AlM: To observe the influence ofphacoemulsification on corneal endothelial cell in patients with the different level of HbA1c.METHODS:With case-control study, 164 eyes from 115 cataract patients were divided into four groups according to the preoperative HbA1c level. Control group A: 43 eyes from 30 cases without diabetes ( HbA1c≤6. 5%). Diabetes groups:group B was consisted of 38 eyes from 26 cases(HbA1c≤6. 5%), 40 eyes of 28 case was in group C (6. 5% 8. 0%). Corneal endothelial microscopy was used to detect the parameters like endothelial cell density ( CD ) , coefficient of variation ( CV ) , percentage of regular hexagonal cells (6A) between pre-operation and post-operation at 1d, 1, 2wk, 1mo. The results were analyzed.RESULTS: The endothelial cell density, CV and 6A cell had no significant difference in four groups before treatment (P>0. 05). The CD and 6A were decreased and CV was increased in all groups after operation of 1d, 1, 2wk and 1mo. The difference was statistically significant (P< 0. 05). There were statistical differences of 6A and CV in diabetes groups compared with control group ( P<0. 05). The decreasing of CD between group A and group B had no difference (P>0. 05). There were statistical differences of CD in group C and group D compared with group A (P<0. 05). There were statistical differences of CD, 6A and CV within diabetes groups (P<0. 05). CONCLUSlON: Cataract phacoemulsification had certain degree damage on corneal endothelial cell. Corneal endothelial appeared the minimal injury when the postoperative HbA1c≤6. 5%. For diabetic cataract patients, the higher HbA1c before, the heavier damaged after the surgery.

Diagnosis, Differential ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Dyspepsia ; diagnosis ; drug therapy ; Humans ; Medicine, Chinese Traditional ; Phytotherapy

Diagnosis, Differential ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Irritable Bowel Syndrome ; diagnosis ; drug therapy ; Medicine, Chinese Traditional ; Phytotherapy ; Reference Standards

Chronic Disease ; Diagnosis, Differential ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Gastritis ; diagnosis ; drug therapy ; Humans ; Medicine, Chinese Traditional ; Phytotherapy ; Reference Standards

AIM: This study aimed at investigating the effects and mechanism of total alkaloids from Rhizoma Coptidis (TA) on ethanol-induced gastric mucosal injury in rats. METHODS: The experimental gastric damages were established by intragastric ethanol, and the protective effects of TA were evaluated by calculating lesion indices contents and superoxide dismutase (SOD) activity from rat gastric mucosa were measured to explore the interrelation between therapeutic effects of TA and these factors. The expressions of neuronal nitrogen monoxide synthase (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS)from ethanol-damaged gastric mucosa in rats were analysised using immunohistochemical method. RESULTS: TA significantly inhibited the gastric injury induced by ethanol ,in dose-dependent manner,and the effect of TA was superior to that of Berberine (Ber). TA obviously antric mucosa. TA significantly suppressed ethanol-induced decreasing nNOS and eNOS expression and elevation of iNOS expression in rat gastric mucosa. CONCLUSION: Rhizoma Coptidis is a potent candidate in therapeutic drugs of human alcohol-induced gastric injury. Its anti-injury effects involve in Ber and other ingredients of TA. The protective mechanisms of TA involve in inhibiting generation of oxygen-derived free radical, accelerating scavenging of free radicals, relieving lipid peroxidation, and maintaining NO content in normal level by inhibiting decreasing of nNOS and eNOS expression and elevation of iNOS expression.

As a functionally and phenotypically distinctive T cell subpopulation, CD4+CD25+ regulatory T cells are anergic and retain their ability to suppress antigen-driven response of CD4+CD25- cells in a contact-dependent manner or through a way of secreting immunosuppressive cytokines such as IL-10 and TGF-beta. Graft-versus-host disease (GVHD) is one of the major complications following allogeneic hematopoietic stem cell transplantation (HSCT). Recently, some researches on the relationship between donor CD4+CD25+ regulatory T cells and GVHD severity produced two contradictory conclusions: one is CD4+CD25+ regulatory T cells that can prevent GVHD efficiently; the other is that GVHD is associated with the increased numbers of peripheral blood CD4+CD25+ regulatory T cells. The answer to this question will provide a new idea for clinic therapy of GVHD. In this review some new research progresses in the related area, such as the CD4+CD25+ regulatory T cells, the phenotype, characteristics, immunoregulatory mechanisms of CD4+CD25+ regulatory T cells, as well as the relation of CD4+CD25+ with GVHD were presented.
CD4 Antigens ; analysis ; Graft vs Host Disease ; etiology ; immunology ; Humans ; Interleukin-2 Receptor alpha Subunit ; analysis ; T-Lymphocytes, Regulatory ; cytology ; immunology ; metabolism

Objective To investigate the role of c-Jun N-terminal kinase (JNK) signal transduction pathway on the up-regulation of the expression of acyl-coenzyme A: cholesterol acyltransferasel (ACAT1) induced by Chlamydia pneumoniae (C. pn), and to discuss the mechanism of macrophages-derived foam cell formation induced by C. pn. Methods C. pn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA) for 48 h, and were randomly allocated into four groups to be incubated continually: control group, C. pn infection group, C. pn and SP600125 (a special JNK inhibitor)group and SP600125 group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellular cholesterol ester were detected by enzyme fluorescence analysis. The expressions of ACAT1 mRNA and protein were determined by reverse transcriptase polymerase chain reaction(RT-PCR) and Western blot, respectively. Results Compared with the control group, the expressions of ACAT1 mRNA and protein were up-regulated in C. pn infection group [(4.16±0.26) vs. (2.17±0.18), (1.20±0.10)vs. (0.61±0.03), both P<0.05], and C. pn-induced foam cell formation was observed. The expressions of ACAT1 mRNA and protein and the foam cell formation were inhibited by SP600125 in a concentration-dependent manner (r = - 0.92, P<0.05; r= - 0. 96, P<0.05, respectively). Conclusions The up-regulation of ACAT1 expression is induced by C. pn via JNK signal transduction pathway, which is involved in the mechanism of C. pn-induced macrophage-derived foam cell formation.

