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Wang C.-J.,Tongji University | Wang C.,Tongji University | Han J.,Pudong New Area Zhoupu Hospital | Wang Y.-K.,Tongji University | And 5 more authors.
Molecular Biology Reports | Year: 2013

This study aimed to evaluate the efficacy of combined treatment with recombinant interleukin-2 (rIL-2) and allicin on pancreatic cancer and explore the potential immunological mechanism. A total of 60 C57/BL6 nude mice pancreatic cancer xenograft models were randomized into four groups of 15 mice per group: control group, allicin treatment group, rIL-2 treatment group, combined treatment with allicin and rIL-2 group. Mice in each group were treated with saline, rIL-2, allicin, or combination of rIL-2 and allicin by weekly i.v injection for four weeks. After four weeks of treatment, eyeballs of the mice were extracted and blood was drawn, percentages of CD4+T, CD8+T and NK cell were analyzed by FACS, IFN-γ level was detected by ELISA. One mouse in each group was sacrificed to measure the weight and volume of the tumor and prepared to the paraffin section of tumor tissue. Apoptosis of the tumor cells was analyzed by TUNEL and FACS. Other mice continued to receive treatment, survival period were compared between each group. We observed a significant suppression of xenograft growth and a significant prolonged survival time in the combined treatment with allicin and rIL-2 group (P < 0.05). The most amount of apoptotic cells were observed in the combined therapy group (P < 0.05). The percentages of CD4+T, CD8+T and NK cell and serum IFN-γ level increased significantly in the combined treatment group compared with other groups (P < 0.05). Combined treatment with allicin and rIL-2 resulted in suppression of tumor growth and prolonged survival time possibly through activation of CD4+T, CD8+T and NK cell. © 2013 Springer Science+Business Media Dordrecht. Source

Wang Y.-K.,Tongji University | Han J.,Pudong New Area Zhoupu Hospital | Xiong W.-J.,Tongji University | Yuan Q.-Y.,Tongji University | And 5 more authors.
Molecules | Year: 2012

Oxidative stress is involved in the development and progression of disease. Because sodium aescinate has been reported to have immunity enhancing and antioxidative effects, we investigated its activity by employing a hepatocellular carcinoma (HCC) mouse model. Sixty BALB/c mice were randomly divided into four groups, including a 1.4 mg/kg treated group (n = 15), a 2.8 mg/kg treated group (n = 15), an untreated hepatocellular carcinoma control group (n = 15) and a normal control group (n = 15). After H22 cells were cultured for one week, we collected 2 × 10 6 cells and injected them subcutaneously as 0.2 mL cell suspensions in sterile saline into the right shoulder region of every mouse. The animals were monitored for changes in activity, physical condition and body weight during the experiment. The next day after injection of H22 cells, animals in these test groups received one intraperitoneal injection of drug or physiological saline for 13 days. Results showed that in the sodium aescinate injection liquid (SAIL)-treated HCC mice, serum interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), Gamma- glutamyltransferase (γ-GT), alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) levels were significantly decreased compared with normal control mice. In addition, treatment with sodium aescinate injection liquid significantly decreased blood and liver malondialdehyde (MDA) levels, increased glutathione (GSH) levels, and antioxidant enzyme [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activities in a dose-dependent manner. We conclude that sodium aescinate injection liquid can decrease oxidative injury and enhance immunity functions in HCC mice. © 2012 by the authors. Source

Wang Y.,Tongji University | Xu X.-Y.,Pudong New Area Zhoupu Hospital | Feng C.-H.,Tongji University | Li Y.-L.,Tongji University | And 5 more authors.
Metabolic Brain Disease | Year: 2015

