Objective To investigate the effects of nitric oxide(NO) and its donor(L-arginine) on focal cerebral ischemic injury in rats. Methods Forty-two healthy male SD rats weighing 250-300g were used. The animals were anesthetized with 20% urethane 1g? kg-1. Common carotid artery (CAA), external carotid artery(ECA) and internal carotid artery were(ICA) exposed through a median incision in the neck. Middle cerebral artery occlusion (MCAO) was produced by insertion of a 40 mm long nylon thread (0.3 mm in diameter) into ICA through ECA. The tip of the nylon thread was made into a ball of 0.5 mm in diameter with heat and the length of insertion was (18.5?0.5)mm on average. The animals were randomly divided into four groups: group 1: sham operation; group 2: ischemia group; group 3: low dose L-arginine(300mg?kg-1 intraperitoneal injection) and group 4: high dose L-arginine(500mg?kg-1 IP). Group 3 and 4 were further divided into 3 subgroups: subgroup A: L-arginine was given 1h after MCAO and the animals were killed 2h after medication (1h + 2h); subgroup B: L-arginine was given 3h after MCAO and the animals were killed 3h after medication(3h + 3h) and subgroup C: L-arginine was given 6h after MCAO and the animals were killed 3h after medication(6h + 3h) . The brain was removed immediately. The volume of cerebral infarct/volume of whole brain was calculated(%) . The NO, MDA content and NOS, SOD activity in the brain tissue of ischemic hemisphere were measured. Results L-arginine significantly decreased cerebral infarct volume and ameliorated focal cerebral ischemia. The effects in high dose group were better than in low dose group. L-arginine significantly increased NO content, decreased MDA content and enhanced the SOD activity in the focal ischemic cerebral tissue. Conclusions It may be concluded that L-arginine has beneficial effect on brain injury in acute ischemic stage and high dose provides better effects.

Objective To evaluate the efficacy of potassium sodium dehydroandroan drographolide succinate (PSDS) combined with routine therapy for rotavirus enteritis in children.MethodsA total of 148 children with rotavirus enteritis were included and divided into an observation group and a control group by random number table method, 74 in each group. The children in the observation group were treated with intravenous PSDS combined with routine therapy, and those in the control group with intravenous ribavirin combined with routine therapy. Serum interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay, and plasma lactate dehydrogenase (LDH), creatine kinase (CK), and creatine kinase-MB (CK-MB) were determined using standard clinical laboratory procedures. The clinical efficacy was evaluated. Results The total efficacy rate in the observation group was significantly higher than that in the control group (91.9%vs. 78.4%;χ2=2.314,P<0.05). After the treatment, the serum levels of IL-6 (18.24 ± 3.62 ng/mlvs. 25.36 ± 5.25 ng/ml; t=2.425,P<0.05) and TNF-α (20.86 ± 4.28 ng/mlvs. 31.22 ± 7.15 ng/ml;t=2.503,P<0.05), and the plasma levels of LDH (104.25 ± 22.06 U/Lvs. 150.26 ± 37.22 U/L;t=2.316,P<0.05), CK (84.25 ± 13.57 U/Lvs. 107.88 ± 16.28 U/L;t=2.327,P<0.05) and CK-MB (22.30 ± 4.24 U/Lvs. 32.26 ± 7.14 U/L;t=2.426,P<0.05) in the observation group was significantly lower than those in the control group. The time to diarrhea resolution (2.42 ± 0.53 dvs.3.56 ± 0.78 d;t=2.316,P<0.05) and the time to fever resolution(2.11 ± 0.32 dvs.2.63 ± 0.43 d;t=2.472,P<0.05) in the observation group were significantly delayed than those in the control group, and the hospital length of stay longer (6.23 ± 1.42 dvs. 4.35 ± 0.96 d;t=2.413,P<0.05).Conclusions PSDS combined with routine therapy may reduce inflammatory response, protect from myocardial injury, and promote recovery in children with RVE.

