scholarly journals Laxative Effect of Spicatoside A by Cholinergic Regulation of Enteric Nerve in Loperamide-Induced Constipation: ICR Mice Model

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 896 ◽  
Author(s):  
Ji Kim ◽  
Ji Park ◽  
Mi Kang ◽  
Hyeon Choi ◽  
Su Bae ◽  
...  
Keyword(s):  
Chronic Constipation ◽  
Water Channel ◽  
Treated Group ◽  
Histological Structure ◽  
Neural Cells ◽  
Mice Model ◽  
Icr Mice ◽  
Cholinergic Regulation ◽  
Spicatoside A ◽  
Vehicle Treated Group

Researches on spicatoside A (SpiA)-containing natural products suggest the possibility of SpiA as a potential laxative to alleviate chronic constipation. However, no studies have been conducted with single compound administration of SpiA. To verify the laxative effects and mechanism of action of SpiA on chronic constipation, we investigated alterations in the excretion parameters, histological structure, and cholinergic regulation of the enteric nerve in the colons of Institute of Cancer Research (ICR) mice with loperamide (Lop)-induced constipation after exposure to 20 mg/kg of SpiA. Decrease in the number, weight and water contents of stools in the Lop+Vehicle treated group significantly recovered after SpiA treatment, and alterations in the histological structure and transmission electron microscopy (TEM) images were improved in the Lop+SpiA treated group. Similar recovery effects were observed in the ability for mucin secretion and expression of the membrane water channel gene (aquaporin 8, AQP8). Furthermore, significant improvements were observed in the acetylcholinesterase (AChE) activity and acetylcholine receptors’ (AChRs) downstream signaling pathway after treatment of SpiA. The levels of gastrointestinal (GI) hormones including cholecystokinin (CCK) and gastrin were also remarkably enhanced in the Lop+SpiA treated group as compared to the Lop+Vehicle treated group. The expression of receptor tyrosine kinase (C-kit) and protein gene product 9.5 (PGP9.5) in Cajal and neural cells, as well as the phosphorylation of myosin light chain (MLC) in smooth muscle cells, were recovered after SpiA exposure. Taken together, the results of the present study provide the first strong evidence that SpiA improves chronic constipation through muscarinic cholinergic regulation of the enteric nerve in a Lop-induced constipation ICR mice model.

scholarly journals Inflammatory response in the mid colon of ICR mice treated with polystyrene microplastics for two weeks

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Yun Ju Choi ◽  
Ji Eun Kim ◽  
Su Jin Lee ◽  
Jeong Eun Gong ◽  
You Jeong Jin ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Oral Administration ◽  
Treated Group ◽  
Nuclear Factor ◽  
Icr Mice ◽  
Pyrin Domain ◽  
Tnf Α ◽  
Vehicle Treated Group ◽  
Light Chain Enhancer ◽  
Necrosis Factor

Abstract Background The oral administration of polystyrene-microplastics (PS-MPs) causes chronic constipation of ICR mice, but there are no reports on their effects on the inflammatory response in the colon. To determine if the oral administration of MPs causes inflammation in the colon, the changes in the apoptosis-associated speck like protein containing a caspase recruitment domain (ASC)-inflammasome pathway, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway, and inflammatory cytokine expression were evaluated in the mid colon of ICR mice treated with 0.5 μm size PS-MPs for two weeks. Results The thicknesses of the mucosa, muscle, flat luminal surface, and crypt layer were decreased significantly (p < 0.01) in the mid colon of the MPs treated group compared to the Vehicle treated group. On the other hand, a remarkable increase in the expression levels of NOD-like receptor pyrin domain-containing protein (NLRP) 3, ASC, and Cleaved Caspase (Cas)-1 protein was observed in the MPs treated group. In addition, similar increasing pattern in the levels of p-NF-κB and phospho-inhibitory subunit of NF-κB (p-IkB) α protein was detected. Four inflammatory cytokines, including NF-κB, interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β, showed an increased expression level after the MPs treatment. Conclusions Therefore, the present study suggests that PS-MPs can be a novel cause of an inflammatory response in the mid colon of ICR mice.

