Decreased tryptophan hydroxylase 2 mRNA and protein expression, decreased brain serotonin concentrations, and anxiety-like behavioral changes in a rat model of simulated transport stress

Stress ◽  
2019 ◽  
Vol 22 (6) ◽  
pp. 707-717 ◽  
Author(s):  
Lili Wang ◽  
Deping Han ◽  
Peng Yin ◽  
Kedao Teng ◽  
Jianqin Xu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Rat Model ◽  
Tryptophan Hydroxylase ◽  
Behavioral Changes ◽  
Brain Serotonin ◽  
Tryptophan Hydroxylase 2 ◽  
Mrna And Protein Expression ◽  
Transport Stress

scholarly journals Brain serotonin deficiency leads to social communication deficits in mice

2015 ◽  
Vol 11 (3) ◽  
pp. 20150057 ◽  
Author(s):  
D. Beis ◽  
K. Holzwarth ◽  
M. Flinders ◽  
M. Bader ◽  
M. Wöhr ◽  
...  
Keyword(s):  
Tryptophan Hydroxylase ◽  
Sexual Preference ◽  
Brain Serotonin ◽  
Adult Males ◽  
Social Situations ◽  
Tryptophan Hydroxylase 2 ◽  
Social Contacts ◽  
Interaction Partners ◽  
Female Urine ◽  
Serotonin Deficiency

A deficit in brain serotonin is thought to be associated with deteriorated stress coping behaviour, affective disorders and exaggerated violence. We challenged this hypothesis in mice with a brain-specific serotonin depletion caused by a tryptophan hydroxylase 2 (TPH2) deficiency. We tested TPH2-deficient ( Tph2 −/– ) animals in two social situations. As juveniles, Tph2 −/− mice displayed reduced social contacts, whereas ultrasonic vocalizations (USVs) were unchanged within same-sex same-genotype pairings. Interestingly, juvenile females vocalized more than males across genotypes. Sexually naive adult males were exposed to fresh male or female urine, followed by an interaction with a conspecific, and re-exposed to urine. Although Tph2 −/− mice showed normal sexual preference, they were hyper-aggressive towards their interaction partners and did not vocalize in response to sexual cues. These results highlight that central serotonin is essential for prosocial behaviour, especially USV production in adulthood, but not for sexual preference.

scholarly journals Inhibition of the SOCS1-JAK2-STAT3 Signaling Pathway Confers Neuroprotection in Rats with Ischemic Stroke

2017 ◽  
Vol 44 (1) ◽  
pp. 85-98 ◽  
Author(s):  
Xiao-Lei Wang ◽  
Chun-Mei Qiao ◽  
Jiong-Ou Liu ◽  
Chun-Yang Li
Keyword(s):  
Ischemic Stroke ◽  
Protein Expression ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Rat Model ◽  
Caspase 3 ◽  
Neuronal Cells ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Mrna And Protein Expression

Background: The present study aims to investigate the protective effects of the SOCS1-JAK2-STAT3 signaling pathway on neurons in a rat model of ischemic stroke. Methods: Our study was conducted using an ischemic stroke rat model. After the microglia were extracted, 40 neonatal Sprague-Dawley (SD) rats were assigned into the blank, AG490, model and negative control (NC) groups. The neurological function of all the rats was evaluated. Histopathological changes were observed. qRT-PCR and western blotting were applied to measure the expression of genes and proteins in the SOCS1-JAK2-STAT3 signaling pathway and related to apoptosis. The TUNEL assay was conducted to calculate the cellular morphology and apoptosis of neuronal cells. Cell viability was detected using the MTT assay. In addition, immunoassays were used to measure the content of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) as well as the levels of oxidative stress. Results: Compared with the blank group, the model and NC groups showed higher neurological function scores—the cytoplasm of the neurons were cavitated, the organelles were reduced with unclear margins, some of the neurons were necrotic, and apoptosis was increased. In addition, the NC and model groups exhibited decreased cell viability, lower mRNA and protein expression of SOCS1 SOCS3 and bcl-2 and reduced SOD and GSH levels but higher mRNA and protein expression levels of AK2, STAT3,Bax and caspase-3 as well as increased protein expression of P-JAK2, P-STAT3 and activated caspase-3 (c-caspase-3). Moreover, the MDA levels were up-regulated in the NC and model groups. In contrast, opposing trends were found in the AG490 group compared with the NC and model groups. Conclusion: These data demonstrate that inhibiting the SOCS1-JAK2-STAT3 signaling pathway can reduce the loss of nerve function and apoptosis of neuronal cells, which provides a new target for the clinical treatment of ischemic stroke.

