Aim To study the effects of extract of astragalus on hippocampal delayed neuronal death of totalcerebral ischemia and 7 days reperfusion in rats.Methods Global ischemia was made by four-vessel occlusion. Electron microscope was used to observe the ultramicrostructure of dorsal hippocampal neurons.Light microscope was used to survey the structure of hippocampal neurons and to count the number of normal neurons in CA1 sector. Glial fibrillary acidic protein(GFAP) was detected by immune histochemistry.Results Compared with ischemia and reperfusion group(I/R),EA improved the ultrastructure of hippocampal neurons, suppressed the decrease of normal neurons in CA1 and degraded the expression of GFAP .The number of normal neurons in I/R group was 38?11.5,and in EA(20,40 mg?kg -1) groups,63?12.8(P

Objective:To investigate the role of alloreactive T cell in clonal deletion and regulatory T cells ( Treg) in transplant tolerance.Methods:F1 mice were bred by crossing female BALB/c mice and male C57BL/6 mice.Within 24 h,newborn C57BL/6 mice were inoculated with F1 spleen cells via the orbital branch of the anterior facial vein.Six weeks later,the mice were subjected to F1 skin grafting to evaluate their tolerance.Proliferation,flow cytometry and adoptive transfer assay were used to analyze clonal deletion of alloreactive T cells and the expression of CD4+Foxp3+T cells in neonatal treated mice.Results: Newborn C57BL/6 mice injected with F1 splenic cells could induce transplantation tolerance,the level of tolerance was associated with the dose of splenic cells.3×107 splenic cells from F1 mice could induce long-term skin graft acceptance in C57BL/6 mice ,1×107splenic cells significantly prolonged the survival of F1 skin grafts,but the grafts completely rejected within 50 days.The mixed lymphocyte reaction ( MLR) experiment in vivo showed that alloreactive T cell in long-term tolerant mice was deleted completely,but a certain amount of reactive T cells existed in the low-dose group mice.Flow cytometry ( FCM) analysis showed that the expression of CD4+Foxp3+T cell in the high-dose group and low-dose group mice had no obvious difference compared with the naive mice.When alloreactive T-cells were injected into tolerant mice,the skin graft rejection was observed,and Treg cells upregulated in graft-rejected mice.Conclusion:The degree of transplantation tolerance depended on the clonal deletion of alloreactive T cells,instead of on the expression of CD4+Foxp3+Treg cells.CD4+Foxp3+regulatory T cells upregulated in graft rejected mice,which may be served as a negative feedback mechanism to control the intensity of rejection.

Objective To evaluate the outcome of patients with low ejection fraction undergoing coronary artery bypass grafting.Methods One hundred and twenty-eight consecutive patients with left ventricular ejection fraction (LVEF) ≤35％,who underwent Off-pump caronary bypass surgery or Cardiopulmonary coronary artery bypass between December 2000 and Novomber 2010 were studied.The outcome of early complication,mortality,LVEF were analyzed.Results LVEF and LVEDD were significantly increased in early postoperation (P ＜ 0.05 ).Use of Intra-aotric balloon counterpulsation(IABP) can decrease early mortality,and postopertive respiratory tract infections,renal insufficiency were found to be the main complications.Conclusions Preoperative low ejection fraction has no relationship with postoperative early mortality.using medicine to adjust heart function,strcity control blood pressure,blood glucose,heart rate preoperation,positive use of IABP postoperativon are key point to decrease early mortality.

Objective To explore the significance and value of the anti-nucleosome antibodies(AnuA)in the diagnosis of system-ic lupus erythematosus(SLE).Methods The serum AnuA was detected in 177 patients with SLE,138 patients with other rheumat-ic diseases and 56 healthy controls by Western blot.The clinical manifestations,autoantibodies and other test results were recorded in the SLE patients.The AnuA and other autoantibodies were analyzed.Results The positive rate of AnuA in the SLE group was significantly higher than that in the disease control group,AnuA was negative in the healthy control group;the sensitivity of AnuA in the SLE group was 48.6% and the specificity was 95.3%;the sensitivity of AnuA was significantly higher than that of the anti-ds-DNA antibodies and anti-Sm antibodies,the difference had statistical significance (P <0.05).The specificity of AnuA was higher than that of ANA and histone (P <0.05 ).The sensitivity of joint detection of AnuA,anti-ds-DNA and anti-Sm antibodies was 89.8%,which was significantly higher than that of a single index detection.The positive rate of AnuA in the active period of SLE was significantly higher than that of the non-active period,moreover higher than that of the ds-DNA antibodies (P <0.05).Conclu-sion AnuA might participate in the pathogenesis of SLE.The joint detection of autoantibodies including AnuA,etc.has importance significance in the diagnosis,condition judgment and curative efficacy evaluation of SLE.

Aim To study the mechanisms of protective effects of extract of astragalus against focal cerebral ischemia/reperfusion injury in rats. Methods Focal cerebral ischemia was induced by intraluminal thread occlusion of middle cerebral artery. Immunohistochemistry was used to determine expression of TNF-?,IL-1? was measured by radioimmunity, and the apoptosis was observed by TUNEL. Results EA(20、40、80 mg?kg -1,ig)could decrease the expression of TNF-? and the level of IL-1? and reduce cell apoptosis. Conclusion EA has inhibitory action on the increase in the expression of TNF-?,the level of IL-1? and the apoptosis of neurons induced by focal cerebral ischemia/reperfusion.

Telomerase, as a highly specific ribonucleoprotein, is composed by the RNA template and protein subunits. It can delay or prevent the process of disc degeneration by maintaining telomere length homeostasis as well as affecting the p53-p21-pRb pathway, p16Ink41-pRb pathway and Wnt/β-catenin signal pathway. Telomerase can regulate the senescence and apoptosis of intervertebral disc cell, expected to prevention and repair reconstruction of the structure by telomerase gene therapy of intervertebral disc degeneration.

