期刊:
Journal of Affective Disorders,2017年224:56-60 ISSN:0165-0327
通讯作者:
Wang, Yuhong
作者机构:
[Meng, Pan; Wang, Yuhong] Hunan Univ Chinese Med, State Key Lab Chinese Med Powder & Med Innovat Hu, Xiangzui Rd, Changsha 410208, Hunan, Peoples R China.;[Han, Yuanshan; Yang, Hui] Hunan Univ Chinese Med, Hosp 1, Cent Lab, Changsha 410007, Hunan, Peoples R China.
通讯机构:
[Wang, Yuhong] H;Hunan Univ Chinese Med, State Key Lab Chinese Med Powder & Med Innovat Hu, Xiangzui Rd, Changsha 410208, Hunan, Peoples R China.
关键词:
Diabetes;Depression;25-hydroxyvitamin D
摘要:
Background: Because of the absence of data on the direct association between vitamin D and depression in patients with diabetes, we examined the association between vitamin D state (assessed by 25-hydroxyvitamin D [ 25(OH) D]) and the prevalence of depression in adult patients with type 2 diabetes mellitus(T2DM). Method: Cross-sectional data were obtained from 2786 patients with T2DM recruited from a Chinese diabetes registry. Patients' records were reviewed to obtain data pertaining to age, sex, Body Mass Index (BMI), marital status, level of education, smoking status, duration of diabetes mellitus, use of insulin, and presence of additional illnesses. A multiple logistic regression analysis adjusted for potential confounders was used to assess independent associations between serum levels of 25 (OH) D and depression (defined by the Patient Health Questionnaire-9). Results: Using the PHQ-9 cutoff value of >= 10, 5.71% (159/2786; 95% CI: 4.85-6.57%) were considered to have depression. The serum 25(OH) D levels were significantly lower in diabetic patients with depression than those patients without depression [10.2(IQR, 7.6-15.2) ng/ml vs. 14.6(IQR, 10.7-19.8)ng/ml, respectively; P < 0.0001]. Multivariate logistic regression analysis considering traditional risk factors and other biomarkers showed an inverse relationship between serum 25 (OH) D levels and depression when serum 25 (OH) D were used as a continuous variable (OR, 0.84; 95% CI, 0.77-0.90; P < 0.001). Compared with the first quartile of serum 25 (OH) D levels, the second quartile OR for depression was 0.83 (95% CI, 0.75-0.92, P=0.012). For the third and fourth quartiles, it was 0.40 (95% CI, 0.33-0.52, P < 0.001) and 0.15 (95% CI, 0.08-0.22; P < 0.001), respectively. Conclusions: We observed a significant negative association between serum levels of 25 (OH) D and depression in Chinese patients with T2DM.
作者机构:
[佘颜] Medical College, Hunan University of Traditional Chinese Medicine, Changsha, 410208, China;[王宇红; 刘芳; 邵乐; 蔡光先; 夏相宜] Training Bases, Hunan Key Lab. of Chinese Materia Medica Powder and Innov. Drugs Estab. by Provincel and Ministry, Changsha, 410208, China
摘要:
目的:观察补阳还五汤精简方对大鼠脑缺血后血管新生及核转录因子 E2相关因子2( Nrf2)/血红素加氧酶-1(HO-1)信号途径的影响。方法120只 SD 大鼠随机分成假手术组、模型组、补阳还五汤组、补阳还五汤精简方组。采用大脑中动脉线栓法建立局灶性脑缺血模型,各组给予相应处理。在 d 1、3、7三个时间点取脑组织进行检测,免疫组织化学法检测血浆Ⅷ因子相关抗原(vWF),测定微血管密度(MVD)。采用 Real-time PCR 和 Western blot 法检测大鼠脑组织中 Nrf2、HO-1基因及蛋白表达。结果①与假手术组比,模型组 vWF 阳性表达微血管在 d 3时表达明显升高(P<0.05),给药组 d 7与模型组比较差异有显著性( P <0.05);②假手术组 Nrf2、HO-1mRNA 及蛋白呈少量表达,模型组 Nrf2蛋白表达水平 d 3与同时间点假手术组比较差异有统计学意义(P <0.01),各给药组能上调 Nrf2mRNA 及蛋白表达,其中 Nrf2mRNA 在 d 7,Nrf2蛋白表达在 d 1及 d 7上调最明显,与同时间点模型组比较差异具有统计学意义(P <0.01)。模型组 HO-1mRNA 及蛋白在 d 7与同时间点假手术组比较差异有统计学意义(P <0.05),各给药组 HO-1mRNA 在 d 3,HO-1蛋白在 d 3及 d 7上调最明显,与同时段模型组比较差异具有统计学意义(P <0.05,P <0.01)。结论补阳还五汤精简方促进脑缺血后血管新生,这一作用可能与调控 Nrf2/ HO-1信号途径的表达有关。
作者:
Bu, Yiwen;Cai, Guoshuai;Shen, Yi;Huang, Chenfei;Zeng, Xi;...