Aim To investigate the effect and the possible mechanism of aminoguanidine(AG)on the lipopolysaccharide(LPS)-induced acute lung injury in rats.Methods Male SD rats were randomly divided into control group,LPS group and AG group.AG was administered in AG group,saline was administered in control group and LPS group.All the groups were further divided into 2 subgroups according to the duration of ALI:3 h+3 h group and 6 h+3 h group.In AG group and LPS group,LPS was administered.Saline was administered in control group.The translocation of NF-?B and the expression of intercellular adhesion molecule-1(ICAM-1)were respectively detected with immunohistochemisty(IHC);the concentrations of TNF-? and IL-6 in lung tissue were evaluated by radioimmunoassay;the pathological changes of lung tissue were observed by light and electron microscope.Results Compared with those of the control group,NF-?B was significantly translocated from the cytoplasm into the nucleus,the expression of NF-?B and ICAM-1 protein were significantly increased.The concentrations of TNF-? and IL-6 in lung tissue were significantly increased in LPS group.Degree of ALI was gradually worsened after administration of LPS.In AG(3 h+3 h)group,the expression of NF-?B and ICAM-1 protein were significantly decreased,the concentrations of TNF-? and IL-6 in lung tissue were significantly decreased and the lung damage was improved compared with those of the LPS(3 h+3 h)group.Conclusions Administration of AG could ameliorate LPS-induced acute lung injury in rats.The possible mechanism was that AG could reduce the expression of iNOS mRNA,inhibited NF-?B activation and subsequently led to the down-regulation of NF-?B-dependent inflammatory gene expression and thus reduced the inflammatory response in lung injury.

Aim To investigate the effect of aminoguanidine (AG) on the lipopolysaccharide (LPS)-induced chronological changes of pulmonary surfactant (PS) and alveolar macrophage (AM) of rats.Methods Acute lung injury was induced by injection(iv) of lipopolysaccharide (LPS 5 mg?kg-1). AG(AG group) or saline(control and LPS group) was administrated respectively at 3 h or 6 h after LPS injection for 3 h.The expressions of SP-A mRNA and SP-A protein in the lung tissue were measured by ISH methods and Western blot;the total protein(TP),total phospholipid(TPL) in the bronchoalveolar lavage fluid (BALF) were detected.Rat AM was isolated from the BALF of adult SD rats and harvested by selective plating technique.The concentrations of Tumor necrosis factor-? (TNF-?),Interleukin-6(IL-6),Nitric oxide (NO) and the activity of lactate dehydrogenase (LDH) in the culture supernatants were detected.Results Compared with the controls,SP-A mRNA and SP-A protein in the LPS groups were significantly and progressively decreased. TPL of LPS group in the BALF was significantly decreased whereas TP concentration was significantly increased.Compared with LPS group at the same time points,treatment with AG at 3 h after LPS the expressions of SP-A mRNA and SP-A protein in lung tissue and TPL in BALF were increased markedly,whereas TP was significantly decreased.LPS treated group,LDH activity,the contents of NO,TNF-? and IL-6 in culture medium were significantly increased compared with that of normal group.The LDH activity,NO contents,TNF-? and IL-6 were decreased in AG group compared with that of LPS group.Conclusion Relatively early administration AG(selective inhibitor of iNOS),can protect lung from LPS-induced injury through increasing the expression of SP-A mRNA,SP-A protein and TPL,and inhibiting over-release of a series of cytokines and inflammatory transmitters from AM.

