Effect of low-intensity focused ultrasound on endothelin-1, nitrogen monoxide and oxytocin receptor in the uterine tissues of Sprague-Dawley rats following abortion

AbstractExtensive studies on focused ultrasound (FUS)-mediated drug delivery through the blood–brain barrier have been published, yet little work has been published on FUS-mediated drug delivery through the blood-spinal cord barrier (BSCB). This work aims to quantify the delivery of the monoclonal antibody trastuzumab to rat spinal cord tissue and characterize its distribution within a model of leptomeningeal metastases. 10 healthy Sprague–Dawley rats were treated with FUS + trastuzumab and sacrificed at 2-h or 24-h post-FUS. A human IgG ELISA (Abcam) was used to measure trastuzumab concentration and a 12 ± fivefold increase was seen in treated tissue over control tissue at 2 h versus no increase at 24 h. Three athymic nude rats were inoculated with MDA-MB-231-H2N HER2 + breast cancer cells between the meninges in the thoracic region of the spinal cord and treated with FUS + trastuzumab. Immunohistochemistry was performed to visualize trastuzumab delivery, and semi-quantitative analysis revealed similar or more intense staining in tumor tissue compared to healthy tissue suggesting a comparable or greater concentration of trastuzumab was achieved. FUS can increase the permeability of the BSCB, improving drug delivery to specifically targeted regions of healthy and pathologic tissue in the spinal cord. The achieved concentrations within the healthy tissue are comparable to those reported in the brain.

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Superoxide Dismutase Expression in the Ovaries of Periodontitis Animal Models Induced by Porphyromonas gingivalis and Treated with Cassava Leaves Extract

Annals of Dentistry ◽

10.22452/adum.vol28no7 ◽

2021 ◽

Vol 28 ◽

pp. 40-46

Author(s):

Agustin Wulan Suci-Dharmayanti ◽

Ajeng Nurwahyuningtyas Anjani ◽

Ari Tri Wanodyo Handayani ◽

Zahreni Hamzah ◽

Zahara Meilawaty ◽

...

Keyword(s):

Animal Models ◽

Porphyromonas Gingivalis ◽

Reproductive Organs ◽

Sprague Dawley ◽

Sex Steroid Hormone ◽

Low Intensity ◽

Fertility Status ◽

Cassava Leaves ◽

Sprague Dawley Rats ◽

Female Reproductive Organs

The ovaries represent the female reproductive organs that determine the women's fertility status and their systemic and oral health, correlating to sex steroid hormone alteration. This study aimed to investigate the effect of cassava leaves extract treatment to SOD expression in the animal model-ovaries after Porphyromonas gingivalis injection. 15 female Sprague Dawley rats were used and divided into five groups: (1) control without cassava leaves extract treatment (C); (2) P. gingivalis without cassava leaves extract treatment (T1); (3) P. gingivalis and cassava leaves extract (T2); (4) P. gingivalis and vitamin C (T3); and (5) P. gingivalis and metronidazole (T4). Animal were euthanised at day seven after the initial treatment to collect ovaries. The ovaries sections were immunohistochemically stained to quantify SOD expression using light microscope while the Image J software was used to quantify the SOD expression. The results showed that all of the follicle types had the same intensity of SOD expression. Most of the follicles exhibited low intensity of SOD expression, except for atretic follicles. In conclusion, P. gingivalis and cassava leaves extract influenced SOD expression in the ovaries of animal models, which increased the SOD expression.

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17β-Estradiol modulates vasoconstriction induced by endothelin-1 following trauma-hemorrhage

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00809.2006 ◽

2007 ◽

Vol 292 (1) ◽

pp. H245-H250 ◽

Cited By ~ 18

Author(s):

Zheng F. Ba ◽

Ailing Lu ◽

Tomoharu Shimizu ◽

László Szalay ◽

Martin G. Schwacha ◽

...

