Aim To investigate the modulation effects of NaHS on arterial vasodilatation functions of renal hy-pertensive rats .Methods Two-kidney , one-c lip ( 2K1C ) renovascular hypertension was induced .Rats were randomly divided into four group:sham group , two-kidney one-clip model ( 2K1C ) group, 2KIC +NaSH( H2 S donor ) group, PPG group.The systolic blood pressure ( SBP ) was measured before the opera-tion and each week after the operation .The carotid ar-tery was collected for morphometric parameters ( outer radius, wall thickness, the radio of wall thickness to outer radius) and the tension of the carotid artery was observed with the isolated artery ring technique .Immu-nohistochemistry was used to determine the protein ex-pression of eNOS , ET-1 protein in carotid artery .Re-sults The blood pressure of 2K1C group and PPG group was higher than that of sham group ( P<0.05) . Compared with 2K1C group,the blood pressure and the rat arteria carotis communis of the radio of wall thick-ness to outer radius of 2K1C+NaHS group decreased significantly , while the relaxation of carotid artery to ACh in NaHS group increased .According to the immu-nohistochemistry results , eNOS expression was upregu-lated while ET-1 was downregulated in 2K1C +NaHS group as compared with 2K1C group.Conclusions Chronical administration of NaHS can decrease blood pressure in renovasocular hypertensive rats .The anti-hypertensive effect of H 2 S maybe associated with im-provement of the arterial functions .

Objective To explore the relationship between drug resistance of leukemic cells and Caspase-3,this study took adriamycin(ADR)-resistant human chronic granulocytic leukemic cell strain K562/AO_2 as research subject,observing the cell survival and the morphological change of cell apoptosis under the action of ADR and arsenic sulfide and the Caspase-3 activity before and after putting in the Caspase-3 inhibitor.Methods ① The 3-(4,5-dimethylthiazo-2-yl)-2,5-diphenyl-tetrazolium bromide(MTT) method was used to determine the cell survival(A value) of K562/AO_(2)cell strain under the action of ADR and arsenic sulfide.② DNA agarose gel electrophoresis was performed to observe the DNA cleavage of apoptotic cells.③ The enzyme colorimetric activity assay(CAA) method was used to measure the change of the Caspase-3 activity of K562/AO_(2) cell strain.Results ① The A value of K562/AO_(2) cells had a time and dosage dependent relation with arsenic sulfide.② Apoptosis occurred in the K562/AO_(2) cell strain affected by arsenic sulfide.③ Compared with the cell strains with the Caspase-3 inhibitor added,the Caspase-3 activity of those without the Caspase-3 inhibitor increased remarkably(P

Purpose To explore the pathological feature of urinary exfoliated cell examination and influence factors by retrospectively comparing the coincidence of diagnosis between urinary exfoliated cell examination and histopathologic results of cystoscopic biopsy. Methods 735 patients underwent both urinary exfoliated cell examination and histopathologic biopsy of cystoscope evaluation from No-vember 2010 to July 2014 in Peking University Shougang Hospital were enrolled in this study. The urinary exfoliated cells were treated with Pap staining, while the histopathologic biopsy were dealt with HE staining. All cases were divided into three groups according to the diagnosis of urinary exfoliated cell examination:negative group ( no cancer or atypical cell detected) , suspicious group ( atypical cell detected) and positive group ( cancer cell detected) . These above diagnoses were confirmed with the histopathologic biopsy. ROC curve analysis, Cochran-Armitage trend test and logistic regression analysis were performed to evaluate the sensitivity and the specificity of urinary exfoliated cell examination as well as the relationship between diagnoses with age and sex. Results The age range of 735 patients (551 male and 184 female) was 28 ~91 years and the median age was 69 years. There were 187 patients in the positive group, including 184 malignant and 3 false-positive cases. The suspicious group, including 186 cases, consisted of 67 malignant, 119 benign reactive changes. Of all 362 cases in the negative group, malignant tumor was detected in 90 cases. For histologic diagnosis, the AUC of ROC(95%CI)was 0. 800 (0. 767~0. 834), displaying significant difference as compared to the histological pathological diagnostic results(P<0. 001). As the cyto-histologic diagnostic level elevated from negative, suspicious to positive, the results of Co-chran-Armitage trend test showed significant differences(Z=15. 83, P<0. 001). If standardized with the histopathologic biopsy re-sults, the AUC (area under curve) of urinary exfoliated cell examination was 0. 800 (0. 767~0. 834) in ROC curve analysis was sig-nificantly larger (P<0. 001). Furthermore, we also found in Logistic regression that the incidence of cancer was 1. 04 (1. 03~1. 05) times higher if aged one year older ( P<0. 001 ) , while there was no significant relationship between the incidence and the sex ( P=0. 655). Conclusions The coincidence rate of urinary exfoliated cell examination increases with the malignant degree. A positive cor-relation is detected between age and the incidence of malignant tumor. Detailed clinical material can markedly improve the sensitivity and accuracy of cyto-histologic diagnosis.