The respective sense and antisense oligodeoxynucleotides and their phosphorothiods, targeting at the bcr/abl, were the hallmark gene of Chronic Myelogenous Leukemia( CML) and c-myb correlates with CML. K562 cells, derived initially from a patient of CML blast crisis, were incubated with bcr/abl antisense oligodeoxynucleotides asODN or c-myb asODN or with both asODN in combinalion. All kinds of asODN could not only significantly inhibit K562 cells survival with the highest inhibitory rate of 64.7%?3.2%, but also dramatically inhibit DNA synthesis and the highest inhibitory rate was 85. 8 %?4.1%, decrease bcr/abl mRNA level almost completely and induce apoptosis significantly. The inhibition effect of antisense oligodeoxynucleotides phosphorothiodes s-asODN was stronger than that of unmodified asODN. The inhibition of the combination of bcr/abl and c-myb asODN was stronger than that of anyone alnoe. All the inhibitions exhibited in sequence-and time-dependent manner. We concluded that bcr/abl in pathogenesis of CML not only increased CML cells proliferation rate, but also decreased CML cells apoptosis rate. c-myb may participate in CML mainly by regulating bcr/abl. Trie results indicated that the modified asODN and multiple asODN targeting several oncogenes may advance to antisense gene therapy.

AIM: The quality standard for Compound Xiaojingtong Capsule(Radix Astragali, Radix Ginseng, Radix Angelicae Sinensis, Rhizoma Chuanxiong, etc.) were studied. METHODS: The TLC method for identification of Radix Ginseng, Radix Angelicae Sinensis, Rhizoma Chuanxiong in these capsules were established. Astragaloside Ⅳ was determined by single wavelength TLC-scanning(? s=530nm). RESULTS: Radix Angelicae Sinensis, Rhizoma Chuanxiong and Radix Ginseng could be detected. Astragaloside Ⅳ showed a linear relationship at the concentration range of 1.1～5.5?g (r=0.9983). The average recovery was 100.1% and RSD was 1.59% (n=6). CONCLUSION: This method is suitable for the quality control of Compound Xiaojingtong Capsule.

Aim To investigate the protective effect of propofol on ischemia-reperfusion(I/R)injury in isolated rat hearts and clarify the possible molecular mechanism from oxidative stress and the apoptosis initiated by mitochondria pathway. Methods The langendorff model of ischemia-reperfusion was used.Forty isolated perfused rat hearts were divided into control,I/R, propofol 15,30,60 ?mol?L-1 groups. Hearts were suffered globally ischemic for 25 min and 30 min with reperfusion. The cardiac function indexs such as the left ventricular developed pressure(LVDP), the left ventricular end diastolic pressure(LVDEP), heart rate (HR), coronary arterial flow (CF) were recorded at the time of equilibrate, before ischemia, the end of reperfusion respectively. The lactate dehydrogenase (LDH), creatine kinase (CK) activities in the flow were measured. The swelling and activity of mitochondria, the activity of Manganese Superoxide Dismutase (Mn-SOD) and content of malondialdehyde (MDA) in myocardium mitochondria were also determined. The incidence of cardiomyocyte apoptosis was evaluated by the TdT-mediated dUTP nick end labeling (TUNEL) staining and the expression of Bcl-2 and Bax were evaluated by Flow Cytometry(FCM). The expression of Caspase-3,8,9 was detected by immunohistochemistry.Results Compared with I/R group, administration of propofol at the concentration of 30 and 60 ?mol?L-1 markedly ameliorated the cardiac function in CF,LVDP and LVDEP(P

AIM To investigate the effect and mechanism of L-arginine(L-Arg) on lipopolysaccharides(LPS)-induced acute lung injury (ALI). METHODS Models of ALI were established by injection (iv) with LPS 5 mg·kg~(-1) in male SD rats. The rats were randomly divided into 3 groups: ① saline group; ② LPS group; ③ L-Arg group. The rats in each group were further divided into 2 subgroups according to L-Arg- supplemented time: 1 h+3 h group and 6 h+3 h group. L-Arg 500 mg·kg~(-1) or saline (saline and LPS groups) was administrated at 1 or 6 h after LPS injection, respectively. The treatment lasted for 3 h, and the rats were sacrificed at 4 or 9 h after LPS injection. Apoptotic rate, caspase 3, and Bcl-2 and Bax were evaluated by flow cytometry, Western blot analysis and immunohistochemistry, respectively; meanwhile, the pathological changes of lung tissue were observed by electron microscope. RESULTS Compared with saline group, apoptosis of pulmonary cells and caspase 3 expression were significantly increased, Bcl-2 was decreased, while Bax was elevated in alveolar and airway epithelial cells in LPS group. Compared with LPS 1 h+3 h group, L-Arg 1 h+3 h decreased apoptotic pulmonary cells〔(23.8±2.8)% vs (15.4±2.3)%〕; moreover, expressions of caspase 3 (0.80±0.06 vs 0.67±0.10) and Bax (0.115±0.012 vs 0.091±0.014) were significantly decreased, while expression of Bcl-2 (0.067±0.011 vs 0.075±0.009) and Bcl-2/Bax ratio (0.586±0.114 vs 0.833±0.142) in alveolar and airway epithelial cells were markedly increased, and lung damage was alleviated. L-Arg 6 h+3 h also reduced apoptotic pulmonary cells and caspase 3 expression compared with LPS group, but the lung injury relieved slightly. CONCLUSION Relatively early administration of L-Arg can protect lungs from LPS-induced injury through inhibiting cell apoptosis, as well as increasing the expression of anti-apoptotic protein Bcl-2 and decreasing the expression of proapoptotic protein Bax and caspase 3.

