Objective By detecting the changes of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)in brain tissue,as well as serum S-100β and neuron specific enolases(NSE)in neonatal rats with hypoxic-ischemic encephalopathy(HIE)under differ-ent treatment regimens,the anti-inflammatory and neuroprotective effects of hydrogen gas were explored.Methods HIE animal model was made from 7-day-old newborn SD rats,and then divided into sham operation group,control group,test group 1(saturated hydro-gen saline group),test group 2(mild hypothermia group),and test group 3(combination group)according to completely random number table method.No special treatment was given in the sham operation group,while the control group only had modeling,test group 1 was in-traperitoneally injected with saturated hydrogen saline after modeling,test group 2 was treated with mild hypothermia after modeling,test group3 was treated with mild hypothermia combined with injection of saturated hydrogen saline after modeling.At 1,3 and 7days after modeling,10 rats from each group were decapitated and brain tissue was collected for enzyme-linked immunosorbent assay(ELISA)de-tection of IL-6 and TNF-α,and serum was collected to detect the expression levels of S-100β and NSE.Results The expression levels of IL-6,TNF-α in the brain tissue,S-100β,and NSE in serum of the control group were increased significantly 1day after modeling,began to decline at 3days,and returned to normal at 7days.Compared with the sham operation group,the expression levels of various indicators in the 1day and 3days were statistically significant(P＜0.05).However,the expression levels of various indicators in test group 1and 2decreased compared with the control group on 1day and 3days after modeling(P＜0.05),but were higher than those in test group 3 and sham operation group,with statistical significance(P＜0.05).There was no statistical significance in the comparison of various indicators between test group 1 and 2 at each stage(P＞0.05).Conclusion Hydrogen treatment can reduce the inflammatory response level of the nervous system to some extent,and also has a certain neuroprotective effect on HIE in neonatal rats.

Objective By detecting the changes of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)in brain tissue,as well as serum S-100β and neuron specific enolases(NSE)in neonatal rats with hypoxic-ischemic encephalopathy(HIE)under differ-ent treatment regimens,the anti-inflammatory and neuroprotective effects of hydrogen gas were explored.Methods HIE animal model was made from 7-day-old newborn SD rats,and then divided into sham operation group,control group,test group 1(saturated hydro-gen saline group),test group 2(mild hypothermia group),and test group 3(combination group)according to completely random number table method.No special treatment was given in the sham operation group,while the control group only had modeling,test group 1 was in-traperitoneally injected with saturated hydrogen saline after modeling,test group 2 was treated with mild hypothermia after modeling,test group3 was treated with mild hypothermia combined with injection of saturated hydrogen saline after modeling.At 1,3 and 7days after modeling,10 rats from each group were decapitated and brain tissue was collected for enzyme-linked immunosorbent assay(ELISA)de-tection of IL-6 and TNF-α,and serum was collected to detect the expression levels of S-100β and NSE.Results The expression levels of IL-6,TNF-α in the brain tissue,S-100β,and NSE in serum of the control group were increased significantly 1day after modeling,began to decline at 3days,and returned to normal at 7days.Compared with the sham operation group,the expression levels of various indicators in the 1day and 3days were statistically significant(P＜0.05).However,the expression levels of various indicators in test group 1and 2decreased compared with the control group on 1day and 3days after modeling(P＜0.05),but were higher than those in test group 3 and sham operation group,with statistical significance(P＜0.05).There was no statistical significance in the comparison of various indicators between test group 1 and 2 at each stage(P＞0.05).Conclusion Hydrogen treatment can reduce the inflammatory response level of the nervous system to some extent,and also has a certain neuroprotective effect on HIE in neonatal rats.

AIM:To investigate the mechanism by which wogonin(WOG)induces ferroptosis in collagen-in-duced arthritis rat fibroblast-like synoviocytes(rat CIA-FLS cells)through the nuclear factor E2-related factor 2(NRF2)/heme oxygenase-1(HO-1)signaling pathway.METHODS:Rat CIA-FLS cells were divided into:control group,low,medium,and high dose of(25,50 and 100 μmol/L)WOG group,ferroptosis inhibitor(LIP-1)group,LIP-1+high dose WOG group,HO-1 agonist cobalt protoporphyrin(COPP)group,and COPP+high dose WOG group.CCK-8 assay was used for cell viability.Crystal violet staining was used for for cell morphology.The levels of oxidative stress markers gluta-thione(GSH),malondialdehyde(MDA),and superoxide dismutase(SOD)were measured.DCFH-DA fluorescent probe was used to detect the intracellular reactive oxygen species(ROS)content as well as Western blot to detect the protein ex-pression levels of Kelch-like ECH-associated protein 1(KEAP-1),NRF2 and HO-1.RESULTS:Compared with the nor-mal control group,administration of WOG treatment resulted in a significant decrease in CIA-FLS cell viability(P<0.01),a significant increase in the level of oxidative stress(P<0.01),a significant increase in the content of ROS(P<0.01),a significant decrease in the level of expression of NRF2 and HO-1 proteins(P<0.01),and a significant increase in the level of KEAP-1(P<0.01)in the rat.Compared with the WOG group,the LIP-1-treated group showed a significant increase in cell viability(P<0.01),a significant decrease in the level of oxidative stress(P<0.01),and a significant de-crease in the content of ROS(P<0.01).Compared with the WOG group,the addition of COPP resulted in a significant in-crease in the protein expression levels of NRF2 and HO-1(P<0.01)and a significant decrease in KEAP-1 levels(P<0.01).CONCLUSION:WOG can induce ferroptosis in rat CIA-FLS cells by promoting oxidative stress through the NRF2/HO-1 signaling pathway.

