Search

It is known that Kv1.3, KCa3.1, CRAC, TRPM7, and Clswell are five important ion channels in T lymphocytes. To investigate the mechanism underlying the protective effects of lentinan against T lymphocytes injury induced by chronic radiation in mice, we determined the expression profiles of Kv1.3, KCa3.1, Orai1, STIM1, TRPM7, and Clswell genes. Mice were injected with different concentrations of lentinan before exposure to 60Co g-ray. Total RNA was then extracted from T lymphocytes in murine spleen. The Real time-PCR was per- formed to detect the expression levels of Kv1.3, KCa3.1, Orai1, STIM1, TRPM7, and Clswell genes. The results show that, out of the six ion channels gene expression detected in the present study, only Kv1.3 and Orai1 were altered by lentinan in mice under chronic radiation stress. Kv1.3 and Orai1 expression were significantly elevated in T-lymphocytes isolated from irradiated mice, and were normalized by lentinan treatment. Our results suggest that that Kv1.3 and Orai1 channels may mediate the anti-radiation effects of lentinan.

Introduction: Luteolin is a flavonoid polyphenolic compound exerting broad pharmacological and medicinal properties. Diabetes-related obesity increases the total blood volume and cardiac output and may increase the myocardial hypertrophy progression. However, the mechanism of luteolin in diabetic myocardial hypertrophy remains uncertain. Therefore, this study aimed to evaluate whether luteolin improved diabetic cardiomyopathy (DCM) by inhibiting the proteasome activity. Methods: Cardiomyopathy was induced in streptozotocin-treated diabetes mellitus (DM) and db/db mice. Luteolin (20 mg kg−1·day−1) was administrated via gavage for 12 weeks. In vitro, high glucose and high insulin (HGI, glucose at 25.5 mM and insulin at 0.1 µM) inducing primary neonatal rat cardiomyocytes (NRCMs) were treated with or without luteolin for 48 h. Echocardiography, reverse transcription quantitative polymerase chain reaction, histology, immunofluorescence, and Western blotting were conducted. Proteasome activities were also detected using a fluorescent peptide substrate. Results: Luteolin administration significantly prevented the onset of cardiac hypertrophy, fibrosis, and dysfunction in type 1 DM (T1DM) and type 2 DM (T2DM). Compared with DCM mice, luteolin groups showed lower serum triglyceride and total cholesterol levels. Furthermore, luteolin attenuated HGI-induced myocardial hypertrophy and reduced atrial natriuretic factor mRNA level in NRCMs. Proteasome activities were inhibited by luteolin in vitro. Luteolin also reduces the proteasome subunit levels (PSMB) 1, PSMB2, and PSMB5 of the 20S proteasome, as well as proteasome-regulated particles (Rpt) 1 and Rpt4 levels of 19S proteasome. Furthermore, luteolin treatment increased protein kinase B (AKT) and GSK-3α/β (inactivation of GSK-3) phosphorylation. The phosphorylation level of AMPK activity was also reversed after the treatment with luteolin in comparison with the HGI-treated group. Conclusion: This study indicates that luteolin protected against DCM in mice, including T1DM and T2DM, by upregulating phosphorylated protein AMPK and AKT/GSK-3 pathways while decreasing the proteasome activity. These findings suggest that luteolin may be a potential therapeutic agent for DCM. [ABSTRACT FROM AUTHOR]