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 Hydroalcoholic extract of Sargassum Oligocystum attenuates pentylenetetrazole-induced seizures by potentiating antioxidant activity in mice

2017 ◽  
Vol 04 (02) ◽  
pp. 159-166
Author(s):  
Ali Movahed ◽  
Mahbubeh Ghaderi ◽  
Adel Daneshi ◽  
Iraj Nabipour ◽  
Mojtaba Keshavarz
Keyword(s):  
Antioxidant Capacity ◽  
Treated Group ◽  
Neural Cells ◽  
Sod Activity ◽  
Hydroalcoholic Extract ◽  
New Antiepileptic Drugs ◽  
Total Antioxidant ◽  
Clonic Seizures ◽  
Vehicle Treated Group ◽  
One Way Anova

AbstractObjectives The aim of this study was to investigate the potential effects of Sargassum oligocystum extract on the pentylenetetrazole (PTZ) seizure and the contribution of antioxidant capacity of this alga to its antiepileptic effect.Methods A dose of 100 mg/kg PTZ was used to induce the seizure in the male albino mice. Extract of Sargassum oligocystum in four doses (100, 200, 400 and 600 mg/kg), diazepam (5 mg/kg) and the vehicle were used 30 min before the injection of PTZ (n = 8). The onsets of clonic and tonic-clonic seizures, as well as the latency of death of animals, were recorded and the total antioxidant capacity (TAC), Superoxide dismutase (SOD) activity and catalase level were measured. Data were analyzed using one-way ANOVA or Kruskal-Wallis tests.Results Sargassum oligocystum extract at the doses of 400 and 600 mg/kg significantly increased the latency of clonic and tonic-clonic seizures. Also, at the doses of 100, 200 and 400 mg/kg significantly increased the TAC. Moreover, Sargassum oligocystum at the doses of 200 and 400 mg/kg increased the SOD activity and at the doses of 400 and 600 mg/kg increased the catalase level in neural cells compared with the vehicle-treated group.Conclusion Sargassum oligocystum extract inhibited PTZ-induced seizure. Attenuation of oxidative stress may partly be responsible for the anticonvulsant effects of this alga in the PTZ-induced seizures. Therefore, marine algae, especially Sargassum oligocystum, may be a valuable target to discover new antiepileptic drugs.

scholarly journals Gynura procumbens Root Extract Ameliorates Ischemia-Induced Neuronal Damage in the Hippocampal CA1 Region by Reducing Neuroinflammation

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 181
Author(s):  
Woosuk Kim ◽  
Hyo Young Jung ◽  
Dae Young Yoo ◽  
Hyun Jung Kwon ◽  
Kyu Ri Hahn ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Neuronal Damage ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Biological Properties ◽  
Root Extract ◽  
Ischemic Damage ◽  
Neuroprotective Effects ◽  
Hippocampal Ca1 ◽  
Vehicle Treated Group

Gynura procumbens has been used in Southeast Asia for the treatment of hypertension, hyperglycemia, and skin problems induced by ultraviolet irradiation. Although considerable studies have reported the biological properties of Gynura procumbens root extract (GPE-R), there are no studies on the effects of GPE-R in brain damages, for example following brain ischemia. In the present study, we screened the neuroprotective effects of GPE-R against ischemic damage and neuroinflammation in the hippocampus based on behavioral, morphological, and biological approaches. Gerbils received oral administration of GPE-R (30 and 300 mg/kg) every day for three weeks and 2 h after the last administration, ischemic surgery was done by occlusion of both common carotid arteries for 5 min. Administration of 300 mg/kg GPE-R significantly reduced ischemia-induced locomotor hyperactivity 1 day after ischemia. Significantly more NeuN-positive neurons were observed in the hippocampal CA1 regions of 300 mg/kg GPE-R-treated animals compared to those in the vehicle-treated group 4 days after ischemia. Administration of GPE-R significantly reduced levels of pro-inflammatory cytokines such as interleukin-1β, -6, and tumor necrosis factor-α 6 h after ischemia/reperfusion. In addition, activated microglia were significantly decreased in the 300 mg/kg GPE-R-treated group four days after ischemia/reperfusion compared to the vehicle-treated group. These results suggest that GPE-R may be one of the possible agents to protect neurons from ischemic damage by reducing inflammatory responses.

