LINE-1 gene hypomethylation and p16 gene hypermethylation in HepG2 cells induced by low-dose and long-term triclosan exposure: The role of hydroxyl group

2016 ◽  
Vol 34 ◽  
pp. 35-44 ◽  
Author(s):  
Liudan Zeng ◽  
Huimin Ma ◽  
Shangxia Pan ◽  
Jing You ◽  
Gan Zhang ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Low Dose ◽  
Hydroxyl Group ◽  
P16 Gene

Short‐ and long‐term responsiveness to low dose growth hormone (GH) in adult GH deficiency: Role of GH receptor polymorphism

2019 ◽  
Vol 31 (4) ◽  
pp. e12692 ◽  
Author(s):  
Antonio Bianchi ◽  
Antonella Giampietro ◽  
Linda Tartaglione ◽  
Sabrina Chiloiro ◽  
Raffaella Gentilella ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Low Dose ◽  
Gh Deficiency ◽  
Gh Receptor ◽  
Adult Gh Deficiency ◽  
Short And Long Term ◽  
Receptor Polymorphism

scholarly journals Neural Plasticity Associated with Hippocampal PKA-CREB and NMDA Signaling Is Involved in the Antidepressant Effect of Repeated Low Dose of Yueju Pill on Chronic Mouse Model of Learned Helplessness

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Zhilu Zou ◽  
Yin Chen ◽  
Qinqin Shen ◽  
Xiaoyan Guo ◽  
Yuxuan Zhang ◽  
...  
Keyword(s):  
Neural Plasticity ◽  
Learned Helplessness ◽  
Low Dose ◽  
Critical Role ◽  
Repeated Administration ◽  
Camp Response Element Binding ◽  
Antidepressant Effect ◽  
Long Term Depression

Yueju pill is a traditional Chinese medicine formulated to treat syndromes of mood disorders. Here, we investigated the therapeutic effect of repeated low dose of Yueju in the animal model mimicking clinical long-term depression condition and the role of neural plasticity associated with PKA- (protein kinase A-) CREB (cAMP response element binding protein) and NMDA (N-methyl-D-aspartate) signaling. We showed that a single low dose of Yueju demonstrated antidepressant effects in tests of tail suspension, forced swim, and novelty-suppressed feeding. A chronic learned helplessness (LH) protocol resulted in a long-term depressive-like condition. Repeated administration of Yueju following chronic LH remarkably alleviated all of depressive-like symptoms measured, whereas conventional antidepressant fluoxetine only showed a minor improvement. In the hippocampus, Yueju and fluoxetine both normalized brain-derived neurotrophic factor (BDNF) and PKA level. Only Yueju, not fluoxetine, rescued the deficits in CREB signaling. The chronic LH upregulated the expression of NMDA receptor subunits NR1, NR2A, and NR2B, which were all attenuated by Yueju. Furthermore, intracerebraventricular administration of NMDA blunted the antidepressant effect of Yueju. These findings supported the antidepressant efficacy of repeated routine low dose of Yueju in a long-term depression model and the critical role of CREB and NMDA signaling.

Catecholamines and pituitary function. IV. Effects of low-dose dopamine infusion and long-term bromocriptine treatment on the abnormal thyrotroph (TSH) dynamics in patients with pathological hyperprolactinaemia

1986 ◽  
Vol 111 (2) ◽  
pp. 154-161 ◽  
Author(s):  
Ildo Nicoletti ◽  
Paolo Filipponi ◽  
Leone Fedeli ◽  
Franca Ambrosi ◽  
Camillo Giammartino ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Low Dose ◽  
Physiological Role ◽  
Serum Concentrations ◽  
Trh Test ◽  
Synthesis Inhibitor ◽  
Tsh Secretion ◽  
Insight Into

