Objective To investigate the possible role of p38 mitogen-activated protein kinase (MAPK) in lung injury following intestinal ischemia reperfusion (II/R) in mice. Methods Intestinal ischemia/reperfusion was induced by occluding the superior mesenteric artery for 45 min followed by 6 h reperfusion. C57BL/6 mice were randomly divided into sham-operated group (sham group), II/R group and II/R plus SB239063 treatment (SB239063 group), n = 6/group. SB239063 (3 mg/kg), a novel second-generation p38 MAPK inhibitor, was administered intraperitoneally one hour before clamping. Pulmonary p38 MAPK and phospho-p38 MAPK protein were measured by Western blotting analysis. Gene expression of TNF-α and IL-1β in the lung was analyzed by RT-PCR. The lung pathology was observed by optical microscope. Results Compared with the sham- operated group, pulmonary p38 MAPK activation was significantly increased 6 h after II/R (P<0. 01), whereas SB239063 could markedly attenuate p38 MAPK activation in lung tissue (P<0. 05). In addition, the increased TNF-α and IL-1β mRNA levels induced by II/R in lungs were significantly blocked by inhibiting p38 MAPK activation (P<0. 05). SB239063 treatment ameliorated the pathologic lung injury induced by II/R. Conclusion p38 MAPK plays an important role in lung injury induced by intestinal ischemia reperfusion (II/R) in mice, and inhibition of p38 MAPK activation prevents lung injury following II/R in mice.

Objective: To explore the role of c-Jun NH2 terminal kinase (JNK) activation and JNK-mediated apoptotic signal pathway in intestinal ischemia/reperfusion (II/R) in mice. Methods: C57BL/6 mice were randomly divided into sham-operated group (n = 6) and II/R groups (n = 36); the latter was further divided according to time after perfusion (0,0. 5,1,4,6 and 12 h). Animal II/R model was established by clamping the superior mesenteric artery (SMA) for 40 min followed by reperfusion. Animals in the sham-operated group received no clamping. Animals in the two groups were sacrificed at defined time points, and the expression of JNK, phosphorylation (phospho-) JNK, cleaved caspase-3,Bcl-2 and Bax protein in the intestinal tissue was examined by Western blotting analysis, and the pathological changes of ileum tissue were observed under optical microscope. Results: Most severe intestinal injury was found at the early stage of reperfusion, and the intestinal tissues almost recovered 12 h later. The phospho-JNK in the intestine was significantly elevated within 1 h after II/R compared with sham group (P<0. 01). Cleaved caspase-3 was significantly increased in II/R group at 0. 5 h, 1 h after reperfusion compared to sham group (P<0. 01); the expression of Bcl-2 protein in II/R group was significantly decreased compared with the sham-operated group (P<0. 01), and there was no significant difference in Bax expression between different groups. Conclusion: JNK phosphorylation plays an essential role in the intestinal damages induced by II/R,possibly through down-regulating Bcl-2 protein expression and caspase-3 dependent apoptosis pathway.

Humans ; Lymphoma, Large B-Cell, Diffuse ; Societies, Medical ; United States

Objective To observe the preventive effect of mannatide on infection and relapse of idiopathic thrombocytopenic purura(ITP).Methods One hundred and twenty children with ITP were randomly divided into mannatide treatment group and prednisone control group.Control group venous dexamethasone of 3 d;then treated by prednisone.Treatment group added mannatide tablets for 1 month.The rates of remission clinical blood,platelet,control time,complicated infection and relapse rates were observed.The levels of plasma immunoglobulin(Ig)G,IgA,IgM were determined before and after mannatide treatment.Results The rate of clinical blood,platelet,control time,infection time was not different in 2 groups.The rates of infection complicated and relapse were all significant lower than that in control group.The plasma IgG,IgA significantly increased than that in control group.The plasma IgM had no significant difference.Conclusion Vaccine therapy can be helpful in protecting and decreasing infection,diminishing relapse of children with ITP,and improve the level of IgG,IgA,and thus improve their immune function.

Objective To review the research advances in molecular biology of vascular restenosis.Methods The literatures about molecular biology of vascular restenosis were reviewed.Results Current transgenic ways had some advantages and disadvantages. Gene therapy with HSV tk, Rb,p21,p27,p53,c myc, c myb, vascular endothelial growth factor,bFGF,platelet derived growth facfor,nuclear factor ?B and so on inhibited vascular restenosis.Conclusion A better transgenic system and gene combination therapy will be effective to treat vascular restenosis.

In this paper, the theoretical and experimental researches concerning the prevention and treatment of myocardial ischemia/reperfusion (I/R) injury by Chinese medicine (CM) therapy of activating blood circulation and removing stasis in recent five years were reviewed, and the mechanisms were summarized. Thereby, based upon the current development of molecular biology and application of new technology, the authors offered their suggestions on the emphasized points and methods of present CM study in this scope.
Drugs, Chinese Herbal ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; methods ; Myocardial Ischemia ; drug therapy ; Myocardial Reperfusion Injury ; drug therapy ; prevention & control ; Phytotherapy

Aclarubicin ; Adolescent ; Adult ; Antineoplastic Combined Chemotherapy Protocols ; Child ; Cytarabine ; Female ; Granulocyte Colony-Stimulating Factor ; Humans ; Male ; Middle Aged ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; therapy ; Young Adult

Choristoma ; Humans ; Male ; Middle Aged ; Thyroid Gland ; pathology ; Tracheal Diseases

Animals ; Drugs, Chinese Herbal ; therapeutic use ; Hepatitis B, Chronic ; complications ; Humans ; Liver Cirrhosis ; drug therapy ; etiology ; prevention & control ; Phytotherapy