Keyword(s):

Control Level ◽

No Synthase ◽

Sprague Dawley ◽

Response Curves ◽

Endothelin 1 ◽

Sprague Dawley Rats ◽

17Β Estradiol ◽

Synthase Inhibitor

Although endothelin-1 (ET-1) induces vasoconstriction, it remains unknown whether 17β-estradiol (E2) treatment following trauma-hemorrhage alters these ET-1-induced vasoconstrictive effects. In addition, the role of the specific estrogen receptor (ER) subtypes (ER-α and ER-β) and the endothelium-localized downstream mechanisms of actions of E2 remain unclear. We hypothesized that E2 attenuates increased ET-1-induced vasoconstriction following trauma-hemorrhage via an ER-β-mediated pathway. To study this, aortic rings were isolated from male Sprague-Dawley rats following trauma-hemorrhage with or without E2 treatment, and alterations in tension were determined in vitro. Dose-response curves to ET-1 were determined, and the vasoactive properties of E2, propylpyrazole triol (PPT, ER-α agonist), and diarylpropionitrile (DPN, ER-β agonist) were determined. The results showed that trauma-hemorrhage significantly increased ET-1-induced vasoconstriction; however, administration of E2 normalized ET-1-induced vasoconstriction in trauma-hemorrhage vessels to the sham-operated control level. The ER-β agonist DPN counteracted ET-1-induced vasoconstriction, whereas the ER-α agonist PPT was ineffective. Moreover, the vasorelaxing effects of E2 were not observed in endothelium-denuded aortic rings or by pretreatment of the rings with a nitric oxide (NO) synthase inhibitor. Cyclooxygenase inhibition with indomethacin had no effect on the action of E2. Thus, E2 administration attenuates ET-1-induced vasoconstriction following trauma-hemorrhage via an ER-β-mediated pathway that is dependent on endothelium-derived NO synthesis.

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Effects of endothelin in portal hypertensive rats

Clinical Science ◽

10.1042/cs0830165 ◽

1992 ◽

Vol 83 (2) ◽

pp. 165-170 ◽

Cited By ~ 19

Author(s):

Pi-Chin Yu ◽

Jon-Son Kuo ◽

Han-Chieh Lin ◽

May C. M. Yang

Keyword(s):

Blood Pressure ◽

Portal Hypertension ◽

Portal Vein ◽

Venous Pressure ◽

Portal Venous Pressure ◽

Portal Vein Ligation ◽

Sprague Dawley ◽

Hypertensive Rats ◽

Endothelin 1 ◽

Sprague Dawley Rats

1. Effects of endothelin-1 on systemic arterial blood pressure, heart rate and portal venous pressure were compared in normal Sprague-Dawley rats and rats with portal hypertension induced by CCl4 and partial portal vein ligation. 2. Endothelin-1 produced biphasic effects on systemic blood pressure and portal venous pressure in all three groups of rats. However, the magnitude of the changes in blood pressure was less in portal hypertensive rats. 3. The ability of endothelin-1 to increase the portal venous pressure was also significantly diminished in portal hypertensive rats. On the other hand, the initial decrease in portal pressure was augmented in rats with partial portal vein ligation, and disappeared at higher dosage in CCl4-treated rats. 4. In accordance with the pressure recording in vivo, the dose-response vasoconstrictive activity of endothelin-1 was significantly attenuated in the intrahepatic vasculature. 5. The plasma immunoreactive endothelin concentration was significantly higher (5.55 ± 0.81 fmol/ml) in Sprague-Dawley rats than in CCl4-treated rats (2.83 ± 0.56 fmol/ml) and rats with partial portal vein ligation (2.68 ± 0.53 fmol/ml). 6. It was concluded that a lower plasma level of endothelin and a reduced vascular responsiveness may contribute, at least in part, to the hyperdynamics of portal hypertension.

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Dose-Dependent Effects of Endothelin-1 on Retinal and Optic Nerve Morphology in Sprague Dawley Rats

Neurochemical Journal ◽

10.1134/s1819712419010045 ◽

2019 ◽

Vol 13 (1) ◽

pp. 73-80 ◽

Cited By ~ 1

Author(s):

Natasha Najwa Nor Arfuzir ◽

Renu Agarwal ◽

Igor Iezhitsa ◽

Puneet Agarwal ◽

Nafeeza Mohd Ismail

Keyword(s):

Optic Nerve ◽

Sprague Dawley ◽

Endothelin 1 ◽

Sprague Dawley Rats ◽

Dose Dependent

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Enalapril attenuates endothelin-1-induced hypertension via increased kinin survival

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00027.2003 ◽

2003 ◽

Vol 284 (6) ◽

pp. H1899-H1903 ◽

Cited By ~ 9

Author(s):

Ahmed A. Elmarakby ◽

Peter Morsing ◽

David M. Pollock

Keyword(s):