scholarly journals Cissus Quadrangularis enhances UCP1 mRNA, indicative of white adipocyte browning and decreases central obesity in humans in a randomized trial

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Saimai Chatree ◽  
Chantacha Sitticharoon ◽  
Pailin Maikaew ◽  
Kitchaya Pongwattanapakin ◽  
Issarawan Keadkraichaiwat ◽  
...  
Keyword(s):  
Treated Group ◽  
Dependent Manner ◽  
Hip Circumference ◽  
White Adipocyte ◽  
Ppar Γ ◽  
White Adipocytes ◽  
Cissus Quadrangularis ◽  
Baseline Values ◽  
Dose Dependent ◽  
Vehicle Treated Group

AbstractObesity is associated with the growth and expansion of adipocytes which could be decreased via several mechanisms. Cissus Quadrangularis (CQ) extract has been shown to reduce obesity in humans; however, its effect on human white adipocytes (hWA) has not been elucidated. This study aimed to investigate the effects of CQ on obesity, lipolysis, and browning of hWA. CQ treatment in obese humans significantly decreased waist circumference at week 4 and week 8 when compared with the baseline values (p < 0.05 all) and significantly decreased hip circumference at week 8 when compared with the baseline and week 4 values (p < 0.05 all). Serum leptin levels of the CQ-treated group were significantly higher at week 8 compared to baseline levels (p < 0.05). In hWA, glycerol release was reduced in the CQ-treated group when compared with the vehicle-treated group. In the browning experiment, pioglitazone, the PPAR-γ agonist, increased UCP1 mRNA when compared to vehicle (p < 0.01). Interestingly, 10, 100, and 1000 ng/ml CQ extract treatment on hWA significantly enhanced UCP1 expression in a dose-dependent manner when compared to pioglitazone treatment (p < 0.001 all). In conclusion, CQ decreased waist and hip circumferences in obese humans and enhanced UCP1 mRNA in hWA suggestive of its action via browning of hWA.

Dose-dependent effect of ANG II-receptor antagonist on myocyte remodeling in rat cardiac hypertrophy

1997 ◽  
Vol 273 (4) ◽  
pp. H1824-H1831 ◽  
Author(s):  
Masakazu Obayashi ◽  
Masafumi Yano ◽  
Michihiro Kohno ◽  
Shigeki Kobayashi ◽  
Taketo Tanigawa ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Receptor Antagonist ◽  
Pressure Overload ◽  
Wall Stress ◽  
Treated Group ◽  
Left Ventricular ◽  
Abdominal Aortic ◽  
Significant Difference ◽  
And Function ◽  
Vehicle Treated Group

The goal of this study was to examine the effect of an angiotensin II type 1 (AT1)-receptor antagonist (TCV-116) on left ventricular (LV) geometry and function during the development of pressure-overload LV hypertrophy. A low (LD; 0.3 mg ⋅ kg−1 ⋅ day−1) or a high (HD; 3.0 mg ⋅ kg−1 ⋅ day−1) dose of TCV-116 was administered to abdominal aortic-banded rats over 4 wk, and hemodynamics and morphology were then evaluated. In both LD and HD groups, peak LV pressures were decreased to a similar extent compared with the vehicle-treated group but stayed at higher levels than in the sham-operated group. In the LD group, both end-diastolic wall thickness (3.08 ± 0.14 mm) and myocyte width (13.3 ± 0.1 μm) decreased compared with those in the vehicle-treated group (3.67 ± 0.19 mm and 15.3 ± 0.1 μm, respectively; both P < 0.05). In the HD group, myocyte length was further decreased (HD: 82.6 ± 2.6, LD: 94.1 ± 2.9 μm; P < 0.05) in association with a reduction in LV midwall radius (HD: 3.36 ± 0.12, LD: 3.60 ± 0.14 mm; P < 0.05) and peak midwall fiber stress (HD: 69 ± 8, LD: 83 ± 10 × 103dyn/cm2; P < 0.05). There was no significant difference in cardiac output among all groups. The AT1-receptor antagonist TCV-116 induced an inhibition of the development of pressure-overload hypertrophy. Morphologically, not only the width but also the length of myocytes was attenuated with TCV-116, leading to a reduction of midwall radius and hence wall stress, which in turn may contribute to a preservation of cardiac output.

