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Wuhan, China

Xia J.-M.,Huazhong University of Science and Technology | Zhang J.,Xiamen University | Zhou W.-X.,Wuhan First Hospital | Liu X.-C.,Huazhong University of Science and Technology | Han M.,Huazhong University of Science and Technology
Journal of Huazhong University of Science and Technology - Medical Science | Year: 2013

Summary: Curcumin, as a main pharmacological component in the traditional Chinese medicine - turmeric, has shown anti-inflammatory, anti-oxidation, anti-tumor and anti-fibrotic effects. This study aimed to investigate the possible underlying signaling pathway which was involved in the inhibition of LDL-induced proliferation of mesangial cells and matrix by curcumin. Rat mesangial cells in vitro were incubated with low-density lipoprotein (LDL) and different concentrations of curcumin (0, 6.25, 12.5, 25.0 μmol/L) or p38 MAPK inhibitor, SB203580 (10 μmol/L). Under LDL incubation, mesangial cells proliferated, the expression of MMP-2 mRNA and protein was decreased, the expression of COX-2 mRNA and protein was increased, reactive oxygen species (ROS) generation was increased and p38 MAPK was activated significantly (P<0.05). When LDL-induced cells were treated with curcumin in the concentration of 12.5 or 25.0 μmol/L, LDL-induced proliferation of mesangial cells was suppressed, the expression of MMP-2 mRNA and protein increased, the expression of COX-2 mRNA and protein downregulated, the production of ROS inhibited and p38 MAPK inactivated (P<0.05). In conclusion, curcumin can inhibit the LDL-induced proliferation of mesangial cells and up-regulate the expression of MMP-2, which may be related with the inhibitory effect of curcumin on COX-2 expression, ROS production and p38 MAPK. © 2013 Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg. Source


Feng X.M.,Wuhan First Hospital
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban | Year: 2010

To evaluate the effect of combined electroacupuncture (EA) and epidural anesthesia in gynecological operation by bispectral index (BIS). Sixty patients of ASA grade I-II, 20-60 years old, being scheduled to receive gynecological operation with epidural anesthesia were randomly assigned to 3 groups equally. Group A was anesthetized with epidural infusion of midazolam in dosage of 0.04 mg/kg, Group B with continuous EA in 30-100 Hz on Zusanli (ST36) and Sanyinjiao (SP6) acupoints, and Group C with both epidural infusion and EA same as those applied in Groups A and B. BIS, blood pressure (BP), heart rate (HR), and blood oxygen saturation (SPO2) were monitored during peri-operative stage, and the post-operation visual analogue scores (VAS) was measured as well. BIS decreased after operation in all groups (P < 0.05), the highest value was shown in Group B (P < 0.05) and the lowest was seen in group C at time of skin incising; while at time of gauze plugging, it was higher in Group B than in other two groups (P < 0.05). Besides, VAS in Group A at 8 h and 24 h after operation was higher than that in the other two groups respectively (P < 0.05). BIS can be taken as an index for objectively evaluating the effect of combined EA and epidural anesthesia in gynecological operation. EA anesthesia has certain analgesic and sedative effects, could effectively release postoperative pain. Source


Ai X.,Military General Hospital of Beijing PLA | Jia Z.,Military General Hospital of Beijing PLA | Liu S.,Wuhan First Hospital | Wang J.,Military General Hospital of Beijing PLA | Zhang X.,Chinese PLA General Hospital
Oncology Reports | Year: 2014

