0.05),and presented significant increase after half a year of retention(P

Objective To determine whether sulfasalazine stimulates hepatic stellate cell (HSC-T6) apoptosis and its possible mechanism. Methods CCK-8 assay, acridine orange/ethidium bromide(AO/EB) and Annexin Ⅴ FITC/PI were used to determine cell growth and cell apoptosis. The expression of NF-?B P65, phospho-IKK and phospho-I?B was detected by Western blotting. The nuclear translocation of HSC-T6 P65 was observed with laser confocal microscopy. Results Sulfasalazine displayed a strong growth inhibition and promoting apoptosis effect on HSC-T6 cells in a dose and time-dependent manner. Sulfasalazine, but not 5-aminosalicylic acid or sulfapyridine, inhibited the activation of NF-?B by down-regulating the expressions of P-IKK, P-I?B and the nuclear translocation of P65. Conclusion Sulfasalazine can inhibit NF-?B activity and promote apoptosis in HSC-T6 cells, where the Rel/NF-?B/I?B/IKK pathway plays an important role in HSC survival.

Objective To investigate the impact of tanshinone Ⅱ A on the level of brain NMDAR1 protein in rats after cardiopulmonary resuscitation and its effects of brain function protection.Methods Seventy-eight SD male rats were randomly (random number) divided into three groups:group A (sham group,n =6),group B (control group,n =36) and group C (Tanshinone Ⅱ A intervention group,n =36).All animals were induced to be models of cardiac arrest by choking.The rats of group C received intravenous injection of Tanshinone Ⅱ A in dose of 15 mg/kg immediately at initiation of resuscitation,while rats of group B were intravenous injected same amount of normal saline instead.Brains tissues of all rats were taken at 1,6,12,24,48 and 72 h after the restoration of spontaneous circulation (ROSC).Immunohistochemical staining method was applied for measuring the levels of brain tissue NMDAR1 and Caspases-3,while water content of the brain was detected by wet and dry weight ratio.The experimentaldata were analyzed by using one-way ANOVA.Results (①)The level of brain NMDAR1 protein in group B increased at 1 h and reached its peak at 6 h after ROSC,then its level gradually declined and dropped below normal at 48 h,72 h,and there were significant difference in variation of NMDAR1 protein levels in comparison with the group A (P ＜ 0.05) ; the NMDAR1 protein levels at 1,6,12 h in group C were significantly lower than those in group B at the same intervals (P ＜ 0.01),but no significant differences were seen at 24,48,72 h (P ＞ 0.05).(②)The level of brain Caspases-3 in group B increased after ROSC,and reached its peak at 48 h after ROSC,then declined and maintained above normal at 72 h,and this variation was significantly different from that of the group A (P ＜ 0.01) ; while the levels of caspase-3 at 1,6,12,24 h in group C were significantly lower than those in group B (P ＜ 0.01),but thses differences at 48,72 h were still significant (P ＜ 0.05).(③)The water content of brain tissue in group B increased at 1 h and reached its peak at 24 h after ROSC,then gradually decreased from 48 h,but maintained above normal at 72 h,and this trend of variation was significantly different from that of group A (P ＜ 0.01 or P ＜ 0.05).Compared with group B,water content of brain tissue in group C decreased more significantly (P ＜ 0.01).Conclusions Tanshinone Ⅱ A down-regulates brain NMDAR1 protein level at early stage in rats as well as significantly inhibits the level of Caspases-3 thereby ameliorating brain edema after cardiopulmonary resuscitation.

Objective To study the activity of N acetylglucosaminyltransferase Ⅲ, Ⅳ and V in extrahepatic cholangiocarcinoma and its significance.Methods The activities of N acetylglucosaminyltransferase(GnT) Ⅲ, Ⅳ and Ⅴ in extrahepatic bile duct carcinoma (EBDC) of 15 cases were determined by reverse phase HPLC (high performance liquid chromatography), and results were compared with benign biliary diseases in 15 cases. Results Compared with normal control, that the specific activities of GnT Ⅲ and GnT Ⅴ increased by 3 3 and 13 5 fold respectively in all of the EBDC samples(all P

OBJECTIVE:To study the general pattern and characteristics of the ADRs associated with Houttuynia cordata injection(HCI).METHODS:An analysis was conducted on55cases of ADRs induced by HCI reported in domestic medical jou_ rnals in recent years.RESULTS:The ADRs of HCI were not related to the dosage given.The onset of ADRs was commonly within30min during infusion.The ADRs mostly occurred in groups of patients under age20and from30to59years of age.The ADRs could involve multiple organs and systems,and the clinical manifestations were varying,of which allergic reaction was the commonest one including anaphylactic shock.CONCLUSION:The mechanism of allergic reaction induced by HCI remains to be further studied.Clinical physicians,nurses and pharmacists should pay more attention to the ADRs of HCI.

