ABSTRACT
Depression is a wellestablished risk factor for cardiac morbidity and mortality in patients with coronary artery disease (CAD). Previous studies have demonstrated that the level of brainderived neurotrophic factor (BDNF) is decreased in depressed patients and this depletion may be reversed by antidepressants. Several recent studies have suggested that BDNF is involved in the pathogenesis of CAD. The aim of the present study was to investigate the possible association between seven single nucleotide polymorphisms (SNPs) of the BDNF gene (SNPs; rs16917204, rs6265, rs7103873, rs16917237, rs56164415, rs13306221 and rs10767664) and coronary artery diseaserelated depression (CADD). In the present study, 616 CAD patients without depression (CADnD) and 155 patients with CADD were recruited, and the response to an eight week sertraline antidepressant treatment regimen was also evaluated. The results demonstrated that a significant association existed between the SNP rs6265, located in exon 4 of the BDNF gene, and CADD [χ2=9.634, P=0.002, odds ratio (OR)=1.486, 95% confidence interval (CI)=1.1561.910]. Another potential association was observed for rs13306221 (χ2=5.194, P=0.023, OR=2.139, 95% CI=1.0964.175) in the promoter region of the BDNF gene. Strong linkage disequilibrium was observed in block 1 (rs16917204, rs6265; D'>0.9). However, there was no evidence of a significant linkage disequilibrium between the seven SNPs in our sample population. Additionally, carriers of the A allele of rs6265 exhibited improved responses to the sertraline treatment (χ2=8.942, P=0.003, OR=2.136, 95% CI=1.2933.528). To the best of our knowledge, these results demonstrate, for the first time, the presence of a significant association between BDNF rs6265 and CADD, the identification of which may facilitate early diagnosis of CADD in the future.
Subject(s)
Antidepressive Agents/therapeutic use , Brain-Derived Neurotrophic Factor/genetics , Coronary Artery Disease/genetics , Depression/drug therapy , Depression/genetics , Polymorphism, Single Nucleotide/genetics , Alleles , Gene Frequency/drug effects , Gene Frequency/genetics , Genotype , Humans , Linkage Disequilibrium/genetics , Middle Aged , Polymorphism, Single Nucleotide/drug effects , Promoter Regions, Genetic/drug effects , Promoter Regions, Genetic/geneticsABSTRACT
BACKGROUND: Recently, melatonin has been associated with cancer both in vitro and in vivo. However, the value of melatonin in the treatment of cancer remains disputable. Hence, we performed a systematic review of randomized controlled trials (RCTs) of melatonin in solid tumor cancer patients and observed its effect on tumor remission, 1-year survival, and side effects due to radiochemotherapy. METHODS: An electronic search was conducted using the databases Pubmed, Medline, EMBASE, Cochrane library, and CNKI, from inception to November 2011. Trials using melatonin as adjunct treatment concurrent with chemotherapy or radiotherapy for cancer were included. Pooled relative risk (RR) for the tumor remission, 1-year survival, and radiochemotherapy-related side effects were calculated using the software Revman 5.0. RESULTS: The search strategy identified 8 eligible RCTs (n = 761), all of which studied solid tumor cancers. The dosage of melatonin used in the 8 included RCTs was 20 mg orally, once a day. Melatonin significantly improved the complete and partial remission (16.5 vs. 32.6%; RR = 1.95, 95% CI, 1.49-2.54; P < 0.00001) as well as 1-year survival rate (28.4 vs. 52.2%; RR = 1.90; 95% CI, 1.28-2.83; P = 0.001), and dramatically decreased radiochemotherapy-related side effects including thrombocytopenia (19.7 vs. 2.2%; RR = 0.13; 95% CI, 0.06-0.28; P < 0.00001), neurotoxicity (15.2 vs. 2.5%; RR = 0.19; 95% CI, 0.09-0.40; P < 0.0001), and fatigue (49.1 vs. 17.2%; RR = 0.37; 95% CI, 0.28-0.48; P < 0.00001). Effects were consistent across different types of cancer. No severe adverse events were reported. CONCLUSIONS: Melatonin as an adjuvant therapy for cancer led to substantial improvements in tumor remission, 1-year survival, and alleviation of radiochemotherapy-related side effects.
Subject(s)
Antineoplastic Agents/therapeutic use , Melatonin/therapeutic use , Neoplasms/drug therapy , Antineoplastic Agents/adverse effects , Antioxidants/adverse effects , Antioxidants/therapeutic use , Combined Modality Therapy , Humans , Melatonin/adverse effects , Neoplasms/pathology , Neoplasms/radiotherapy , Radiation Injuries/epidemiology , Randomized Controlled Trials as Topic , Remission Induction/methods , Survival RateABSTRACT
A new jacaranone derivative, 2-(1,6-dihydroxy-4-oxocyclohex-2-enyl) acetic acid (1), has been isolated from the whole plants of Senecio scandens var. incisus, together with three known compounds: 2'-(p-hydroxyl-cinnamoyl)-6'-jacaranone-D-glucopyranoside (2), 2'-caffeoyl-6'-jacaranone-D-glucopyranoside (3) and kampferol-3-rhamnoside (4). Their structures were elucidated on the basis of spectroscopic data analyses and by comparison with the related known compounds. Cytotoxic activities of 1 against three human tumour cell lines have been evaluated by the MTT method.