scholarly journals Uridine stimulate laxative effect in the loperamide-induced constipation of SD rats through regulation of the mAChRs signaling pathway and mucin secretion

2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Ji Eun Kim ◽  
Jun Go ◽  
Ji Eun Sung ◽  
Hyun Ah Lee ◽  
Woo Bin Yun ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Mucin Secretion ◽  
Sd Rats ◽  
Laxative Effect

scholarly journals Maren Pills Improve Constipation via Regulating AQP3 and NF-κB Signaling Pathway in Slow Transit Constipation In Vitro and In Vivo

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Yu Zhan ◽  
Xuegui Tang ◽  
Hong Xu ◽  
Shiyu Tang
Keyword(s):  
Signaling Pathway ◽  
Vital Role ◽  
Slow Transit Constipation ◽  
Dependent Manner ◽  
Water Metabolism ◽  
Laxative Effect ◽  
Irritable Bowel ◽  
Ht 29

Background. Maren pills have been used to treat constipation. Aquaporin 3 (AQP3) plays a vital role in regulating water transfer in the colon. It has been reported that the downregulation of AQP3 can regulate liquid water metabolism and intestinal permeability in irritable bowel syndrome (IBS) rats’ colon via NF-κB pathway. In this study, we investigated whether the laxative effect of Maren pills is associated with the regulation of AQP3 and NF-κB signaling pathway in the colon. Methods. The compound diphenoxylate suspension-induced STC rats received Maren pills intragastrically for 1 consecutive week to evaluate the laxative effect of Maren pills involving the regulation of AQP3 and NF-κB signaling pathway. Moreover, human intestinal epithelial cells (HT-29) were treated with drug serum to obtain in vitro data. Results. Our results revealed that treatment with Maren pills increased the stool number, moisture content of feces, and intestinal transit rate in a dose-dependent manner. Maren pills significantly increased the AQP3, fibrosis transmembrane conductance regulator (CFTR), and protein kinase A (PKA) proteins in the colon of rats and in HT-29 cells. Mechanistically, Maren pills obviously inhibited the activation of NF-κB pathway in the colon of rats and in HT-29 cells. Conclusion. These results suggest that the laxative effect of Maren pills is associated with the increased expression of AQP3 by downregulating NF-κB signal pathway.

miR-223 Promotes Smooth Muscle Cell Proliferation and Atherosclerotic Plaque Formation by Inhibiting Phosphatase and Tensin Homolog (PTEN)/ Phosphatidylinositol 3-Kinase (PI3K) and Protein Kinase B (AKT) Signaling Pathway

2020 ◽  
Vol 10 (5) ◽  
pp. 719-723
Author(s):  
Xiaofang Tao ◽  
Nianhua Fei
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Plaque Formation ◽  
Akt Signaling Pathway ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
Sd Rats ◽  
Vsmcs Proliferation

Abnormal vascular smooth muscle cells (VSMCs) proliferation is the pathological basis of atherosclerosis (AS) pathogenesis. miR-223 is abnormally expressed in AS plaques and affects the proliferation of VSMCs, but the mechanism of miR-223 affecting the proliferation of VSMCs is unclear. Our study intends to investigate the mechanism of miR-223 in VSMCs proliferation and AS formation. Healthy SD rats and miR-223 knockout SD rats took high-fat diet to induce AS model. Oil red O staining was done to observe AS formation. miR-223 mimics/NC was transferred to VSMCs followed by analysis of miR-214 expression by real-time PCR, cell proliferation by CCK8 assay, phosphatase and tensin homolog gene (PTEN) level by Western blot detection. Compared with control group, after knocking out miR-223, the AS level was significantly decreased and PTEN expression was significantly elevated (P < 0 05). After transfection of miR-223 mimics into VSMCs, PTEN expression protein was significantly decreased and the number of cells was increased (P < 0 05). In addition, the luciferase signal of miR-223 mimics and pmirGLO-PTEN-3 UTR-wt co-transfection group was significantly reduced (P < 0 05). miR-223 promotes VSMCs proliferation and AS plaque formation by targeting PTEN/PI3K/Akt signaling pathway.