Objective To investigate the mechanisms of Chlamydia pneumoniae (C. pn)-induced foam cell formation, the expression of ATP binding cassette transporter AI ( ABCA1 ) and perexisome prolif-erator-activated receptor γ (PPARγ) were examined. Methods THP-1 monneytes were induced into mac-rophages after the addition of 160 nmol/L phorbol myristate acetate (PMA) for 72 h. THP-1-dorived macro-phages when co-cuhured 50 mg/L low density lipoprotein (LDL) were designated randomly in four groups: control (uninfected) group, C. pn infection group, rosiglitazone + C. pn infection group and rosiglitazone group. Lipid droplets in cytoplasm were observed by oil red O staining. The contents of intracellnlur choles-terol ester were detected by enzyme-flnoreseence. The expression of ABCA1, PPARγ, mRNA and protein were determined by RT-PCR and Western blot, respectively. Results C. pn down-regulated the expression of ABCA1, PPARγ at mRNA and protein levels in a concentration-dependent manner in THP-1-derived mac-rophages when co-incubated with LDL. Resiglitazone not only concentration-dependently alleviated the down-regulation of ABCA1 expression by C. pn infection (P<0.05), but also markedly suppressed the accumula- tion of lipid droplets and cholesteryl ester by C. pn at higher concentrations ( 10 and 20 μaol/L). Condu-sion C. pn induces foam cell formation by down-regulating the expression of ABCA1 via PPART pathway, which may provide a new evidence for the development and progression of atherosclerosis initiated by C. pn infection.

AIM: To investigate the signal transduction mechanism of Chlamydia pneumoniae (Cpn) in down-regulating the expression of ATP binding cassette A1 (ABCA1) and ATP binding cassette G1 (ABCG1),the key molecules in cholesterol efflux and atherogenesis,from THP-1-derived macrophages. METHODS: Cpn was propagated in Hep-2 cells. THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate (PMA) for 48 h,and were randomly allocated into 4 groups to incubate continually: control group,50 mg/L low density lipoprotein (LDL); Cpn infection group,Cpn (1×10~6 IFU) and 50 mg/L LDL; Cpn and SP600125 (a special JNK inhibiter) group,THP-1 macrophages were previously treated with different concentrations (1-20 μmol/L) of SP600125 for 1 h,and then infected with Cpn (1×10~6 IFU) and 50 mg/L LDL; SP600125 group,SP600125(20 μmol/L)and 50 mg/L LDL. The expressions of ABCA1/ABCG1 and peroxisome proliferator-activated receptor γ (PPARγ) from each group were detected then. The cholesterol efflux was detected by enzyme-fluorescence. The expressions of ABCA1/ABCG1 and PPARγ mRNA and protein were determined by RT-PCR and Western blotting,respectively. RESULTS: Cpn not only down-regulated the ABCA1/ABCG1 expression,but also down-regulated the expression of PPARγ,which regulated the ABCA1/ABCG1 genes transcriptions. However,the mentioned effects of Cpn infection were restrained by the special JNK inhibitor SP600125 in a dose-dependent manner. CONCLUSION: Chlamydia pneumoniae may down-regulate ABCA1/ABCG1 expression from THP-1-derived macrophages via JNK-PPARγ signal transduction pathway.

Objective:To investigate the effects of Chlamydia pneumoniae(Cpn) on SR-A1 and CD36 expression in THP-1-derived macrophages and role of c-Jun NH_2-terminal signal transduction pathway in the process.Methods:Cpn was propagated in Hep-2 cells.THP-1 monocytes were induced into macrophages by 160 nmol/L phorbol myristate acetate(PMA)for 48h,and were randomly allocated into four groups to be incubated continually: control group;Cpn infection group;Cpn and SP600125(a JNK inhibiter)group and SP600125 group.Lipid droplets in cytoplasm were observed by oil red O staining.The contents of intracellular cholesterol ester were detected by enzyme-fluorescence.The expression of SR-A1 and CD36mRNA and protein were determined by RT-PCR and Western blot, respectively. Results:THP-1-derived macrophages infected with Cpn resulted in large accumulation of lipid droplets and foam cell formation when co-cultured with LDL.Meanwhile,the expression of SR-A1 mRNA and protein were up-regulated by Cpn infection (P<0.05).However,the expressions of CD36 mRNA and protein in THP-1-derived macrophages infected with Cpn were unchanged.Moreover,the up-regulation of SR-A1 and foam cell formation induced by Cpn could be restrained by the JNK inhibiter SP600125 in a dose-dependent manner,and SP600125 had little impact on the expression of CD36 in THP-1-derived macrophages infected with Cpn.Conclusion:The up-regulation of SR-A1 but not CD36 expression is involved in mechanisms of Cpn inducing foam cell formation.And Chlamydia pneumoniae up-regulates the expression of SR-A1 via the JNK signal transduction pathway.This may be a novel mechanism for the foam cell formation induced by Cpn.