By using extracellular single unit recording technique, locally suppressive effects of a single dose of ketamine on sub-cutaneous (s. c. ) bee venom-induced increase in firing of wide dynamic-range (WDR) neurons in spinal dorsal horn were investi-gated on urcthane-chloralose anesthetized cats. Injection of bee venom s.c. into the cutaneous receptive field (RF) resulted in asingle phase of prolonged, persistently increased firing of WDR neurons over background activity for more than 1 h. Local pre-treatment with ketamine (100 mM, 0. 1 m l) into the center of RF where bee venom was injected produced a dramatic suppressionof the increased neuronal firing by 60% (3.10± 0.42 spikes/s, n= 5) when compared with saline pre-treated group (7.61 ± 0.17spikes/ s. n = 5 ). Moreover, local post-treatment with the same dose of ketamine also produced a profound suppression of the in-creased neuronal activity by 81% (1.51±0.06 spikes/s, n=5) when compared with the saline post-treated group (7.76±0.15spikes s, n=5). However, s.c. administration with the same dose of ketamine into a symmetrical region on the bee venom un-treated contralateral hindpaw produced no affection on the increased firing of the WDR neurons, suggesting that the suppressiveaction of local ketamine was not the result of systemic effects. The present result suggests that ketamine may exert its localantinociceptive effects mainly through the peripheral NMDA receptors in addition to its partially potential blocking effects onsodium and voltage-sensitive calcium channels.

Objective To observe the effects of arsenic trioxide(As2O3)on the expressions of TNF-?,Fas and bcl-2 in lung adenocarcinoma cells(LAC)and to explore the mechanism of arsenic trioxide inducing apoptosis.Methods The expressions of TNF-?,Fas and bcl-2 in lung adenocarcinoma cells pretreated by arsenious acid were determined by the double antibody sandwich ABC-ELISA method.Results Compared with the control group,As2O3 showed no effects on the contents of bcl-2 in lung adenocarcinoma cells after 72 hours treatment,but increased the contents of TNF-? and Fas significantly,and the effects in different concentration groups had significant differences.The protein expressions of TNF-? and Fas showed a tendency of concentration-dependent increasing.Conclusions The results suggest that As2O3 induces the apoptosis of LAC cells possibly by up-regulating the expression of TNF-? and Fas.

【Objective】 To explore the therapeutic mechanismof arsenic trioxide(AS2O3),the active component of arsenolitumininhibitingtumor.【Methods】Humanlung adenocarcinoma cells(LAC) at logarithmic growth phase were culturedin vitro for 24 hours,and then were cocultured with arsenic trioxide(AS2O3) in the dosages of 0.75,1.0,1.5 and 2.0 mg/Lrespectively.Meanwhile,model control group was set up.The morphological features of LAC in different groups were observed under reverse microscope,growth-inhibitory rate of LAC was examined by methylthiazolyltetrazolium(MTT) assay,andthe expression of p53 gene was detected by enzyme-linked immunosorbent assay(ELISA) method.【Results】AS2O3in different dosages obviously inhibited the proliferation of LACin a time-effect manner,and markedly increased the expression of p53 gene(P

Objective To describe clinical features,polysomnographic (PSG) alterations and characteristics of motor and distribution during rapid eye movement (REM) sleep in narcoleptic patients with REM sleep behavior disorder (RBD).Methods We retrospectively summarized general features of 22 narcoleptic patients with RBD,96 narcoleptic patients without RBD and 21 healthy subjects as controls.We compared their PSG and the related indexes in 3 groups.Then we analyzed a full-night video-PSG recording in a continuous series in 22 narcoleptic patients with RBD to identify their motor behavior and distribution features.Results There was no significant difference in PSG parameter and correlation index between the narcoleptic patients with RBD group and without RBD group.However,compared with normal control group (20.15 ± 4.52),narcoleptic patients with or without RBD (24.07 ± 5.44,23.40 ± 4.50) showed increased the body mass index(F =4.869,P =0.009),shortened NREM sleep and REM sleep (min) latency at night (4.41 ±7.01,3.55 ±3.98 and 14.69 ±9.62,x2 =31.697,P =0.000;69.39 ±81.39,71.04 ±74.45and 115.31 ± 45.13,x2 =11.485,P =0.003),increased percentage of sleep stage 1,decreased percentage of slow wave sleep,delayed the arousal time and increased number of arousal episode longer than 5 minutes.In narcoleptic patients with RBD,RBD episodes occurred frequentlyatany stage of REM sleep through whole night and the frequency of vocalizations did not significantly differ between the two halves of the night.Pantomimes were significantly more frequent in RBD episodes of the second half of the night.Conclusions The prevalence of RBD is high in narcoleptic patients.Sleep architecture doesn' t differ between narcoleptic patients with and without RBD.There is no correlation between the occurrence of RBD and narcoleptic duration.In narcoleptic patients with RBD,vocalizations and pantomimes accounted formajor proportion of RBD episodes while aggressive-violent movements are rare.