Acute Disease ; Animals ; Endotoxins ; blood ; Nitric Oxide ; blood ; Pancreatitis ; blood ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; blood

Objective To observe temporal expression of matrix metalloproteinases(MMP-13) and tissue inhibitor of metalloproteina-ses-1 (TIMP-1) in lung of newborn rats with hyperoxia induced chronic lung disease (CLD),and to explore the relationship of CLD with MMPs.Methods The neonatal rats within 24 hours after birth were randomly divided into hyperoxia-exposed group(n=40) and control group(n=40).On postnatal 1,3,7,14 and 21 days,lung tissue of rats in 2 groups were collected.Lung histological changes were evaluated by hematoxylin and eosin and Masson stain;Collagen Ⅰ was detected by enzyme linked immunoadsorbent assay;MMP-13 and TIMP-1 were identifide by immunohistochemistry.Results Exposured to hyperoxia enviroment for 21 days,the number of alveolar decreased,terminal air space enlarged,inter-alveolar septa thickened,and deposition of interstitial collagen fibers.On 14 and 21 days,collagen Ⅰ in the lung of hyperoxia-exposed group increased significantly compared with that of control group(P0.05),obviously decreased on 21 day(P

Objective To explore the effects of the neonatal handling and enriched environmental stimulation on brain damage in neonatal rats with hypoglycemia.Methods Thirty-six neonatal rats were randomly divided into the normal group,hypoglycemia intervention group and the hypoglycemia non-intervention group.Those rats in hypoglycemia intervention and hypoglycemia non-intervention groups were weaned for 12 h,then the blood sugar of both groups were monitored.After neonatal rat models with hyperglycemia were prepared,the rats in hypoglycemia intervention group received the neonatal handling for 14 d and then were kept in an enriched stimulation environment for another 14 d.Rats in normal group and hypoglycemia non-intervention group were fed in the routine way.Neonatal handling was done when the rats were born for 24 h.The rat was rubbed with the brush from head to tail softly.Rats in the hypoglycemia non-intervention group was not handled.The enriched environment stimulation was used after 15 d when the rats were born.Rats in the hypoglycemia intervention group was put into the enriched environment for 1 h per day until 28 d when the rats were born,and rats in the hypoglycemia non-intervention group was put into the normal environment.Then the body weight was scaled at 0 d,7 d,14 d,21 d and 28 d when the rats were born.Space learning and memory were tested with Morris earter at their third month's age.After that,changes of pathology was observed in their occipital cortex.Results The weight increase,the ability of space learning,memory and the number of survival pyramid neurons of occipital cortex in normal group were better than those in hypoglycemia intervention and hypoglycemia non-intervention group(Pa

Objective To observe the effect ofYinqiao Powder on the mouse models with upper respiratory trace mucosal immunity dysfunction infected with influenza virus A, and explore mechanism of action.Methods The mouse models of upper respiratory trace mucosal immunity dysfunction induced by cold stimulation with the influenza A/PR/8/34 (H1N1) virus through the nasal cavity were established. The mice were randomly divided into normal group, model group, positive medicine (Ribavirin) group, andYinqiao Powder group. All administration groups received gavage with relevant medicine, and then mortality, the life prolonging rate, average survival time and the lung index of each group were observed.Results Compared with the model group, the mortalities in positive medicine group andYinqiao Powder group decreased significantly (P<0.05,P<0.01), with longer survival time. The lung indexes in positive medicine group andYinqiao Powder group decreased significantly (P<0.05,P<0.01), and the inhibition ratios of lung index were 35.5% and 24.6%, respectively.ConclusionYinqiao Powder can realize the protective effects on upper respiratory infection through upregulating the mucosal immunity of the upper respiratory tract of mouse models.

