Changes in nitric oxide, zinc and metallothionein levels in limbic regions at pre-pubertal and post-pubertal ages presented in an animal model of schizophrenia

2021 ◽  
Vol 111 ◽  
pp. 101889
Author(s):  
Israel Camacho-Abrego ◽  
Sonia Irais González-Cano ◽  
Patricia Aguilar-Alonso ◽  
Eduardo Brambila ◽  
Fidel de la Cruz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Limbic Regions

scholarly journals Anti-Inflammatory Effect of Phytoncide in an Animal Model of Gastrointestinal Inflammation

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1895
Author(s):  
Azra Memon ◽  
Bae Yong Kim ◽  
Se-eun Kim ◽  
Yuliya Pyao ◽  
Yeong-Geun Lee ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Gastric Ulcer ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Inos Expression ◽  
Gastrointestinal Inflammation ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Inflammatory Effect

Background: Phytoncide is known to have antimicrobial and anti-inflammatory properties. Purpose: This study was carried out to confirm the anti-inflammatory activity of two types of phytoncide extracts from pinecone waste. Methods: We made two types of animal models to evaluate the efficacy, an indomethacin-induced gastroenteritis rat model and a dextran sulfate sodium-induced colitis mouse model. Result: In the gastroenteritis experiment, the expression of induced-nitric oxide synthase (iNOS), a marker for inflammation, decreased in the phytoncide-supplemented groups, and gastric ulcer development was significantly inhibited (p < 0.05). In the colitis experiment, the shortening of the colon length and the iNOS expression were significantly suppressed in the phytoncide-supplemented group (p < 0.05). Conclusions: Through this study, we confirmed that phytoncide can directly inhibit inflammation in digestive organs. Although further research is needed, we conclude that phytoncide has potential anti-inflammatory properties in the digestive tract and can be developed as a functional agent.

scholarly journals Effect of Low-Frequency Therapeutic Ultrasound on Induction of Nitric Oxide in CKD: Potential to Prevent Acute Kidney Injury

2020 ◽  
Vol 6 (6) ◽  
pp. 453-460
Author(s):  
Michael W. Dae ◽  
Kathleen D. Liu ◽  
Richard J. Solomon ◽  
Dong W. Gao ◽  
Carol A. Stillson
Keyword(s):  
Nitric Oxide ◽  
Acute Kidney Injury ◽  
Animal Model ◽  
Blood Flow ◽  
Radionuclide Imaging ◽  
Therapeutic Ultrasound ◽  
Low Frequency ◽  
Kidney Injury ◽  
Large Animal Model ◽  
Large Animal

<b><i>Introduction:</i></b> Post-contrast acute kidney injury (PC-AKI) develops in a significant proportion of patients with CKD after invasive cardiology procedures and is strongly associated with adverse outcomes. <b><i>Objective:</i></b> We sought to determine whether increased intrarenal nitric oxide (NO) would prevent PC-AKI. <b><i>Methods:</i></b> To create a large animal model of CKD, we infused 250 micron particles into the renal arteries in 56 ± 8 kg pigs. We used a low-frequency therapeutic ultrasound device (LOTUS – 29 kHz, 0.4 W/cm<sup>2</sup>) to induce NO release. NO and laser Doppler probes were used to assess changes in NO content and blood flow. Glomerular filtration rate (GFR) was measured by technetium-diethylene-triamine-pentaacetic acid (Tc-99m-DTPA) radionuclide imaging. PC-AKI was induced by intravenous infusion of 7 cm<sup>3</sup>/kg diatrizoate. In patients with CKD, we measured GFR at baseline and during LOTUS using Tc-99m--DTPA radionuclide imaging. <b><i>Results:</i></b> In the pig model, CKD developed over 4 weeks (serum creatinine [Cr], mg/dL, 1.0 ± 0.2–2.6 ± 0.9, <i>p</i> &#x3c; 0.01, <i>n</i> = 12). NO and renal blood flow (RBF) increased in cortex and medulla during LOTUS. GFR increased 75 ± 24% (<i>p</i> = 0.016, <i>n</i> = 3). PC-AKI developed following diatrizoate i.v. infusion (Cr 2.6 ± 0.7 baseline to 3.4 ± 0.6 at 24 h, <i>p</i> &#x3c; 0.01, <i>n</i> = 3). LOTUS (starting 15 min prior to contrast and lasting for 90 min) prevented PC-AKI in the same animals 1 week later (Cr 2.5 ± 0.4 baseline to 2.6 ± 0.7 at 24 h, <i>p</i> = ns, <i>n</i> = 3). In patients with CKD (<i>n</i> = 10), there was an overall 25% increase in GFR in response to LOTUS (<i>p</i> &#x3c; 0.01). <b><i>Conclusions:</i></b> LOTUS increased intrarenal NO, RBF, and GFR and prevented PC-AKI in a large animal model of CKD, and significantly increased GFR in patients with CKD. This novel approach may provide a noninvasive nonpharmacological means to prevent PC-AKI in high-risk patients.