AIM: To investigate the effects of sodium hydrosulfide ( NaHS ) , a donor of hydrogen sulfide ( H2 S) , on the membrane permeability , intracellular Ca 2+concentration ( [ Ca2+] i ) and the release of IL-1βinduced by a-denosine triphosphate (ATP) in rat microglia, and to explore the effect of H2S on ATP-P2X purinergic signaling pathway and the molecular mechanism of its neuroprotective effect .METHODS: Rat microglia in logarithmic growth phase were used in the study.The [Ca2+]i was detected by Fura-2/AM staining.Fluorescent dye YO-PRO-1 was used to observe the membrane permeability.Interleukin-1β(IL-1β) was measured by rat IL-1βELISA kits.RESULTS:The YO-PRO-1 flu-orescence intensity was obviously elevated by ATP induction in a dose -dependent manner in the rat microglia , but this effect was counteracted by NaHS pretreatment (P<0.05).[Ca2+]i rapidly increased and then decreased slowly , forming a sta-ble platform for a long time when rat microglia were treated with ATP .Ca2+spike activity induced by ATP had no change , but the platform disappeared (P<0.05) after NaHS pretreatment.The ATP and LPS together facilitated the release of IL-1β, but the phenomenon was inhibited by NaHS (P<0.05).CONCLUSION:Hydrogen sulfide may decrease the mem-brane permeability , calcium inflow and IL-1βrelease in rat microglia activated by high dose of ATP .The cytoprotection of hydrogen sulfide may be mediated by purinergic signaling pathway .

AIM: To explore the neuroprotective action of progesterone(PROG), which has been proved to be a "neuroactive steroid". METHODS: The model of focal cerebral ischemia was established in rats by reverserble inserting a nylon thread with a diameter of 0.2 mm into the anterior cerebral artery through the internal carotid artery. The effect of PROG was assessed by determining water,sodium, potassium, and calcium contents in striatum of rats subjected to 2 h ischemia followed by 22 h reperfusion. RESULTS: The water,sodium,and calcium contents of middle cerebral artery occlusion(MCAO) striatum were obviously higher,the potassium content was obviously lower than those of non-MCAO striatum in I/R and DMSO groups,but there was no significant difference between these two groups.Compared with the result in I/R and DMSO groups , water, sodium and calcium contents significantly decreased, but potassium(P0.05). CONCLUSION: Treatment with PROG can significantly reduce the striatal injury of rats with cerebral ischmia-reperfusion.

AIM: To explore the effect of allicin on hippocampal neuronal apoptosis induced by global cerebral ischemia - reperfusion and its mechanisms. METHODS: Wistar rats were subjected to 15 min global cerebral ischemia followed by 72 h reperfusion. Flow cytometry (FCM) was used to evaluate the rate of hippocampal neuronal apoptosis and colorimetric method was used for the measurement of nitric oxide (NO) , malondialdehyde (MDA) contents and superoxide dismutase (SOD) activity in hippocampal tissue. RESULTS: Neuronal apoptotic rate, nitric oxide and malondialdehyde contents in hippocampal tissues of rats in I - R group were significantly higher than those in sham group. However, superoxide dismutase activity in hippocampal tissues of rats in I - R group was obviously lower than that in sham group. Allicin pretreatment inhibited the above changes in a dose-dependent manner. CONCLUSION: Allicin hihibits hippocampal neuronal apoptosis induced by global ischemia-reperfusion insult through anti - oxidation. The anti - oxidation action of allicin may be one of the mechanisms of inhibitory effects on hippocampal neuronal apoptosis.