Numerous studies have investigated the deleterious effects of maternal depression on child outcomes. Knowledge of characteristics of these mothers is incomplete, as most studies utilize small samples or limit investigation to the postpartum period. Utilizing data from a nationally representative sample of 7,211 fathers and mothers living in households with children aged 5-17 years who participated in the Medical Expenditure Panel Survey (MEPS) 2004-2006, the Patient Health Questionnaire-2 (PHQ-2) was used to assess parental depressive symptoms, the Short Form-12 (SF-12) was used to examine paternal and maternal physical health, and the Columbia Impairment Scale was used to measure child behavioral or emotional problems. In multivariate analyses, maternal unemployment (AOR 1.76, 95% CI 1.31-2.35); living with smokers (AOR 1.82, 95% CI 1.12-2.94); poor maternal physical health (AOR 2.31; 95% CI 1.81-2.94); living with children with behavioral or emotional problems (AOR 2.95, 95% CI 2.30-3.96); and paternal depressive symptoms (AOR 5.11, 95% CI 1.97-13.25) each were independently associated with increased rates of maternal depressive symptoms. This paper is the first we are aware of to use a nationally representative sample to investigate characteristics associated with maternal depressive symptoms and found that maternal unemployment, living with smokers, poor maternal physical health, having children with behavioral or emotional problems, and paternal depressive symptoms are each independently associated with maternal depressive symptoms. In these data, paternal depressive symptoms are associated with the greatest risk of mothers exhibiting depressive symptoms, a finding that we believe has never before been shown. Keywords Maternal depressive symptoms * Child behavior * Child emotional problems, Introduction Maternal depression is a significant public health problem, and identification of these mothers is critical for effective intervention. Maternal depression during the postpartum period has been reported in almost [...]

Extensive research shows maternal depression to be associated with poorer child outcomes, and characteristics of these mothers have been described. Recent research describes associations of paternal depressive symptoms and child behavioral and emotional outcomes, but characteristics of these fathers have not been investigated. This study describes characteristics of fathers with depressive symptoms in the USA. Utilizing data from 7,247 fathers and mothers living in households with children aged 5-17 years who participated in the Medical Expenditure Panel Survey 2004-2006, the Patient Health Questionnaire-2 was used to assess parental depressive symptoms, the Short Form-12 was used to examine paternal and maternal physical health, the Columbia Impairment Scale was used to measure child behavioral or emotional problems, and the Children with Special Health Care Needs Screener was used to identify children with special health care needs. In multivariate analyses, poverty (AOR 1.52; 95% CI 1.05-2.22), maternal depressive symptoms (AOR 5.77; 95% CI 4.18-7.95), living with a child with special health care needs (AOR 1.42, 95% CI 1.04-1.94), poor paternal physical health (AOR 3.31; 95% CI 2.50-4.38) and paternal unemployment (AOR 6.49; 95% CI 4.12-10.22) were independently associated with increased rates of paternal depressive symptoms. These are the first data that demonstrate that poverty, paternal physical health problems, having a child with special health care needs, maternal depressive symptoms, and paternal unemployment are independently associated with paternal depressive symptoms, with paternal unemployment associated with the highest rates of such problems. Keywords Paternal depressive symptoms * Child behavior * Child emotional problems, Introduction Depression has been described as an epidemic in the United States, with lifetime incidence rates estimated at 17% in women and 9% in men [1-3], with a point prevalence [...]

This study aimed to investigate the effects of caprylic acid (C8:0) on lipid metabolism and inflammation, and examine the mechanisms underlying these effects in mice and cells. Fifty-six 6-week-old male C57BL/6J mice were randomly allocated to four groups fed a high-fat diet (HFD) without or with 2% C8:0, palmitic acid (C16:0) or eicosapentaenoic acid (EPA). RAW246.7 cells were randomly divided into five groups: normal, lipopolysaccharide (LPS), LPS+C8:0, LPS+EPA and LPS+cAMP. The serum lipid profiles, inflammatory biomolecules, and ABCA1 and JAK2/STAT3 mRNA and protein expression were measured. C8:0 decreased TC and LDL-C, and increased the HDL-C/LDL-C ratio after injection of LPS. Without LPS, it decreased TC in mice (P < 0.05). Moreover, C8:0 decreased the inflammatory response after LPS treatment in both mice and cells (P < 0.05). Mechanistic investigations in C57BL/6J mouse aortas after injection of LPS indicated that C8:0 resulted in higher ABCA1 and JAK2/STAT3 expression than that with HFD, C16:0 and EPA, and resulted in lower TNF-α, NF-κB mRNA expression than that with HFD (P < 0.05). In RAW 264.7 cells, C8:0 resulted in lower expression of pNF-κBP65 than that in the LPS group, and higher protein expression of ABCA1, p-JAK2 and p-STAT3 than that in the LPS and LPS+cAMP groups (P < 0.05). Our studies demonstrated that C8:0 may play an important role in lipid metabolism and the inflammatory response, and the mechanism may be associated with ABCA1 and the p-JAK2/p-STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]