scholarly journals Effects of Chinese Formula Jueyin Granules on Psoriasis in an Animal Model

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Tian Ma ◽  
Wen-cheng Jiang ◽  
Xin Li ◽  
Jie Chen ◽  
Tie-jun Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Epithelial Cells ◽  
Mouse Model ◽  
Granular Layer ◽  
Granular Cell ◽  
Epidermal Hyperplasia ◽  
Elisa Method ◽  
Vaginal Epithelial Cells ◽  
Cell Layers

Although Traditional Chinese medicine (TCM) is known to be effective for psoriasis patients, the responsible mechanisms still remain poorly understood. In this study, we aimed to evaluate the effect of one formula, named Jueyin granules (JYG) in the mouse model of the vaginal epithelium and tail epidermis. Additionally, we also determined the anti-inflammatory effects of JYG in an imiquimod- (IMQ-) induced psoriasis-like skin mouse model. Our results show that JYG can attenuate the IMQ-induced psoriasis-like inflammation, accompanied with increased epidermal hyperplasia. We also measured estrogenic stage mitosis of vaginal epithelial cells and the formation of granular cell layers in male mouse tails per 100 scales, as well as the tissue nitric oxide (NO) and malondialdehyde (MDA) levels using the ELISA method. The results suggest that JYG significantly inhibited mitosis in mouse vaginal epithelial cells, promoted the formation of the squamous epidermal granular layer in mice tails, and reduced the levels of NO and MDA in an imiquimod-induced psoriasis-like skin mouse model after 14 d (P<0.05). These results demonstrate that JYG might be an effective clinical treatment for psoriasis and the effects may be related to inhibited keratinocytes proliferation, improved parakeratotic epidermal cells, and reduced expression of NO and MDA.

scholarly journals The Role of Nitric Oxide in Resolution of Vasospasam Corresponding with Cerebral Vasospasms after Subarachnoid Haemorrhage: Animal Model

2008 ◽  
Vol 8 (2) ◽  
pp. 177-182
Author(s):  
Kemal Dizdarević
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Subarachnoid Haemorrhage ◽  
Cerebral Vasospasm ◽  
Subarachnoid Space ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Control Group ◽  
Blood Products

