Altered levels of BMD, PRL, BAP and TRACP-5b in male chronic patients with schizophrenia
3区 · 综合性期刊
作者: Du, Xiangdong ; Ye, Fei ; Li, Jin ; Zhao, Yaqin ; Xiao, Wenhuan ; Tang, Xiaowei ; Zhang, Xiaobin
Bone mineral density (BMD) has been found to decrease in schizophrenia patients. We examined BMD and the levels of prolactin (PRL), bone alkaline phosphatase (BAP) and tartrate resistant acid phosphatase isoform 5b (TRACP-5b) in male chronic schizophrenia patients and compared them with healthy controls in a Chinese Han population, which has not been reported before. Male patients with chronic schizophrenia (SPs; n = 79) and healthy controls (HCs; n = 56) were recruited. BMD and plasma PRL, BAP and TRACP-5b levels were measured and compared between the two groups. The SPs group was further divided into two subgroups: the elevated PRL group (PRL ≥ 25 ng/ml, EPRL; n = 38) and the normal PRL group (PRL < 25 ng/ml, NPRL; n = 41) in accordance with PRL levels. The levels of BAP and TRACP-5b were measured using sandwich enzyme-linked immunosorbent assay (ELISA) while serum PRL was measured with an Access Immunoassay Analyzer. BMD was determined by quantitative computed tomography. BMD levels significantly decreased and serum PRL and TRACP-5b levels were significantly higher in male chronic schizophrenia patients. The EPRL group had remarkably lower BMD and BAP level and higher TRACP-5b levels compared with the NPRL group and HCs. Moreover, there was a negative correlation between BMD and TRACP-5b in the EPRL group. We found that BMD, BAP and TRACP-5b levels in the EPRL group were significantly different than HCs and the NPRL group. PRL levels in schizophrenia patients may be related to BMD and bone metabolism. Monitoring BMD and markers of bone metabolism in clinical practice may therefore be helpful to understand the bone health status of schizophrenia patients.
2015-11-01·Nutricion hospitalaria4区 · 医学
NUTRITIONAL AND METABOLIC ASSESSMENT IN OVERWEIGHT PATIENTS WITH AND WITHOUT HYPERPROLACTINEMIA CAUSED BY PROLACTINOMA.
prolactinomas are pituitary adenomas that express and secrete prolactin. These patients are overweight and the mechanisms are being studied.
assess nutritional and metabolic status of overweight patients with and without hyperprolactinemia caused by prolactinoma and compare them.
MATERIALS AND METHODS:
cross-sectional study, patients with body mass index (BMI) ≥ 25 kg/m2 with and without prolactinoma: 1) 20 normoprolactinemic (NPrl) with prolactinoma; 2) 23 hyperprolactinemic (HPrl) with prolactinoma; 3) 28 controls without prolactinoma or alterations in prolactin levels. Evaluated through anthropometric, dietetics, and biochemical assessment.
of the 71 patients evaluated, most were obese women with macroprolactinomas. All three groups had diets with low caloric and monounsaturated fatty acid (MUFA) intake, the NPrl group had low carbohydrate (CHO) intake and high lipid (LIP) and saturated fatty acid (SFA) intake, and the NPrl and HPrl groups had appropriate intake of polyunsaturated fatty acids (PUFA). The HPrl group had elevated total cholesterol. HDL cholesterol was below the recommended threshold for most patients. No statistically significant differences were found in anthropometric and biochemical variables among the groups.
most patients with prolactinomas and controls are obese and metabolically similar regardless of prolactin levels. All groups presented low caloric and MUFA intake. Protein, LIP, SFA, and cholesterol were significantly different among the groups, the NPrl group ingested less amount of protein and greater of fat. Snacking between meals and changes of food consumption on weekends was reported by most patients. This is the first study comparing patients with prolactinomas and controls, both with overweight, regarding food consumption and feeding behavior.
2014-01-01·PLoS One3区 · 综合性期刊
NPRL-Z-1, as a new topoisomerase II poison, induces cell apoptosis and ROS generation in human renal carcinoma cells
NPRL-Z-1 is a 4β-[(4"-benzamido)-amino]-4'-O-demethyl-epipodophyllotoxin derivative. Previous reports have shown that NPRL-Z-1 possesses anticancer activity. Here NPRL-Z-1 displayed cytotoxic effects against four human cancer cell lines (HCT 116, A549, ACHN, and A498) and exhibited potent activity in A498 human renal carcinoma cells, with an IC50 value of 2.38 µM via the MTT assay. We also found that NPRL-Z-1 induced cell cycle arrest in G1-phase and detected DNA double-strand breaks in A498 cells. NPRL-Z-1 induced ataxia telangiectasia-mutated (ATM) protein kinase phosphorylation at serine 1981, leading to the activation of DNA damage signaling pathways, including Chk2, histone H2AX, and p53/p21. By ICE assay, the data suggested that NPRL-Z-1 acted on and stabilized the topoisomerase II (TOP2)-DNA complex, leading to TOP2cc formation. NPRL-Z-1-induced DNA damage signaling and apoptotic death was also reversed by TOP2α or TOP2β knockdown. In addition, NPRL-Z-1 inhibited the Akt signaling pathway and induced reactive oxygen species (ROS) generation. These results demonstrated that NPRL-Z-1 appeared to be a novel TOP2 poison and ROS generator. Thus, NPRL-Z-1 may present a significant potential anticancer candidate against renal carcinoma.