AIM: To explore the role of NO in the induction of brain ischemic tolerance (BIT) by observing changes of NOS activity and NO_2-/NO_3- content following a transient cerebral ischemia. METHODS: The rat 4-vessel occluding brain ischemic model was used. 140 male Wistar rats were divided into sham, cerebral ischemic preconditioning (CIP), ischemic insult and CIP+ischemic insult groups. An occlusion of the 4 vessels for 3 min was normally used as CIP, and a relative long one for 10 min was used as ischemic insult. When CIP was followed by ischemic insult, the interval between them was 3 d. The CA1 region of the hippocampus of rats was dissected out at 0 h, 2 h, 16 h, 24 h, 36 h, 72 h and 7 d after the last time of ischemia to assay its NOS activity and NO_2-/NO_3- content. RESULTS: The NOS activity and NO_2-/NO_3- content began to increase at 16 h, peaked at 24 h and decreased to basal level at 36 h of reperfusion after CIP. The duration of the up-regulation of NOS activity and NO_2-/NO_3- content was much shorter than that of BIT, which usually takes place 1-7 d after CIP. The pattern of upregulation of the NOS activity and NO_2-/NO_3- content was similar to the CIP group, but the maximum (24 h) was much more than that in CIP group (P

Objective To study the dynamic expression and distribution of high mobility group box 1 (HMGB-1)in diffuse axonal injury (DAI)in rats and to clarify its involvement in the inflammatory reaction after DAI in rats,in order to provide new targets for the clinical treatment of DAI.Methods A DAI model was established using a coronal rotation device and evaluated by HE,Glees-Marsland silver staining,and Mallory phosphotungstic acid hematoxylin staining.Immunohistochemistry,Western blot and RT-PCR were used to detect the expression and distribution of HMGB-1 in the cortex of DAI rats at 6 h,1 d,3 d and 7 d.And TUNEL was used to examine the apoptosis of neurons in DAI rats.Results Immunohistochemical results showed that at 6 h and 1 d after DAI,the number of HMGB-1-positive cells decreased,but at 3 and 7 d it began to increase.Western blot also showed that during the early stage after DAI (6 h and 1 d),the level of HMGB-1 protein in the cortex was significantly lower than that in the control group,but at the late stage (3 and 7 d)after DAI it significantly increased compared with that in the control group until 7 d.RT-PCR showed that at 6 h after DAI there was no significant increase in the level of HMGB-1mRNA,but at 1 d there was a slight increase compared with the control group;at 3 and 7 d,it showed an obvious significance.TUNEL staining indicated that the significant neuronal apoptosis appeared as early as 6 h after DAI,and reached the peak at 3 d;it started to decrease at 7 d but still remained at a relatively high level.Conclusion The dynamic expression and distribution of HMGB-1 showed significant changes with the time course after DAI in rats.They decreased at the early stage but increased at the late stage.At the early stage, HMGB-1 is mainly passively released by the necrotic neurons,and at the late stage it may be actively secreted by the active inflammatory cells.HMGB-1 may mediate the post-DAI neural cell apoptosis by inducing the inflammatory reaction.

Aim To investigate the protective effects of hydrogen sulfide ( H2 S) on focal cerebral ischemia/reperfusion injury in rats and the possible mechanisms. Methods Male Sprague Dawley rats were divided into three groups randomly: sham-operated group, cerebral ischemia/ reperfusion ( I/R) group and sodium hydro-sulfide ( NaHS ) + I/R group. The left temporary middle cerebral artery occlusion ( MCAO ) model was established by the line-embolism method. After rats were suffered 2h/24h ischemia/reperfusion stress, the mortality rate was evaluated, and the nervous function-al defect degree was evaluated by Longe scoring, the volumes of cerebral infarction was evaluated by 2 ,3 ,5-triphenyltetrazolium chloride ( TTC) staining, and the expression of P2X7 receptor protein in brain tissue was detected by the immunofluorescence method. Results The mortality rate in NaHS + I/R rats ( 29.41%) was obviously lower than those of I/R group ( 42 . 86%) . The nervous defect scores in NaHS + I/R rats were significant lower than those of I/R group ( P <0.05 ) . The volumes of cerebral infarction in NaHS +I/R group (21.88% ±3.53%) were significant lower than those of I/R group ( 36.71% ±3.73%) ( P <0.01 ) . The results of immunofluorescence showed that the positive expression cells of P2X7 receptor protein in cerebral cortex and hippocampal CA1 area of I/R group were significantly higher than those of sham-op-erated group(P<0. 01). However, compared with I/R group, the positive expression cells of P2X7 receptor protein in cerebral cortex and hippocampal CA1 area of NaHS + I/R group were significantly decreased ( P<0. 01). Conclusions H2S exerts the neuroprotective effect on focal cerebral ischemia/reperfusion injury in rats, and the protective mechanism might be associated with down-regulating the expression of P2X7 receptor protein in brain tissue.