scholarly journals Hydrogen Sulfide Prevents Mesenteric Adipose Tissue Damage, Endothelial Dysfunction, and Redox Imbalance From High Fructose Diet-Induced Injury in Aged Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Oleh Revenko ◽  
Yaroslav Pavlovskiy ◽  
Maryana Savytska ◽  
Antonina Yashchenko ◽  
Vasyl Kovalyshyn ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Hydrogen Sulfide ◽  
Tissue Damage ◽  
Redox Balance ◽  
Treated Group ◽  
Advanced Age ◽  
Aged Rats ◽  
Key Factors ◽  
High Fructose ◽  
Vehicle Treated Group

A high fructose diet (HFD) and advanced age are key factors for the gradual loss of physiological integrity of adipose tissue. Endogenous hydrogen sulfide (H2S) has beneficial effects on cytoprotection and redox balance. But its interactive effects on age-related damage of mesenteric vessels and connective and adipose tissues (MA) during HFD which could be the base of the development of effective physiological-based therapeutic strategy are unknown. The aim of study was to investigate age- and HFD-induced mesenteric cellular changes and activities of enzymes in H2S synthesis and to test the effects of sodium hydrosulfide (NaHS) which is considered an H2S donor on them. Adult and aged male rats on a standard diet (SD) or 4-week HFD were exposed to acute water-immersion restraint stress (WIRS) for evaluation of mesenteric subcellular and cellular adaptive responses by electron microscopy. The effects of exogenous NaHS (5.6 mg/kg/day for 9 days) versus vehicle on mesentery changes were investigated. Serum glucose level, thiobarbituric acid reactive substances (TBARS), and activities of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS), thiosulfate-dithiol sulfurtransferase (TST), and sulfite oxidase (SO) were examined by spectrophotometry. In both adult and aged SD groups, treatment with NaHS protected mesenteric cells after WIRS. In both groups, the treatment with NaHS also protected MA mitochondria, microvascular endothelial and sub-endothelial structures, and fibroblasts versus the vehicle-treated group that had signs of damage. HFD increased MA injury and mitochondrial changes in both aged and adult rats. HFD-associated malfunction is characterized by low activities of CSE, CBS, TST, SO, and increased TBARS. Finally, we demonstrated that pretreatment with NaHS inhibited MA and mitochondria alterations in aged rats exposed to HFD and WIRS, lowered TBARS, and enhanced H2S enzyme activities in contrast to the vehicle-treated group. Mitochondrial integrity alterations, endothelial damage, and redox imbalance are key factors for rat mesenteric adipose tissue damage during advanced age. These alterations and MA hypertrophic changes retain the central for HFD-induced damage. Moreover, H2S signaling contributes to MA and mitochondria redox balance that is crucial for advanced age and HFD injury. The future study of H2S donors’ effects on mesenteric cells is fundamental to define novel therapeutic strategies against metabolic changes.

Abstract 274: Polarization of Macrophage Confers Regenerative Capacity of Using Adipose Derived Regenerative Cells

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Satoshi Shintani ◽  
Yuuki Shimizu ◽  
Changning Hao ◽  
Kazuhisa Kondo ◽  
Ryo Hayashida ◽  
...  
Keyword(s):  
Umbilical Vein ◽  
Lymphatic Endothelial Cell ◽  
Limb Ischemia ◽  
Treated Group ◽  
Tube Formation ◽  
Mice Model ◽  
Ischemic Tissue ◽  
Regenerative Cells ◽  
Anti Inflammatory

