Parabens are widely used in personal care products due to their antimicrobial effects. Although the toxicity of parabens has been reported, little information is available on the toxicity of butylparaben (BP) on oocyte maturation. Therefore, we investigated the effects of various concentrations of BP (0 μM, 100 μM, 200 μM, 300 μM, 400 μM, and 500 μM) on the in vitro maturation of porcine oocytes. BP supplementation at a concentration greater than 300 μM significantly reduced the proportion of complete cumulus cell expansion and metaphase II oocytes compared to the control. The 300 μM BP significantly decreased fertilization, cleavage, and blastocyst formation rates with lower total cell numbers and a higher rate of apoptosis in blastocysts compared to the control. The BP-treated oocytes showed significantly higher reactive oxygen species (ROS) levels, and lower glutathione (GSH) levels than the control. BP significantly increased the aberrant mitochondrial distribution and decreased mitochondrial function compared to the control. BP-treated oocytes exhibited significantly higher percentage of γ-H2AX, annexin V-positive oocytes and expression of LC3 than the control. In conclusion, we demonstrated that BP impaired oocyte maturation and subsequent embryonic development, by inducing ROS generation and reducing GSH levels. Furthermore, BP disrupted mitochondrial function and triggered DNA damage, early apoptosis, and autophagy in oocytes.
Mast cell-mediated allergic inflammation is involved in many diseases such as asthma, sinusitis, and rheumatoid arthritis. Mast cells induce synthesis and production of pro-inflammatory cytokines including tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-6 with immune regulatory properties. The formulated ethanol extract of Artemisia asiatica Nakai (DA-9601) has been reported to have antioxidative and anti-inflammatory activities. In this report, we investigated the effect of DA-9601 on the expression of pro-inflammatory cytokines by the activated human mast cell line HMC-1 and studied its possible mechanisms of action. DA-9601 dose-dependently decreased the gene expression and production of TNF-alpha, IL-1beta, and IL-6 on phorbol 12-myristate 13-acetate (PMA)- and calcium ionophore A23187-stimulated HMC-1 cells. In addition, DA-9601 attenuated PMA- and A23187-induced activation of NF-kappaB as indicated by inhibition of degradation of IkappaBalpha, nuclear translocation of NF-kappaB, NF-kappaB/DNA binding, and NF-kappaB-dependent gene reporter assay. Our in vitro studies provide evidence that DA-9601 might contribute to the treatment of mast cell-derived allergic inflammatory diseases.
Symptoms of Parkinson' s disease (PD) caused by loss of dopaminergic neurons are accompanied by movement disorders, including tremors, rigidity, bradykinesia, and akinesia. Non-human primate (NHP) models with PD play an essential role in the analysis of PD pathophysiology and behavior symptoms. As impairments of hand dexterity function can affect activities of daily living in patients with PD, research on hand dexterity function in NHP models with chronic PD is essential. Traditional rating scales previously used in the evaluation of animal spontaneous behavior were insufficient due to factors related to subjectivity and passivity. Thus, experimentally designed applications for an appropriate apparatus are necessary. In this study, we aimed to longitudinally assess hand dexterity function using hand dexterity task (HDT) in NHP-PD models. To validate this assessment, we analyzed the alteration in Parkinsonian tremor signs and the functionality of presynaptic dopaminergic neuron using positron emission tomography imaging of dopamine transporters in these models. In addition, a significant inverse correlation between HDT and DAT level was identified, but no local bias was found. The correlation with intention tremor signs was lower than the resting tremor. In conclusion, the evaluation of HDT may reflect behavioral symptoms of NHP-PD models. Furthermore, HDT was effectively used to experimentally distinguish intention tremors from other tremors.
32Symptoms of Parkinson's disease (PD) caused by loss of dopaminergic neurons are 33 accompanied by movement disorders, including tremors, rigidity, bradykinesia, and akinesia. 34 Non-human primate (NHP) models with PD play an essential role in the analysis of PD 35 pathophysiology and behavior symptoms. As impairments of hand dexterity function can affect 36 activities of daily living in patients with PD, research on hand dexterity function in NHP 37 models with chronic PD is essential. Traditional rating scales previously used in the evaluation 38 of animal spontaneous behavior were insufficient due to factors related to subjectivity and 39 passivity. Thus, experimentally designed applications for an appropriate apparatus are 40 necessary. In this study, we aimed to longitudinally assess hand dexterity function using hand 41 dexterity task (HDT) in NHP-PD models. To validate this assessment, we analyzed an 42 alteration in Parkinsonian tremor symptoms, loss of dopaminergic neuron, and positron 43 emission tomography (PET) imaging of dopamine transporters (DAT) in these models. HDT 44 latency significantly increased in NHP-PD models. In addition, a significant inverse correlation 45 between HDT and DAT was identified, but no local bias was found. The correlation with 46 intention tremor symptoms was lower than the resting tremor. In conclusion, the evaluation of 47 HDT may reflect behavioral symptoms of NHP-PD models. Furthermore, HDT was effectively 48 used to experimentally distinguish intention tremors from other tremors. 50 Symptoms of Parkinson's disease (PD) caused by loss of dopaminergic neurons are 51 accompanied by movement disorders, including tremors, rigidity, bradykinesia, and akinesia 52 [1, 2]. As impairments of hand dexterity function can affect activities of daily living in patients 53 with PD, such as buttoning a shirt or picking up a fork, recent studies have attempted to identify 54 related pathological processes, such as apraxia, to develop a treatment strategy [3, 4]. Various 55 methods have been developed to assess hand dexterity dysfunction in patients with PD [5-7]. 56 Non-human primate (NHP) of PD models play an essential role in the analysis of PD 57 pathophysiology and behavior symptoms [8]. However, methods that can be applied to NHP 58 models with PD are limited and confined to those based on visual phenotype observations. 59 Traditional rating scales previously used in the evaluation of animal spontaneous behavior were 60 problematic due to factors related to subjectivity and passivity [9]. Observation methods can 61 neither eliminate idiosyncrasies of each observer's subjective judgment (subjectivity) nor 62 separate bradykinesia from temporary spontaneous laziness of the subjects (passivity). In 63 particular, distinguishing parkinsonian symptoms, such as bradykinesia, from spontaneous 64 laziness in NHP-PD models was challenging [9]. 65To overcome these challenges, experimentally designed applications of an appropriate 66 apparatus are necessary. An apparatus for the hand ...
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