OBJECTIVETo investigate the changes in the levels of monocarboxylate transporter-2 in spinal cord horn in a rat model of chronic inflammatory pain.

METHODSMale SD rats weighting 180 - 220 g were randomly divided into two groups(n = 48): normal saline group (NS group), complete Freund's adjuvant group (CFA group). Rats were given injections of CFA 100 µl in left hind paw in group CFA, and an equal volume of saline was given injection in group NS. Mechanical withdraw threshold(MWT) and thermal withdraw latency(TWL) were measured at before injection(T0 and 3 h, 1 d, 3 d, 7 d, 14 d, and 21 d after injection(T1-7). Four rats were chosen from each group at T0-7 and sacrificed, and L4-5 segments of the spinal cord horn were removed for measurement of the expression of monocarboxylate transporter-2 by Western blot analysis.

RESULTSIn CFA group, mechanical hyperalgesia and allodynia appeared on the 3 h after CFA injection, then until the day 14. The expression of monocarboxylate transporter-2 in the spinal dorsal horn of rats in CFA group was significantly higher than that in normal control group at T1-6(P <0.05). The protein level of monocarboxylate transporter-2 was apparently correlated with MWT and TWL(P <0.01 and P <0.05) in CFA group.

CONCLUSIONThe level of monocarboxylate transporter-2 in spinal dorsal horn is significantly increased in a rat model of chronic inflammatory pain and the change may involve in the formation and maintenance of central sensitization in spinal cord of chronic inflammatory uain.

Animals ; Disease Models, Animal ; Freund's Adjuvant ; Hyperalgesia ; chemically induced ; Inflammation ; chemically induced ; metabolism ; Male ; Monocarboxylic Acid Transporters ; metabolism ; Pain ; chemically induced ; metabolism ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; metabolism ; physiopathology

AIMTo investigate the bio-affinities of ligustilide and butylidenephthalide to rat aortic smooth muscle cells and the inhibitory effects of them on bFGF-stimulated proliferation of rat vascular smooth muscle cell (VSMC).

METHODSVSMCs were cultured from rat aorta pectoralis and identified by an immunohistochemical method. The bio-affinities between solute (ligustilide or butylidenephthalide) and cell membrane were measured by rat aortic cell membrane chromatography (CMC). The inhibitory effects of ligustilide and butylidenephthalide on bFGF-stimulated VSMC proliferation were evaluated by MIT colorimetric method.

RESULTSBoth ligustilide and butylidenephthalide had selective affinities to rat aortic smooth muscle cell as the same as verapamil, one of the calcium ion antagonists. They could potently inhibit the bFGF-stimulated VSMC proliferation at the concentrations of 5.5 and 11.1 micromol x L(-1), separately (P < 0.05), but had no effects on the normal VSMC growth.

CONCLUSIONBoth ligustilide and butylidenephthalide can inhibit the abnormal proliferation of VSMC induced by bFGF.

4-Butyrolactone ; analogs & derivatives ; isolation & purification ; pharmacology ; Animals ; Aorta, Thoracic ; cytology ; Cell Proliferation ; drug effects ; Cells, Cultured ; Female ; Fibroblast Growth Factor 2 ; antagonists & inhibitors ; Ligusticum ; chemistry ; Male ; Muscle, Smooth, Vascular ; cytology ; drug effects ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Phthalic Anhydrides ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley

AIMTo study the protective effects of EA against cer ebral ischemia-reperfusion injury. METHODSAcute cerebral ischemia w as produced by the occlusion of bilateral common carotid arteries of mice .The s urvival time in 12 h of the mice was observed, and the mortalities in 2 h, 6 h, 12 h were recorded. Pulsinelli four-vessel occlusion method was used to make ce rebral ischemia-reperfusion model of rats. The EEG and the reappearing time of righting reflex were recorded and the activity of GSH-Px,LDH,NOS in the brain w as tested. Researching the iNOS expression in hippocampiwith immunocytochemistry method and measure the mean optical density. RESULTSEA can decrease the mortalities and prolong the survival t ime in 12 h of the mice. EA can promote the recovery of the EEG and the RR after cerebral ischemia-reperfusion operation in rats and enhance the activities of the GSH-Px LDH, reduce the activity of the NOS. EA also inhibits the expression of iNOS and reduce it's value of mean optical density in hippocampi of the rat s. CONCLUSIONEA has protective effects against cerebral ischemai-r eperfusion injury.

AIM Protective effects of extract of astragalus on injuries of global cerebral ischemia/reperfusion in rats and anoxia in mice. METHODS Acute anoxia in mice were produced by hypoxia under normal pressure and decapitation. In these two models the survival time and persistent time of gasping were observed. The global ischemia and reperfusion in rats was made by four-vessel occlusion (4-VO). After 20 min ischemia and 24 h reperfusion, the brain index and water content in brain was detected. MDA content and SOD activity of brain homogenate were tested. Endothelin concentration was determined both in plasma and hippocampus. The pathological changes of cortex tissue were observed by light microscope. RESULTS EA(50,100 mg?kg -1) significantly prolonged the survival time and persistent time of gasping in mice subjected to acute anoxia. EA(20,40,80 mg?kg -1) markedly reduced brain edema induced by global ischemia and reperfusion. EA(40,80 mg?kg -1) decreased MDA content and increased SOD activity in brain homogenate, and also inhibited ET concentration both in plasma and hippocampus. The pathological changes of cortex tissue were less serious in rats treated with EA. CONCLUSION EA has protective effects on cerebral ischemia and anoxia injuries that may relate to anti-oxidation and inhibition of ET production.