Background: Recent studies indicate that macrophages (Mφ) have conflicting characteristics, pro-inflammatory or anti-inflammatory phenotypes. We previously demonstrated that implantation of adipose derived regenerative cells (ADRCs) augmented angiogenesis and lymph angiogenesis by modulating Mφ phenotype in animal models. We thus examine whether Mφ polarization to M2 type is important for neovascularization in various models. Methods and Results: Culture medium of ADRCs accelerated not only migration of human umbilical vein endothelial cells (HUVECs) but also polarization of M2 type Mφ. Cultured ADRCs released SDF-1, VEGF-C, and prostaglandin E2 (PGE2). PGE2 plays a key role for the polarization of M2 type Mφ via EP2/4 receptors. Matrigel tube formation assay conformed that ADRCs were incorporated into HUVEC network. In vivo, implanted ADRCs participated in the formation of capillary networks in ischemic tissue. In a mice model of tail lymphedema, the number of bone marrow derived Mφ was significantly higher in the ADRCs treated group than in the un-treated group. Most of Mφ differentiated into lymphatic endothelial cell in the edematous tissue and were polarized to M2 phenotype. Moreover, in a mice model of hind limb ischemia, implantation of ADRCs facilitated the polarization of Mφ into M2 type Mφ and up regulated IL-10 expression to suppress inflammation at ischemic tissue. Conclusion: Polarization into anti-inflammatory phenotype of Mφ plays an important role for regenerative action of ADRCs.

Abstract P422: Chronic Nicotine Exposure Increases Hematoma Growth Following Intracerebral Hemorrhage in Young Rats of Both Sexes

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Ashish K Rehni ◽  
Sunjoo Cho ◽  
Hever Navarro Quero ◽  
Miguel A Perez-pinzon ◽  
Ami P Raval ◽  
...  
Keyword(s):  
Treated Group ◽  
Vehicle Group ◽  
Female Group ◽  
Nicotine Exposure ◽  
Hematoma Volume ◽  
Treated Male ◽  
Male Group ◽  
Neurological Score ◽  
Hematoma Growth ◽  
Vehicle Treated Group

Spontaneous intracerebral hemorrhage (sICH) is the deadliest stroke subtype. There is strong evidence that tobacco use / smoking increases the risk of sICH, and some epidemiological studies have observed sex differences in sICH outcomes. However, systematic controlled studies on the effect of tobacco / smoking on post-sICH outcomes in both sexes are lacking. Therefore, we determined the effect of nicotine exposure on outcomes following collagenase-induced sICH both sexes. Young animals of both sexes were randomly divided into nicotine (4.5 mg / kg / day b.w.) and vehicle (saline) treatment groups (using osmotic pumps for two to three weeks). sICH in females was induced during the diestrous stage of estrous cycle. sICH was induced by collagenase injection into the right striatum and ~24 hours later, neurological scores were evaluated, rats were euthanized, and brains were sectioned to measure hematoma volume. Hematoma volumes for male rats was 42% higher (p<0.01) in the nicotine-treated group (139 ± 9 mm 3 , n=10) versus vehicle-treated group (98 ± 9 mm 3 , n=10). Hematoma volumes for female rats was 48% higher (p<0.01) in the nicotine-treated group (134 ± 11 mm 3 , n=10) versus vehicle-treated group (90 ± 7 mm 3 , n=10). Hematoma volumes for the vehicle and nicotine-treated male groups were not different from their respective female groups. The neurological score for the nicotine-treated male group (9.3 ± 0.6) was significantly higher (p<0.05) when compared to vehicle group (7.4 ± 0.6). The neurological score for the nicotine-treated female group (10.7 ± 0.2) was significantly higher (p<0.001) than the vehicle group (7.7 ± 0.7). The neurological score for the vehicle-treated male group was not different from its respective female group. However, the neurological score for the nicotine-treated male group was significantly lower than the female group. Our results show that chronic nicotine exposure increases hematoma volume post-sICH in animals of both sexes. Future studies into the mechanism of nicotine-induced increase in hematoma growth following sICH are required. Support: James and Esther King Biomedical Research Grant 9JK08

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