Di-(2-ethylhexyl) phthalate could disrupt the insulin signaling pathway in liver of SD rats and L02 cells via PPARγ

2017 ◽  
Vol 316 ◽  
pp. 17-26 ◽  
Author(s):  
Wang Zhang ◽  
Xin -yue Shen ◽  
Wen-wen Zhang ◽  
Hao Chen ◽  
Wei-ping Xu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Insulin Signaling ◽  
Insulin Signaling Pathway ◽  
Sd Rats ◽  
Ethylhexyl Phthalate ◽  
L02 Cells

scholarly journals Effects of TLR3 and TLR9 Signaling Pathway on Brain Protection in Rats Undergoing Sevoflurane Pretreatment during Cardiopulmonary Bypass

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Zhou Nan ◽  
Zhou Jin ◽  
Cao Huijuan ◽  
Zhang Tiezheng ◽  
Chen Keyan
Keyword(s):  
Brain Injury ◽  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
Sham Group ◽  
Brain Protection ◽  
Rat Models ◽  
Tlr9 Expression ◽  
Sd Rats ◽  
Tlr3 Expression ◽  
Tlr9 Signaling

Objective. To investigate the effects of TLR3 and TLR9 signaling pathway on brain injury during CPB in rats pretreated with sevoflurane and its possible molecular mechanism. Methods. SD rats were randomly assigned to sham group, CPB group, and Sev group. Brain tissue was obtained at before CPB (T0), at CPB for 30 minutes (T1), 1 hour after CPB (T3), and 3 hours after CPB (T5). ELISA was used to measure S100-β and IL-6. Western blot was utilized to determine TLR3 and TLR9 expression. TUNEL was applied to detect neuronal apoptosis. Results. Compared with CPB group, at T1, at termination after 1 hour of CPB (T2), T3, 2 hours after CPB (T4) and T5, S100-β and IL-6 decreased in Sev group. Compared with CPB group, IFN-β were increased in Sev group, except T0. Compared with CPB group, TLR3 expression increased, and TLR9 and NF-κB decreased in Sev group. The apoptotic neurons were less in Sev group than in CPB group (P<0.05). Conclusion. Sevoflurane intervention can activate TLR3 and TLR9 signaling pathway, upregulate TLR3 expression and downstream TRIF expression, decrease TLR9 expression, and downregulate downstream NF-κB expression in CPB rat models, thereby mitigating brain injury induced by inflammatory response during CPB.

scholarly journals Oral administration of polystyrene microplastics for 2 weeks induces chronic constipation in ICR mice

2021 ◽  
Author(s):  
Yun Ju Choi ◽  
Jun Woo Park ◽  
Ji Eun Kim ◽  
Su Jin Lee ◽  
Jeong Eun Gong ◽  
...  
Keyword(s):  
Oral Administration ◽  
Signaling Pathway ◽  
Transverse Colon ◽  
Chronic Constipation ◽  
Molecular Mechanisms ◽  
Chloride Ion ◽  
Mucin Secretion ◽  
Icr Mice ◽  
Water Transportation ◽  
Gi Motility

Abstract Objective: Indirect evidence has determined the possibility that microplastics (MP) induce constipation, although direct scientific proof for constipation induction in animals remains unclear. Thus, this study is aimed to investigate whether oral administration of polystyrene MP causes constipation.Methods: An alteration in the constipation parameters and their molecular mechanisms was analyzed in ICR mice treated with 0.5 μm polystyrene (PS)-MP for 2 weeks. Results: Significant alterations in water consumption, stool weight, stool water contents, and stool morphology were detected in MP treated ICR mice, as compared to Vehicle treated group. Also, the gastrointestinal (GI) motility and intestinal length were decreased, while the histopathological structure and cytological structure of the transverse colon were remarkably altered in treated mice. Mice exposed to MP also showed a significant decrease in the GI hormone concentration, muscarinic acetylcholine receptors (mAChRs) expression and their downstream signaling pathway, as well as mucin secretion and transcription of the MUC1, MUC2 and Klf4 genes. Subsequent to MP treatment, concentrations of chloride ion and expressions of its channel (CFTR and CIC-2) were decreased, whereas expressions of AQP3 and 8 for water transportation were downregulated by activation of the MAPK/NF-kB signaling pathway. These regulation on water and chloride transportation were verified in intestinal epithelioid cell line (IEC18) after MP treatment. Conclusion: These results are the first to suggest that oral administration of PS-MP induces chronic constipation through the dysregulation of GI motility, mucin secretion, and chloride ion and water transportation in the transverse colon.

scholarly journals Laxative Effects of Phlorotannins Derived from Ecklonia cava on Loperamide-Induced Constipation in SD Rats