Objective To investigate the protective effect of heat shock protein (HSP) 70 on the acute lung injury (ALI) of rats with heat stroke.Methods Sixty four rats were randomly (by employing a random number table) assigned into a sham-heated group (Sham group),heat stress group (HS group),and HS plus gluttamine treatment group (HS+GLN group) and HS plus quercet in treatment group (HS+QU group),16 each.All rats were housed in a artificial climate chamber,with the rats in the sham groups exposed to a temperature of 23 ℃ and humidity of 55％ ± 5％,while the rats of HS,HS+GLN and HS+QU groups to an ambient temperature of 39 ℃ and humidity of 65％.During heat stress or sham heating,rectal temperature (Tr),systolic blood pressure (SBP) and pulse rate (PR) were monitored to observe the difference in heat stress response among the groups.The time point at which the SBP started to drop from the peak level was taken as the point of HS onset.At the onset of HS,heat exposure was terminated,then the rats were immediately removed from the chamber,and returned to room temperature.The rats were scarified 0h and 6h after HS onset respectively.After bronchoalveolar lavage fluid (BALF) was collected,the lungs of all animals were harvested for pathological examination of lung injury.The concentrations of IL-1β,TNF-α and IL-6 in BALF and HSP70 in lung homogenate were measured by using an enzyme linked immunosorbent assay kit.Results Compared with HS and HS+QU groups,the rats in HS+GLN group required significantly greater heat load to induce HS (P＜0.001),and had longer survival time span after HS onset.Compared with Sham group,the concentration of HSP70 in lung homogenate in HS group increased in a time-dependent manner (P＜0.001).In comparison with HS group,the concentration of HSP70 in lung homogenate from HS+GLN group was significantly elevated at each time point (P＜0.001),while the treatment with QU significantly inhibited the expression of HSP70 (P＜0.001).The concentration of IL-1β,TNF-α and IL-6 in BALF significantly decreased in HS+GLN group compared with those in HS group and HS+QU group (P＜0.001).The pathological results showed that the lung injury was milder in HS+GLN group,while the opposite in HS+QU group.Conclusion HSP70 could protect HS rats against ALI by enhancing their thermo-tolerance and inhibiting inflammatory response.

Objective To investigate the role of oxidative stress in acute liver injury in a heat stroke model of conscious rats,and to explore its underlying mechanism.Methods Thirty-two rats were randomly (by using a random number table) assigned into a sham-heated control group (Sham group,n=8),a sham-heated group treated with NAC (Sham-NAC group,n=8),a heat stroke group (HS group,n=8) and a heat stoke group treated with NAC (HS-NAC,n=8).Rats were prepared with pre-warm chamber to initiate heat stoke.The change of rectum temperature (Tr),heart rate (HR) and systolic blood pressure (SBP) were monitored,and the time point of HS onset was recorded.Rats were sacrificed 12h after HS onset.ALT,serum TBIL,IL-6,IL-1β,TNF-α,MDA,T-SOD and GSH in the liver homogenates were measured.Liver tissues were harvested for determining the concentration of reactive oxygen species (ROS),neutrophil infiltration and the histological changes.Results During HS onset,no significant differences were observed in Tr,HR,SBP and heat exposure time between HS group and HS-NAC group (P＞0.05).However,the survival time was significantly longer in HS-NAC group than in HS group (P=0.039).12 hours after HS onset,the concentrations of ROS and MDA in the liver homogenates were significantly higher in HS group than in the other groups (P=0.000),while the concentrations of T-SOD and GSH were much lower than in the other groups (P=0.000).The serum concentrations of ALT and TBIL were significantly higher in HS group than in the other groups (P=0.000).Compare with HS group,the pathological injury was alleviated in HS-NAC group (P=0.000).The neutrophil infiltration level and the concentrations of IL-6,IL-1 β and TNF-α in liver tissue were significantly higher in HS group than in HS-NAC group (P=0.000).Conclusion Oxidative stress may play an important role in the pathogenesis of HS liver injury through its cytotoxic effect and by inducing inflammatory responses.

Objective To observe the immunological effect of tumor cell vaccines to mouse hepatoma A(HepA) treated by Haematoxylin. Methods HepA cell was treated by 0.1% Haematoxylin and made into three vaccines: HepA vaccine with complete Freund' s adjuvant, HepA vaccine with incomplete Freund' s adjuvant; and HepA vaccine without any adjuvants. Five times of immunization were given the grouped mice with the above three vaccines, then active HepA cells (1×105 for each mouse) were inoculated by intraperitoneal injection to attack them; reckoning the mean survival time (MST) of the grouped mice, comparing the immunoprotective action of the three vaccines to the tmnor-bearing mice. Those mice only receiving normal saline (equal volume to the vaccine) were as a control group. Results MST of control group was (23.30±1.24) day; MST of mice receiving H22 vaccine with complete adjuvant was (43.90±15.20) day (P<0.02); MST of mice receiving H22 vaccine with incomplete adjuvant was (39.60±13.77) day (P<0.05); and MST of mice receiving HepA vaccine without any adjuvant was (38.40±12.54) day (P<0.05); As compared with the control group, the three treated groups showed a life-lengthening rate (LLR) 88.41%, 69.96 % and 64.81% respectively. Conclusion The vaccines treated by Haematoxylin give a marked immunoprotective action to those tumor-bearing mice. The HepA vaccine' s immunological effect is increased by the Freund' s adjuvant (complete or incomplete).