Abstract. In order to gain further insight into the role of dopamine (DA) in the control of TSH release and to investigate whether an increased or defective DA inhibition on pituitary thyrotrophs may be considered responsible for the abnormal TSH dynamics in pathological hyperprolactinaemia, we examined the effect of low-dose DA infusion on TRH stimulated TSH secretion in normally cycling women and in patients with pathological hyperprolactinaemia. The effect of long-term bromocriptine therapy on TSH dynamics was also evaluated in a selected group of hyperprolactinaemic women. Fifty-two hyperprolactinaemic patients with no other signs of pituitary or thyroid dysfunction had significantly higher mean TSH serum concentrations and mean TSH peak values after TRH administration than 75 healthy controls. Furthermore, the TSH rises induced by the DA-synthesis inhibitor α-methyl-p-tyrosine (AMPT, 500 mg orally) were enhanced in both prolactinoma and 'idiopathic hyperprolactinaemia' patients as compared with controls. There was a positive correlation between the TRH- and AMPT-induced TSH rises in the hyperprolactinaemic group. Low-dose DA infusion (0.1 μg/kg min) reduced TSH response to TRH in both regularly cycling women and patients with hyperprolactinaemic amenorrhoea. Long-term bromocriptine therapy (2.5 mg tid over 60– 150 days) not only normalized serum Prl levels, but also reduced the TSH response to TRH in 7 hyperprolactinaemic women who had presented exaggerated TSH responses to the basal TRH test. These findings confirm that DA plays a physiological role in the inhibition of TSH release, probably at the level of the anterior pituitary. The fact that both low-dose DA infusion and long-term bromocriptine treatment effectively reduced TSH release in hyperprolactinaemic patients seems to indicate that endogenous DA inhibition of pituitary thyrotrophs is reduced rather than enhanced in pathological hyperprolactinaemia.

The metabolic responses of HepG2 cells to the exposure of mycotoxin deoxynivalenol

2016 ◽  
Vol 9 (4) ◽  
pp. 577-586 ◽  
Author(s):  
Y. Liu ◽  
R. Ran ◽  
C. Hu ◽  
B. Cui ◽  
Y. Xu ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Redox Homeostasis ◽  
Short Term ◽  
Cellular Mechanisms ◽  
Metabolomics Data ◽  
Toxicological Effects ◽  
In Vitro Systems

As the number of reported deoxynivalenol (DON) contamination incidents increased steadily over the past decades, there has been a widespread interest in understanding the cellular mechanisms of the toxicological effects of DON using in vitro systems and omics technologies. The present investigation was conducted to understand the metabolomic changes in human hepatocellular carcinoma cells (HepG2) exposed to 10 μM DON for short term (4 h) and long term (12 h) periods, using a non-targeted metabolomics approach. Our results revealed a remarkable metabolic shift from short term to long term exposure to DON in HepG2 cells. Our metabolomics data also confirmed the role of DON induced oxidative stress in DON toxicity. Coupled with pattern recognition and pathway analysis, effects of DON on redox homeostasis, energy balance, lipid metabolism, and potential toxicological mechanisms were discussed, which would facilitate further studies on the risk assessment of the dietary mycotoxin DON.

scholarly journals miR-146a attenuates apoptosis and modulates autophagy by targeting TAF9b/P53 pathway in doxorubicin-induced cardiotoxicity

2019 ◽  
Vol 10 (9) ◽  
Author(s):  
Jian-An Pan ◽  
Yong Tang ◽  
Jian-Ying Yu ◽  
Hui Zhang ◽  
Jun-Feng Zhang ◽  
...  
Keyword(s):  
Protective Factor ◽  
Low Dose ◽  
Tata Binding Protein ◽  
Wild Type ◽  
P53 Pathway ◽  
The Stability ◽  
Dose Dependent

Abstract Clinical therapy of doxorubicin (DOX) is limited due to its cardiotoxicity. miR-146a was proved as a protective factor in many cardiovascular diseases, but its role in chronic DOX-induced cardiotoxicity is unclear. The objective of this study was to demonstrate the role of miR-146a in low-dose long-term DOX-induced cardiotoxicity. Experiments have shown that DOX intervention caused a dose-dependent and time-dependent cardiotoxicity involving the increased of apoptosis and dysregulation of autophagy. The cardiotoxicity was inhibited by overexpressed miR-146a and was more severe when miR-146a was downgraded. Further research proved that miR-146a targeted TATA-binding protein (TBP) associated factor 9b (TAF9b), a coactivator and stabilizer of P53, indirectly destroyed the stability of P53, thereby inhibiting apoptosis and improving autophagy in cardiomyocytes. Besides, miR-146a knockout mice were used for in vivo validation. In the DOX-induced model, miR-146a deficiency made it worse whether in cardiac function, cardiomyocyte apoptosis or basal level of autophagy, than wild-type. In conclusion, miR-146a partially reversed the DOX-induced cardiotoxicity by targeting TAF9b/P53 pathway to attenuate apoptosis and adjust autophagy levels.

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