Molecules ◽  
2021 ◽  
Vol 26 (23) ◽  
pp. 7209
Author(s):  
Ji-Eun Kim ◽  
Yun-Ju Choi ◽  
Su-Jin Lee ◽  
Jeong-Eun Gong ◽  
You-Jung Jin ◽  
...  
Keyword(s):  
Gastrointestinal Motility ◽  
Water Channel ◽  
Treated Group ◽  
Fecal Microbiota ◽  
Mucin Secretion ◽  
Sd Rats ◽  
Cholinergic Regulation ◽  
Laxative Effects ◽  
Channel Expression ◽  
Muscarinic Cholinergic

This study investigated the laxative effects of phlorotannins (Pt) derived from Ecklonia cava (E. cave) on chronic constipation by evaluating alterations in stool parameters, gastrointestinal motility, histopathological structure, mucin secretion, gastrointestinal hormones, muscarinic cholinergic regulation, and fecal microbiota in SD rats with loperamide (Lop)-induced constipation subjected to Pt treatment. Stool-related parameters (including stool number, weight, and water contents), gastrointestinal motility, and length of intestine were significantly enhanced in the Lop+Pt-treated group as compared to the Lop+Vehicle-treated group. A similar recovery was detected in the histopathological and cytological structure of the mid-colon of Lop+Pt-treated rats, although the level of mucin secretion remained constant. Moreover, rats with Lop-induced constipation subjected to Pt treatment showed significant improvements in water channel expression, gastrointestinal hormone secretions, and expression of muscarinic acetylcholine receptors M2/M3 (mAChRs M2/M3) and their mediators of muscarinic cholinergic regulation. Furthermore, the Lop+Pt-treated group showed a significant recovery of Bifidobacteriaceae, Muribaculaceae, Clostridiaceae, and Eubacteriaceae families in fecal microbiota. Taken together, these results provide the first evidence that exposure of SD rats with Lop-induced constipation to Pt improves the constipation phenotype through the regulation of membrane water channel expression, GI hormones, the mAChR signaling pathway, and fecal microbiota.

scholarly journals Metformin attenuates LPS-induced neuronal injury and cognitive impairments by blocking NF-κB pathway

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Chenliang Zhou ◽  
Bo Peng ◽  
Zhenghui Qin ◽  
Wei Zhu ◽  
Cuiping Guo
Keyword(s):  
Synaptic Plasticity ◽  
Signaling Pathway ◽  
Hippocampal Neurons ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Neuronal Damage ◽  
Cognitive Impairments ◽  
Neuronal Injury ◽  
Sd Rats ◽  
Primary Hippocampal Neurons

Abstract Background Neuroinflammatory response is considered to be a high-risk factor for cognitive impairments in the brain. Lipopolysaccharides (LPS) is an endotoxin that induces acute inflammatory responses in injected bodies. However, the molecular mechanisms underlying LPS-associated cognitive impairments still remain unclear. Methods Here, primary hippocampal neurons were treated with LPS, and western blotting and immunofluorescence were used to investigate whether LPS induces neurons damage. At the same time, SD rats were injected with LPS (830 μg/Kg) intraperitoneally, and Open field test, Novel Objective Recognition test, Fear condition test were used to detect cognitive function. LTP was used to assess synaptic plasticity, and molecular biology technology was used to assess the NF-κB pathway, while ELISA was used to detect inflammatory factors. In addition, metformin was used to treat primary hippocampal neurons, and intraventricularly administered to SD rats. The same molecular technics, behavioral and electrophysiological tests were used to examine whether metformin could alleviate the LPS-associated neuronal damage, as well as synaptic plasticity, and behavioral alterations in SD rats. Results Altogether, neuronal damage were observed in primary hippocampal neurons after LPS intervention, which were alleviated by metformin treatment. At the same time, LPS injection in rat triggers cognitive impairment through activation of NF-κB signaling pathway, and metformin administration alleviates the LPS-induced memory dysfunction and improves synaptic plasticity. Conclusion These findings highlight a novel pathogenic mechanism of LPS-related cognitive impairments through activation of NF-κB signaling pathway, and accumulation of inflammatory mediators, which induces neuronal pathologic changes and cognitive impairments. However, metformin attenuates LPS-induced neuronal injury and cognitive impairments by blocking NF-κB pathway.

scholarly journals Quercetin promotes gastrointestinal motility and mucin secretion in loperamide-induced constipation of SD rats through regulation of the mAChRs downstream signal

2018 ◽  
Vol 56 (1) ◽  
pp. 309-317 ◽  
Author(s):  
Ji Eun Kim ◽  
Mi Rim Lee ◽  
Jin Ju Park ◽  
Jun Young Choi ◽  
Bo Ram Song ◽  
...  
Keyword(s):  
Gastrointestinal Motility ◽  
Mucin Secretion ◽  
Sd Rats
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