Objective: To prepare oxymatrine phospholipid complex solid lipid nanoparticles(OMT-PC-SLN) lyophilized powder and evaluate its pharmaceutical properties. Method: Pseudo-ternary phase diagram was employed to optimize the formula of microemulsion;single factor experiments were adopted to optimize the formulation process of OMT-PC-SLN lyophilized powder with encapsulation efficiency as index;the morphology of this preparation was observed by transmission electron microscope(TEM).The particle size was measured by particle size analyzer and the in vitro release performance of OMT-PC-SLN lyophilized powder was examined. Result: Optimal formulation process was as following:taking soybean phospholipid and polyethylene glycol 15-hydroxystearate(Kolliphor HS 15) as the emulsifier,ethanol as co-emulsifier,ratio of emulsifier to co-emulsifier(K_m)=3:2,oil phase:(emulsifier+co-emulsifier)=1:9,oxymatrine phospholipid complex-stearic acid-soybean phospholipid-Kolliphor HS 15-ethanol(30:100:180:360:360);taking 50 mL of 4%mannitol solution as the external aqueous phase,ice bath stirring at 1 000 r·min^-1 and solidifying for 1 h,precooled at -20℃ for 24 h,took out and dried for 24 h.OMT-PC-SLN lyophilized powder was spherical in appearance with encapsulation efficiency of (38.09±1.24)%,average particle size of 785.5 nm,polydispersity coefficient(PDI) of 0.456 and the Zeta potential of -24.82 mV.The cumulative release rates of OMT-PC-SLN lyophilized powder were 72.63%at 2 h and 98.42%at 12 h;the cumulative release rate of oxymatrine(crude drug) was 98.60%at 2 h. Conclusion: This optimized formulation process of OMT-PC-SLN lyophilized powder is stable with good repeatability;compared with oxymatrine,OMT-PC-SLN lyophilized powder has a certain sustained-release effect.

Objective: To investigate the impact of gender and age on in-hospital major adverse cardiovascular and cerebrovascular events of patients with acute ST-segment elevation myocardial infarction (STEMI). Methods: This is a retrospective single-center study. A total of consecutive 1 102 patients with acute STEMI admitted to our hospital from January 2001 to December 2010 were recruited and clinical data were analyzed. The primary end point was in-hospital death due to any cause, and the secondary end point was in-hospital composite end point including death, re-infarction and stroke. Multivariate logistic regression analyses were performed to identify the risk factors of in hospital death and composite end point. Results: The study population included 283(25.7%(283/1 102)) female patients and female patients were older than male patients ((68.7±11.2)years vs. (59.2±12.5)years, P<0.001). Compared with male patients, less female patients received primary percutaneous coronary intervention (50.9%(144/283) vs. 70.9%(581/819), P<0.001), had higher rates of in hospital death(10.6%(30/283)vs. 6.0%(36/819), P<0.001) and composite endpoint(14.1%(40/283)vs. 7.0%(57/819), P<0.001). Among STEMI patients aged <60 years, no differences were found in in-hospital mortality (1.7%(1/58)vs. 1.4%(6/437)) and composite endpoint(3.6%(3/58)vs. 3.4%(15/437)) rates between female and male patients (both P>0.05). Among STEMI patients aged ≥60 years, female patients had higher in-hospital mortality (12.9%(29/225)vs. 7.9%(30/382), P<0.001), and there was no difference on composite endpoint between female and male patients (16.4%(37/225)vs. 11.0%(42/382), P=0.054). Multivariate logistic regression analysis showed that female gender was not the independent risk factor of in-hospital death(OR=1.029, 95%CI 0.564-1.877, P=0.926) and composite end point(OR=1.593, 95%CI 0.989-2.566, P=0.055), but age was the independent risk factor of in-hospital death(OR=1.065, 95%CI 1.037-1.094, P<0.001) and composite end point(OR=1.050, 95%CI 1.029-1.071, P<0.001)in STEMI patients. Multivariate logistic regression analysis also showed that female was not the independent risk factor of in-hospital death(OR=1.539, 95%CI 0.572-4.142, P=0.394) and composite end point(OR=1.563, 95%CI 0.689-3.546, P=0.285), but age was the independent risk factor of in-hospital death(OR=1.052, 95%CI 1.011-1.096, P=0.013) and composite end point(OR=1.042, 95%CI 1.008-1.077, P=0.016)in STEMI patients received primary percutaneous coronary intervention. Conclusion Female patients with STEMI have higher incidence of in-hospital major adverse cardiovascular and cerebrovascular events than male patients, and age is the independent risk factor of in-hospital major adverse cardiovascular and cerebrovascular events of STEMI patients.