期刊:
Cancer Letters,2016年383(2):261-271 ISSN:0304-3835
通讯作者:
Cao, Deliang;Liao, Duan-Fang
作者机构:
[Huang, Chenfei; Shen, Yi; Cao, Yu; Bu, Yiwen; Cao, Deliang] Southern Illinois Univ, Sch Med, Simmons Canc Inst, Dept Med Microbiol Immunol & Cell Biol, 913 N Rutledge St, Springfield, IL 62794 USA.;[Cai, Guoshuai] Geisel Sch Med Dartmouth, Dept Genet, Hanover, NH 03755 USA.;[Zeng, Xi] Univ South China, Canc Res Inst, Hengyang 421001, Hunan, Peoples R China.;[Wang, Yuhong; Cao, Deliang; Huang, Dan; Liao, Duan-Fang; Cai, Chuan] Hunan Univ Chinese Med, State Key Lab Chinese Med Powder & Med Innovat Hu, Div Stem Cell Regulat & Applicat, Changsha 410208, Hunan, Peoples R China.;[Liao, Duan-Fang] Hunan Univ Tradit Chinese Med, Div Stem Cell Regulat & Applicat, 1 Xiangzui Rd, Changsha 410208, Hunan, Peoples R China.
通讯机构:
[Cao, Deliang] S;[Liao, Duan-Fang] H;Southern Illinois Univ, Sch Med, Simmons Canc Inst, Dept Med Microbiol Immunol & Cell Biol, 913 N Rutledge St, Springfield, IL 62794 USA.;Hunan Univ Tradit Chinese Med, Div Stem Cell Regulat & Applicat, 1 Xiangzui Rd, Changsha 410208, Hunan, Peoples R China.
关键词:
NF-kappa B RelA/p65;ABCC6;RITA;Chemoresistance
摘要:
Inactivation of p53 occurs frequently in various cancers. RITA is a promising anticancer small molecule that dissociates p53-MDM2 interaction, reactivates p53 and induces exclusive apoptosis in cancer cells, but acquired RITA resistance remains a major drawback. This study found that the site-differential phosphorylation of nuclear factor-kappa B (NF-kappa B) RelA/p65 creates a barcode for RITA chemosensitivity in cancer cells. In naive MCF7 and HCT116 cells where RITA triggered vast apoptosis, phosphorylation of RelA/p65 increased at Ser536, but decreased at Ser276 and Ser468; oppositely, in RITA-resistant cells, RelA/p65 phosphorylation decreased at Ser536, but increased at Ser276 and Ser468. A phosphomimetic mutation at Ser536 (p65/S536D) or silencing of endogenous RelA/p65 resensitized the RITA-resistant cells to RITA while the phosphomimetic mutant at Ser276 (p65/S276D) led to RITA resistance of naive cells. In mouse xenografts, intratumoral delivery of the phosphomimetic p65/S536D mutant increased the antitumor activity of RITA. Furthermore, in the RITA-resistant cells ATP-binding cassette transporter ABCC6 was upregulated, and silencing of ABCC6 expression in these cells restored RITA sensitivity. In the naive cells, ABCC6 delivery led to RITA resistance and blockage of p65/S536D mutant-induced RITA sensitivity. Taken together, these data suggest that the site-differential phosphorylation of RelA/p65 modulates RITA sensitivity in cancer cells, which may provide an avenue to manipulate RITA resistance. (C) 2016 Elsevier Ireland Ltd. All rights reserved.