Objective To evaluate the effects of L-aronine(L-Arg) on LPS-induced lung mitochondrial injury in rats.Methods Twenty.four male SD rats weighing 230-270 g were randomly divided into 3 groups(n=8 each):groupⅠsham operation(S);group ⅡLPS and group Ⅲ LPS+L-Arg.LPS 5 mg/kg in normal saline(NS)1 ml/kg waft given iv in group Ⅱ and Ⅲ while in group Ⅰ NS 1 ml/kg was given iv instead of LPS. L-Arg 500 ms/kg in NS 1 ml/kg was given intrapefitoneally(IP)at 3 h after LPS administration in group Ⅲ,while in group Ⅰ I and Ⅱ NS1 ml/kg was injected IP instead of L-Arg.The animals were sacrificed at 3 h after L-Arg injection by exsanguination and the lungs were immediately removed.The mitochondrias of the lungs were isolated by differentia centrifugation.The activities of SOD,GSH-Px,ATPase,inducible,constitutive and total nitric oxide synthase(iNOS,cNOS,NOS)and MDA and NO contents,the degree of mitochondrial swelling,mitocho-ndrial activity and membrBne fluidity of mitochondria wefe measured.Ultrastructure of cells in lung was examined wlth eleciron microscope.Results The SOD,GSH-Px.ATPase and mitochondriai activities and the membrane fluidity of mitochondria were significantly decreased,while the MDA and NO contents and iNOS,NOS activities and the degree of mitochondriM swelling in the lung were significantly increased in group LPS as compared with group S.The lung cytoplasm and mitoehondria swelled,the cfistae were disrupted,dissolved or disappeared in LPS group(Ⅱ).The LPS-induced changes were ameliorated by L-Arg in group Ⅲ as compared with group Ⅱ.Conclusion L-Arg can attenuate lung mitochondrinl injury induced by LPS by enhancing antioxidative effects.

Objective: To investigate the beneficial effect of NG-nitro-L-arginine(L-NA) on cerebral ischemic injury and the possible mechanism by evaluating the effect of nitric oxide synthase(NOS) inhibitor,L-NA,on the contents of aspartate,glutamate,glycine and?-aminobutyric acid(GABA),respectively,in striatum,hippocampus and cortex of rat brain following cerebral ischemia. Methods:The model of focal cerebral ischemia in rat was prepared.Rats were divided into sham-operated group,ischemic group and L-NA group.Each group was further divided into 3 subgroup(n=6 for each): the middle cerebral artery occlusion(MCAO) was maintained for 2,6 and 12h,respectively.L-NA(20 mg/kg,ip) was administrated after MCAO,two times a day,for 3 consecutive days.The changes of infarcted volume and the contents of amino acids were assayed. Results:The infarcted volume(IV%) was not significantly different among the ischemic groups with or without L-NA administrated 2 or 6 h after MCAO;and was markedly decreased in the ischemic group with L-NA administrated 12 h after MCAO(P