Type 2 diabetes mellitus (T2DM) is associated with cognitive dysfunction. Previous studies have reported the relationship between cerebral metabolite changes and glucose levels. However, the specific aspects of cognition that are affected by metabolic changes in T2DM- related cognitive impairment remain undetermined. In this study, 188 T2DM patients and 266 controls were recruited. Proton magnetic resonance spectra with a single voxel stimulated echo acquisition mode (STEAM) were acquired fromthe left hippocampus and the frontal lobe. Presence of T2DM negatively affected the scores of Mini-Mental State Examination (MMSE), sub-tests (i.e., attention and language) of MMSE, Montreal Cognitive Assessment (MoCA) according to the Beijing version, and sub-tests (i.e., visuospatial/executive reasoning, attention, and language) of MoCA, rather than the Wechsler Memory Scale – Revised in China (WMS-RC), and all memory sub-tests contained with the MMSE and MoCA frameworks. T2DMpositively affected creatine and myoinositol peak areas from the left hippocampus, rather than metabolites in the left frontal lobe. Negative correlations were shown between the left hippocampal myoinositol levels and language scores, and between the left hippocampal creatine levels and visuospatial/executive scores in T2DM. These findings suggest that T2DM may be an independent risk factor for cognitive impairment. Further, the cognitive domains of visuospatial /executive reasoning, attention and language may be predominantly impaired in the early phases of T2DM-related cognitive impairment. In addition, left hippocampal myoinositol and creatine concentrations were associated with cognitive impairment in patients with T2DM. © The Author(s) 2015. Source

Ge X.,Tongji University | Xu X.-Y.,Pudong New Area Zhoupu Hospital | Feng C.-H.,Tongji University | Wang Y.,Tongji University | And 2 more authors.
BMC Neurology | Year: 2013

Background: We examined the clinical value of two serum markers of low-grade inflammation, C-reactive protein (CRP) and receptor of advanced glycation products (RAGE), as prognostic indices for cognitive decline.Methods: Patients with cognitive impairment (n = 377) and controls (n = 66) were examined by blood biochemistry tests, including ELISAs of serum CRP and RAGE, the Mini-mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA), and STEAM 1H-MRS of the left hippocampus and thalamus.Results: Compared to the control group, the cognitive impairment group was older (63.10 ± 9.70 years vs. 55.09 ± 10.77 years, P = 0.000) and had fewer years of formal education (9.01 ± 4.01 vs. 12.94 ± 3.0, P = 0.000). There were no significant differences in the frequencies of type 2 diabetes, hypertension, or hyperlipidemia between groups. Serum CRP and RAGE were higher in the cognitive impairment group (CRP: 2.08 mg/L, range 1.07 - 3.36 mg/L vs. 0.21 mg/L, range 0.18 - 0.42 mg/L; RAGE: 4.01, range 2.49 - 5.71, vs. 2.28, range 1.84 - 3.03; P < 0.05 for both). In patients with cognitive impairment, there were negative correlations between cognitive function (as measured by MMSE and MoCA) and both CRP and RAGE levels (P < 0.05). Patients over 55 years exhibited a positive correlation between CRP and myo-inositol peak area in the left hippocampus (P < 0.05), while there was no relationship between RAGE and any metabolite (P > 0.05). Multiple linear regression revealed that CRP was influenced by hypertension (P = 0.026) and cognitive impairment (P = 0.042).Conclusions: Chronic low-grade inflammation is present in patients with cognitive impairment. Serum CRP, RAGE, and left hippocampal myo-inositol may provide prognostic information on cognitive decline. © 2013 Ge et al.; licensee BioMed Central Ltd. Source

Liu B.,Tongji University | Che W.,Tongji University | Zheng C.,Pudong New Area Zhoupu Hospital | Liu W.,Tongji University | And 5 more authors.
Cellular Physiology and Biochemistry | Year: 2013

Background: SIRT5 is located in the mitochondria, and plays a crucial role in the regulation of metabolic process and cellular apoptosis. Cardiomyocytes are abundant in mitochondria. However, the role of SIRT5 in oxidative stress-induced apoptosis is still unknown in cardiomyocytes. Methods and Results: Western blots analysis revealed that SIRT5 is significantly down-regulated in cardiomyocytes upon oxidative stress. MTT assay, DAPI staining, and caspase 3/7 activity assay were used to estimate apoptosis development. The result suggested that compared with the wild-type group, SIRT5 knockdown results in a marked reduction in cell viability, and a significant increase in the number of apoptotic cells and the caspase 3/7 activity. Protein immunoprecipitation revealed a direct interaction between Bcl-Xl and SIRT5. Apoptosis assay and western blot anaylsis suggested that SIRT5 levels could affect the levels of Bcl-Xl expression, but have no effect on the apoptosis development in Bcl-Xl knockdown cells. Conclusion: This study reveals a novel role of SIRT5 in the regulation of oxidative stress-induced apoptosis in cardiomyocytes. Pharmacological interventions on SIRT5 expression may be useful in the treatment of oxidative stress-related cardiac injury. © 2013 S. Karger AG, Basel. Source

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