Targeted Manipulation of Brain Serotonin: RNAi-Mediated Knockdown of Tryptophan Hydroxylase 2 in Rats

2019 ◽  
Vol 10 (7) ◽  
pp. 3207-3217 ◽  
Author(s):  
Susann Matthes ◽  
Valentina Mosienko ◽  
Elena Popova ◽  
Marion Rivalan ◽  
Michael Bader ◽  
...  
Keyword(s):  
Tryptophan Hydroxylase ◽  
Brain Serotonin ◽  
Tryptophan Hydroxylase 2

scholarly journals Tryptophan hydroxylase 2 genotype determines brain serotonin synthesis but not tissue content in C57Bl/6 and BALB/c congenic mice

2010 ◽  
Vol 481 (1) ◽  
pp. 6-11 ◽  
Author(s):  
William B. Siesser ◽  
Xiaodong Zhang ◽  
Jacob P.R. Jacobsen ◽  
Tatyana D. Sotnikova ◽  
Raul R. Gainetdinov ◽  
...  
Keyword(s):  
Tryptophan Hydroxylase ◽  
Brain Serotonin ◽  
Serotonin Synthesis ◽  
Tryptophan Hydroxylase 2 ◽  
Congenic Mice ◽  
Tissue Content

scholarly journals The disappearance of IPO in myocardium of diabetes mellitus rats is associated with the increase of succinate dehydrogenase-flavin protein

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mengyuan Deng ◽  
Wei Chen ◽  
Haiying Wang ◽  
Yan Wang ◽  
Wenjing Zhou ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Tolerance ◽  
Protein Expression ◽  
Rat Model ◽  
Glucose Tolerance Test ◽  
Blood Gas Analysis ◽  
Tolerance Test ◽  
Gas Analysis ◽  
Blood Gas ◽  
Mrna And Protein Expression

Abstract Background The aim of the present study was to investigate whether the disappearance of ischemic post-processing (IPO) in the myocardium of diabetes mellitus (DM) is associated with the increase of succinate dehydrogenase-flavin protein (SDHA). Methods A total of 50 Sprague Dawley rats, weighing 300–400 g, were divided into 5 groups according to the random number table method, each with 10 rats. After DM rats were fed a high-fat and -sugar diet for 4 weeks, they were injected with Streptozotocin to establish the diabetic rat model. Normal rats were fed the same regular diet for the same number of weeks. Next, the above rats were taken to establish a cardiopulmonary bypass (CPB) model. Intraperitoneal glucose tolerance test (IPGTT) and oral glucose tolerance test (OGTT) were used to detect whether the DM rat model was established successfully. Taking blood from the femoral artery to collect the blood-gas analysis indicators, and judged whether the CPB model is established. After perfusion was performed according to the experimental strategy, the area of myocardial infarction (MI), and serum creatine kinase isoenzyme (CK-MB) and cardiac troponin (CTnI) levels were measured. Finally, the relative mRNA and protein expression of SDHA was detected. Results The OGTT and IPGTT suggested that the DM rat model was successfully established. The arterial blood gas analysis indicated that the CPB model was successfully established. As compared with the N group, the heart function of the IR group was significantly reduced, the levels of myocardial enzyme markers, the area of MI, as well as the relative mRNA and protein expression of SDHA, were all increased. As compared with the IR group, the CK-MB and CTnI levels in the IPO group, the MI area, relative mRNA and protein expression of SDHA decreased. As compared with the IPO group, the myocardial enzyme content in the DM + IPO group, the MI area and the relative mRNA and protein expression of SDHA increased. As compared with the DM + IPO group, in the DM + IPO + dme group, the myocardial enzyme content, area of MI and relative mRNA and protein expression were all decreased. Conclusion IPO can inhibit the expression of SDHA, reduce MIRI and exert a cardioprotective effect in the normal rats. However, the protective effect of IPO disappears in the diabetic rats. The inhibitor dme combined with IPO can increase the expression of SDHA and restore the protective effect of IPO in DM myocardia.

scholarly journals Mogroside IIe Ameliorates Cardiomyopathy by Suppressing Cardiomyocyte Apoptosis in a Type 2 Diabetic Model

2021 ◽  
Vol 12 ◽  
Author(s):  
Xin Cai ◽  
Lingmin He ◽  
Guoao Zhou ◽  
Shenghua Li ◽  
Xinghua Liao
Keyword(s):  
Protein Expression ◽  
Rat Model ◽  
Heart Function ◽  
Interleukin 1 ◽  
Fasting Blood Glucose ◽  
Density Lipoprotein ◽  
Apoptotic Pathway ◽  
Sd Rat ◽  
Mrna And Protein Expression

Mogroside IIe is primarily present in the unripe fruit of Siraitia grosvenorii (Swingle) C. Jeffrey, and it is the predominant saponin component. The purpose of this study was to investigate the effects of mogroside IIe (MGE IIe) on myocardial cell apoptosis in diabetic cardiomyopathy (DCM) rats by establishing a high-sugar and high-fat diet–induced model of type 2 diabetes (T2D) in SD rats and a homocysteine (Hcy)-induced apoptotic model in rat H9c2 cardiomyocytes. The results showed that MGE IIe decreased the levels of fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL) levels, but increased the levels of high-density lipoprotein (HDL) in the SD rat model. Furthermore, MGE IIe decreased the levels of lactate dehydrogenase 2 (LDH2), creatine phosphokinase isoenzyme (CKMB), and creatine kinase (CK), and improved heart function. Additionally, MGE IIe inhibited the secretion of interleukin-1 (IL-1), IL-6, and tumor necrosis factor-α (TNF-α), improved myocardial morphology, and reduced myocardial apoptosis in the SD rat model. Furthermore, MGE IIe inhibited the mRNA and protein expression of active-caspase-3, -8, -9, -12, and Bax and Cyt-C, and promoted the mRNA and protein expression of Bcl-2 in the SD rat model. Furthermore, MGE IIe suppressed homocysteine-induced apoptosis of H9c2 cells by inhibiting the activity of caspases-3, -8, -9, and -12. In conclusion, MGE IIe inhibits the apoptotic pathway, thereby relieving DCM in vivo and in vitro.

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