Objective To investigate the value of cardiac troponin Ⅰ (cTn Ⅰ) in diagnosis of multi-trauma patients combined with myocardiac contusion.Methods A retrospective review was made on 98 cases of multi-trauma patients combined with blunt chest trauma.The groups were identified according to whether the patients were associated with myocardiac contusion or not,including myocardiac contusion group (n =48) and non-myocardiac contusion group (n =50).The detection and diagnosis of myocardiac contusion in the use of different cut-off points of cTn Ⅰ and creatine kinase MB isoenzyme/creatine kinase (CKMB/CK) or their combination were compared between groups.Results cTn Ⅰ ≥0.60 ng/ml had a specificity of 90.0％,a sensitivity of 64.6％ and a Youden index of 0.54 in diagnosis of myocardiac contusion,indicating a best diagnostic accuracy as a single parameter.As compared with the single use of cTn Ⅰ ≥ 0.60 ng/ml or CKMB/CK ≥ 6％ in diagnosis of myocardiac contusion,the combined use of two parameters presented a significantly higher diagnostic sensitivity (85.4％ vs 64.6％ ; 85.4％ vs 27.1％ respectively,both P ＜ 0.05),but no markedly lower specificity (84.0％ vs 90.0％ ; 84.0％ vs 88.0％ respectively,both P ＞0.05).cTn Ⅰ level was positively correlated with ISS score of the multi-trauma patients combined with myocardiac contusion (r =0.534,P ＜ 0.01).Mortality rate in patients with severely increased cTn Ⅰ was much higher than that in patients with mild-moderately increased cTn Ⅰ (P ＜ 0.01).Conclusions cTn Ⅰ ≥0.60 ng/ml presents a high sensitivity and preferable specificity for diagnosis of multiple trauma patients combined with myocardiac contusion.It can be served as a biomarker for diagnosis of MC and its combination with CKMB/CK≥6％ improves the diagnostic sensitivity.cTn Ⅰ can be used as an assessment indicator for the early risk stratification and outcome in multi-trauma patients combined with myocardiac contusion.

Objective To investigate the changes of the N-acetylaspartate(NAA) concentrations in different brain regions and executive function skills in alcohol dependence,and to study the relationship between NAA levels and cognitive functions in subjects.Methods 49 male,non-smoking,alcohol-dependent patients and 45 healthy control subjects were measured with Proton 1H Magnetic resonance spectroscopy (MRS) and Wisconsin Card Sorting Test (WCST).Results Alcoholics had lower NAA/Cr ratios in prefrontal grey matter(GM) (1.59± 0.13) and white matter(WM) (1.58±0.12) regions and performed poorly on executive function tests compared to controls (P＜0.001).NAA/Cr in left prefrontal regions positively correlated with certain parameters of EF testing (number of correct responses 30.37± 3.73,perseverative errors 11.49± 3.39,random errors 6.18± 2.64,categories completed 2.08± 1.59)in alcoholic group (P＜0.01).NAA/Cr in prefrontal WM regions correlated with certain parameters of EF testing in alcoholic group (number of correct responses r=0.379,categories completed r=0.433,P＜ 0.05).Conclusion Long-term,chronic alcoholism will damage neuronal viability and cognitive functions,which suggests that NAA concentrations can reflect the extent of damage of cognitive functions with decreased levels reflecting neuronal loss.

BACKGROUND: This study was undertaken to investigate the expression of hypoxia-inducible factor-1α (HIF-1α) in rat cerebral cortex and the effects of β-sodium aescinate (SA) administration after return of spontaneous circulation (ROSC).METHODS: Sixty rats were divided into three groups: SA group, injected intraperitoneally with SA instantly after ROSC; control group, injected intraperitoneally with normal saline; and sham-operated group, without cardiac arrest or SA. The cardiac arrest model was established using asphyxiation and intravenous potassium chloride. Blood was sampled 1, 6, 12, and 24 hours after ROSC. Protein and mRNA levels of HIF-1α, VEGF and EPO were detected in the cerebral cortex by immunohistochemistry and real-time RT-PCR; serum levels of NSE and S100β were determined by enzyme-linked immunosorbent assays.RESULTS: Serum S100β and NSE were signifi cantly increased in the control group versus the sham-operated group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were signifi cantly increased in the control rats (P<0.05). Serum NSE and S100β were significantly decreased in the SA group versus the control group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were signifi cantly increased in the SA group (P<0.05).CONCLUSIONS: The expression of HIF-1α is increased in rat cerebral cortex after ROSC, and SA up-regulates the expression of HIF-1α. The up-regulation of HIF-1α improves the resistance of the cortex to ischemia and hypoxia and contributes to neuroprotection, possibly because of up-regulation of EPO and VEGF expression.