Angiotensin Ii ◽

Receptor Antagonist ◽

Neutral Endopeptidase ◽

Sprague Dawley ◽

Angiotensin Ii Receptor ◽

Angiotensin Ii Receptor Antagonist ◽

Endothelin 1 ◽

Sprague Dawley Rats ◽

Vasodilator Activity ◽

Induced Hypertension

Recent studies have shown that angiotensin-converting enzyme (ACE) inhibitors attenuate endothelin-1 (ET-1)-induced hypertension, but the mechanisms for this effect have not been clarified. Initial experiments were conducted to contrast the effect of the ACE inhibitor enalapril, the combined ACE-neutral endopeptidase inhibitor omapatrilat, and the angiotensin II receptor antagonist candesartan on the hypertensive and renal response to ET-1 in anesthetized Sprague-Dawley rats. Acute intravenous infusion of ET-1 (10 pmol · kg−1 · min−1) for 60 min significantly increased mean arterial pressure (MAP) from 125 ± 8 to 145 ± 8 mmHg ( P < 0.05) and significantly decreased glomerular filtration rate (GFR) from 0.31 ± 0.09 to 0.13 ± 0.05 ml · min−1 · 100 g kidney wt−1. Pretreatment with enalapril (10 mg/kg iv) before ET-1 infusion inhibited the increase in MAP (121 ± 4 vs. 126 ± 4 mmHg) before and during ET-1 infusion, respectively ( P < 0.05) without blocking the effect of ET-1 on GFR. In contrast, neither omapatrilat (30 mg/kg) nor candesartan (10 mg/kg) had any effect on ET-1-induced increases in MAP or decreases in GFR. To determine whether the effect of enalapril was due to the decrease in angiotensin II or increase in kinin formation, rats were given REF-000359 (1 mg/kg iv), a selective B2 receptor antagonist, with or without enalapril before ET-1 infusion. REF-000359 completely blocked the effect of enalapril on ET-1 infusion (MAP was 117 ± 5 vs. 135 ± 5 mmHg before and during ET-1 infusion, respectively, P < 0.05). REF-000359 alone had no effect on the response to ET-1 infusion (MAP was 117 ± 4 vs. 144 ± 4 mmHg before and during ET-1 infusion, respectively, P < 0.05). REF-000359 with or without enalapril had no significant effect on the ability of ET-1 infusion to decrease GFR. These findings support the hypothesis that decreased catabolism of bradykinin and its subsequent vasodilator activity oppose the actions of ET-1 to increase MAP.

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Increased Activity of the Intracardiac Oxytocinergic System in the Development of Postinfarction Heart Failure

BioMed Research International ◽

10.1155/2016/3652068 ◽

2016 ◽

Vol 2016 ◽

pp. 1-7 ◽

Cited By ~ 5

Author(s):

Agnieszka Wsol ◽

Kaja Kasarello ◽

Marek Kuch ◽

Kamila Gala ◽

Agnieszka Cudnoch-Jedrzejewska

Keyword(s):

Heart Failure ◽

Mrna Expression ◽

Protein Level ◽

Oxytocin Receptor ◽

Sprague Dawley ◽

Rt Pcr ◽

Sham Surgery ◽

Sprague Dawley Rats ◽

The Right ◽

Increased Activity

Aim.The present study was designed to test the hypothesis that the development of postinfarction heart failure is associated with a change of activity of the intracardiac oxytocinergic system.Methods.Experiments were performed on male Sprague-Dawley rats subjected to myocardial infarction or sham surgery. Four weeks after the surgery, blood samples were collected and the samples of the left ventricle (LV) and right ventricle (RV) were harvested for evaluation of the mRNA expression (RT-PCR) of oxytocin (OT), oxytocin receptor (OTR), natriuretic peptides, and the level of OT and OTR protein (ELISA). The concentration of N-terminal B-type natriuretic peptide was measured to determine the presence of heart failure.Results.Plasma NT-proBNP concentration was higher in the infarcted rats. In the infarcted rats, the expression of OT mRNA and the OT protein level were higher in the RV. There were no significant differences between infarcted and noninfarcted rats in the expression of OT mRNA and in the OT protein level in the fragments of the LV. In both the left and the right ventricles, OTR mRNA expression was lower but the level of OTR protein was higher in the infarcted rats.Conclusions.In the present study, we indicate that postinfarction heart failure is associated with an increased activity of the intracardiac oxytocinergic system.

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