Inhibition of Notch signaling pathways, consisting of 4 highly conserved receptors (Notch 1-4), induces expression of Krüppel-like transcription factors (KLFs) linked to bladder cancer tumorigenesis and metastasis. Effects of Notch-1 knockdown on cell proliferation, differentiation and KLF4 levels in bladder cancer cell lines were investigated. PsiRNA1-mediated Notch-1 and KLF4 knockdown models and control model without the psiRNA1 vector were constructed using bladder cancer cell lines T24 and BIU87. Cell proliferation, apoptosis and expression of Notch-1 and KLF4 were assessed using 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry assay with Annexin V-FITC/PI staining, and reverse transcriptase polymerase chain reaction (RT-PCR) and western blot analysis, respectively. Proliferation was assessed in Notch-1 and/or KLF4 knockdown. The results showed that Notch-1 mRNA and protein expression levels were significantly lower following psiRNA1 vector transfection in both cell lines (P<0.05). Growth and proliferation of both cell lines were significantly inhibited by Notch-1 knockdown (P<0.05), and more G0/G1 arrest and apoptosis were observed compared to those in the control groups (P<0.05). The effects were time-dependent, peaking between 24-48 h and declining by 72 h. KLF4 expression was significantly higher in the Notch-1 knockdown group than in control cells (P<0.05). Notch-1 knockdown cell proliferation was significantly lower than that of Notch-1 and KLF4 knockdown (P<0.05). In conclusion, Notch-1 may act as an oncogene, regulating the proliferation and differentiation of bladder cancer cells by inhibiting KLF4. Pending further exploration of pathway variations and crosstalk, these pathways may be useful targets for bladder cancer therapy. Source


Zhou Y.,University of Tennessee Health Science Center | Yuan J.,Wuhan First Hospital | Zhou B.,University of Tennessee Health Science Center | Lee A.J.,University of Tennessee Health Science Center | And 2 more authors.
Immunology | Year: 2011

Autoimmune inner ear disease is characterized by progressive, bilateral although asymmetric, sensorineural hearing loss. Patients with autoimmune inner ear disease had higher frequencies of interferon-γ-producing T cells than did control subjects tested. Human adipose-derived mesenchymal stem cells (hASCs) were recently found to suppress effector T cells and inflammatory responses and therefore have beneficial effects in various autoimmune diseases. The aim of this study was to examine the immunosuppressive activity of hASCs on autoreactive T cells from the experimental autoimmune hearing loss (EAHL) murine model. Female BALB/c mice underwent β-tubulin immunization to develop EAHL; mice with EAHL were given hASCs or PBS intraperitoneally once a week for 6 consecutive weeks. Auditory brainstem responses were examined over time. The T helper type 1 (Th1)/Th17-mediated autoreactive responses were examined by determining the proliferative response and cytokine profile of splenocytes stimulated with β-tubulin. The frequency of regulatory T (Treg) cells and their suppressive capacity on autoreactive T cells were also determined. Systemic infusion of hASCs significantly improved hearing function and protected hair cells in established EAHL. The hASCs decreased the proliferation of antigen-specific Th1/Th17 cells and induced the production of anti-inflammatory cytokine interleukin-10 in splenocytes. They also induced the generation of antigen-specific CD4 +CD25 +Foxp3 + Treg cells with the capacity to suppress autoantigen-specific T-cell responses. The experiment demonstrated that hASCs are one of the important regulators of immune tolerance with the capacity to suppress effector T cells and to induce the generation of antigen-specific Treg cells. © 2011 The Authors. Immunology © 2011 Blackwell Publishing Ltd. Source


Zhou B.,University of Tennessee Health Science Center | Yuan J.,Wuhan First Hospital | Zhou Y.,University of Tennessee Health Science Center | Ghawji M.,University of Tennessee Health Science Center | And 6 more authors.
Clinical Immunology | Year: 2011

Rheumatoid arthritis is a chronic autoimmune disease and affecting approximately 1% of the population. Human adipose-derived mesenchymal stem cells (hASCs) were recently found to suppress effector T cell and inflammatory responses and, thus, to have beneficial effects in various autoimmune diseases. In this study, we examined whether hASCs could play a protective and/or therapeutic role in collagen-induced arthritis (CIA). We showed that hASCs both prevented and treated CIA by significantly reducing the incidence and severity of experimental arthritis. We further demonstrated that treatment with hASCs inhibited the production of various inflammatory mediators, decreased antigen-specific Th1/Th17 cell expansion, and induced the production of anti-inflammatory cytokine interleukin-10. Moreover, hASCs could induce the generation of antigen-specific Treg cells with the capacity to suppress collagen-specific T cell responses. © 2011. Source

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