Intracranial aneurysmal rupture is the common cause of spontaneous subarachnoid haemorrhage (SAH). This haemorrhage is typically diffuse and located in extracerebral subarachnoid space in which main cerebral arterial branches are situated. The intimate and long-term contact of arterial wall and blood products in the closed space causes the cerebral vasospasm as a serious and frequent complication of SAH. It is connected with significant morbidity and mortality due to developing of focal cerebral ischaemia and subsequently cerebral infarction. The aim of our experimental research was to create the animal model of vasospasm using the femoral artery due to examination of reduced basic dilator activity cause in arterial wall after SAH. The important characteristic of major cerebral arteries is their localization in the closed subarachnoid space which enables their to have long-term contact with blood products after haemorrhage. Thirty six femoral arteries (FA) of eighteen female rats weighing about 300 g were used. In vivo, femoral arteries are microsurgically prepared in both inguinal regions in all rats. Eighteen arteries were encompassed by polytetrafluoroethylene (PTFE) material forming closed tube and autologous blood was injected in the tube around the arterial wall. Additional eighteen arteries, as a control group, were also put in PTFE tube but without exposing to the blood. All rats are left to live for eight days. Afterwards, rats were sacrificed and their arteries were in vitro examined including an isometric tension measurement and histological changes analysis. The tension was measured during application of vasoconstrictors and vasodilatators (nitric oxide, NO). FA exposed to periadventitial blood exhibit hyper reactivity to constrictors (KCl, phenylephrine, acetylcholine) compared to control group. It was also found that NO donor (sodium nitroprusside) diminished arterial spasm induced by blood and vasoconstrictors. In conclusion, FA can be used as a model for vasospasm correlating with cerebral vasospasm after SAH and therefore this model can be utilized in future experiments assessing cerebral vasospasm. The reduced basic dilator activity of spastic femoral artery is caused by an absence of gaseous messenger NO next to the arteries but not by diminished response vasculature to NO. Absence of NO after SAH probably causes the reduced basic dilator activity of cerebral arteries as well. The guanylate-cyclase level in the arterial wall is consequently reduced after SAH primary due to absence of NO but not due to direct reduction of enzyme activities caused by process of blood degradation inside of subarachnoid space.

Role of Nitric Oxide in the Enhancement of Pentylenetetrazole-Induced Seizures Caused by Shigella dysenteriae

1999 ◽  
Vol 67 (12) ◽  
pp. 6364-6368 ◽  
Author(s):  
Judith Balter-Seri ◽  
Yael Yuhas ◽  
Abraham Weizman ◽  
Yehuda Nofech-Mozes ◽  
Elizabeth Kaminsky ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Potent Inhibitor ◽  
Elevated Serum ◽  
Selective Inhibitor ◽  
No Synthase ◽  
Shigella Dysenteriae ◽  
Contrast Injection ◽  
The Mean

ABSTRACT Convulsions and encephalopathy are frequent complications of childhood shigellosis. We studied the role of nitric oxide (NO) inShigella-related seizures in an animal model. Pretreatment of mice with Shigella dysenteriae 60R sonicate elevated serum NO levels and enhanced the convulsive response to pentylenetetrazole (PTZ), as indicated by a higher mean convulsion score and a higher number of mice responding with seizures. Treatment of the mice with S-methylisothiourea sulfate (SMT), a potent inhibitor of inducible NO synthase (NOS), prevented the elevation of serum NO levels and concomitantly reduced the enhanced response to PTZ. The mean convulsion scores were 0.7, 0.7, 1.3, and 0.8 for mice treated with saline, saline and SMT, S. dysenteriae 60R sonicate, and S. dysenteriae60R sonicate with SMT, respectively (P = 0.001 for 60R sonicate versus saline and P = 0.013 for 60R sonicate versus 60R sonicate with SMT). The corresponding seizure rates were 40, 44, 75, and 47% for saline, saline with SMT, S. dysenteriae 60R sonicate, and S. dysenteriae 60R sonicate with SMT, respectively (P = 0.0004 for 60R sonicate versus saline and P = 0.005 for 60R sonicate versus 60R sonicate with SMT). In contrast, injection of N-nitro-l-arginine, a selective inhibitor of constitutive NOS, neither abolished the elevation of serum NO nor attenuated the enhancement of seizures. These findings indicate that NO, induced by S. dysenteriae 60R sonicate, is involved in enhancing the susceptibility to seizures caused by S. dysenteriae.

Sign in / Sign up

Export Citation Format

Share Document