippocampal CA1 area in the Hypothermia group demonstrated obvious LC3 granules formation, the NDS score of the Normothermia group and the Mild hypothermia group in ROSC24h、ROSC48h、ROSC72h were 320vs205、285vs140、266vs120, respectively.The apoptotic index of the hippocampal CA1 area in the Normothemia group in ROSC72h was higher than the Mild hypothermia group,(P<0.05).Conclusions Mild hypothermia after cardiopulmonary resuscitation promotes autophagy of the hippocampal CA1 area neurons in rats and reduce neuronal apoptosis.

AIM: To explore the effect and possible mechanism of type 2 innate lymphoid cell (ILC2) on the development of chronic renal failure (CRF).METHODS: The patients with chronic renal failure (n=36) in the Fist Affiliated Hospital of Sun Yat-sen University from March 2016 to December 2016 were selected, and 32 healthy persons in the same period were enrolled in the study for control.The proportion of ILC2 in the PBMC of CRF patients and healthy controls was detected by flow cytometry, IL-13 concentration in the plasma was measured by ELISA.The isolated PBMCs from the patients and healthy persons were divided into 3 groups (control group, cytokine group, intervention group) and cultured in vitro for 3 days, respespestively, then IL-13 concentration was measured by ELISA.The protein levels of phosphorylated signal transducers and activators of transcription 6 (p-STAT6) in the PBMC of healthy controls before stimulation and after stimulation for 15 min, 30 min, 1 h, 2 h were determined by Western blot.RESULTS: The proportion of ILC2 in the PBMC and the plasma IL-13 concentration of CRF patients was higher than that in the healthy controls (P<0.05).In the culture supernatant in vitro, IL-13 concentration in the 3 subgroups of CRF patients (control group, cytokine group, intervention group) were all higher than that in the healthy controls (P<0.05), both the 2 groups showed a trend that the active IL-13 concentration in cytokine group was higher than that in control group, and that in intervention group was lower than that in cytokine group.The protein levels of p-STAT6 in cytokine stimulated-PBMC with a time dependent manner.CONCLUSION: The percentage of ILC2 in the PBMC is elevated in CRF patients.Furthermore, the ILC2 secret large amount of IL-13 to mediate the polarization of Th2 cells to regulate immunity through activating p-STAT6.

Aim To explore the best way of calculating antihypertensive effect of nifedipine GITS on trough to peak ratio (T/PR), and smoothness index (SI) of the drug from ambulatory blood pressure monitoring (ABPM). Methods 32 cases of mild to moderate essential hypertension patients were enrolled and each was given 30 mg of nifedipine GITS once daily. ABPM was repeated for four weeks. ABPM data were analyzed statistically and T/PR calculated by both individual and whole group way. Results The casual blood pressure(CBP) and ABP were lowered by (24?12)/(12?8) mmHg and ( 14.5 ? 3.9 )/( 11.2 ? 3.0) mmHg .The T/PR by individual way was 0.65 ? 0.23 for SBP and 0.66 ? 0.25 for DBP, while by whole group way 0.62 for SBP and 0.68 for DBP. The smoothness index (SI), a new method for assessing the homogeneity of 24 hour blood pressure reduction by antihypertensive therapy, was 3.74 for SBP and 3.77 for DBP after treatment. Conclusion Nifedipine GITS lowers blood pressure effectively and smoothly for 24 hours long. Antihypertensive effects can be reflected by T/PR and SI.

Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.

AIM: To investigate the effect of cobalt chloride (CoCl2) on the apoptosis of neural stem cells (NSCs) and the expression of microRNA-26a (miR-26a) in vitro, and to explore the mechanisms of NSC apoptosis in-duced by CoCl 2 .METHODS:NSCs were exposed to CoCl 2 at different doses (200~600μmol/L) for 24 h.The cell via-bility and apoptosis were measured by CCK-8 assay and TUNEL method.The expression of miR-26a-3p, miR-26a-5p, GSK-3β, caspase-3, Bcl-2 and Bax was examined by real-time PCR.The protein levels of Bcl-2 and Bax were detected by Western blotting .RESULTS: The cell viability was inhibited and the apoptosis of NSCs was increased significantly by CoCl2 in a dose-dependent manner (P<0.05).CoCl2 at concentration of 400μmol/L for 24 h was used to induce apopto-sis and the expression of miR-26a was down-regulated compared with control (P<0.05).Exposure to CoCl2 at concentra-tion of 400μmol/L up-regulated the expression of GSK-3β, caspase-3 and Bax , down-regulated the expression of Bcl-2 and Bcl-2/Bax (P<0.05).CONCLUSION:CoCl2 at concentration of 400μmol/L induces the apoptosis of NSCs obviously . CoCl2 may induce the NSC apoptosis by mitochondrial apoptotic pathway .Declining miR-26a may be related to NSC apopto-sis.

Objective To study the effect of neuronal Nogo-66 receptor (NgR1) antagonist,soluble Nogo-66 receptor (sNgR1-Fc),on promoting the endogenous neural precursor cells (NPCs) differentiating into neurons in order to clarify the mechanism.Methods The cortical infarction was induced by photochemistry,named photothrombotic cortical injury (PCI).Twelve Sprague Dawley rats were randomly divided (random number) into three groups:Sham-operated group,PBS group,and sNgR1-Fc group.PBS (PBS group) or sNgR1-Fc (sNgR1-Fc group) was injected into the lateral ventricle of brain with a minipump.BrdU (Bromodeoxyuridine) was injected into the peritoneal cavity 4-6 days after PCI.The subdentate gyrus zone (SGZ) of brain from sacrificed rat was harvested for Immunohistochemistry to observe the ratio of NeuN +/BrdU + cells 35 days after PCI.Proteins including Nestin、Notch1 and Mash1 were detected by Western Blot.Results The cortical infarction in rat was successfully induced by photochemistry.Thirty-five days after PCI,the BrdU + cells number and theratio of NeuN +/BrdU + in the SGZ of the ipsilateral cerebrum hemisphere with PCI were significantly higher in sNgR1-Fc group than those in PBS group (P ＜ 0.05).The levels of Notch1,Mash1 and Neuro D in the sNgR1-Fc group were significantly higher than those in the PBS group (P ＜ 0.05),which were significantly higher than those in the Sham-operated group.Conclusions sNgR1-Fc could promote the endogenous NPCs differentiating into neurons in a cortical infarction model.The mechanisms may be attributed to the Notch/bHLH (proneural basic helix-loop-helix genes) signaling way.