Dose dependent effects of antipsychotics оn prolactin and corticosterone concentration in phencyclidine animal model of schizophrenia

The effect of long-term methamphetamine (MAP) treatment on intracranial self-stimulation of the lateral hypotholamus and locomotor traces was assessed. An attempt was made to provide a useful animal model for understanding anhedonia, stereotypy, and reoccurrence of liability, which are analogous to symptoms of schizophrenia. The frequency of intracranial self-stimulation (ICSS) as used as a measure of the animals' "hedonic–anhedonic" state. Following long-term MAP treatment (3 mg/kg), rats gradually showed stereotyped behavior, and became inactive and unresponsive to ICSS. These behavioral changes and decreased ICSS lasted several weeks after cessation of chronic MAP treatment and seemed to suggest post-MAP chronic psychosis and (or) anhedonia, two of the negative symptoms of schizophrenia. The traces of rat behavior affected by chronic MAP treatment were classified into three types, peripheral, mixed, and fixed, occurring in a dose-dependent manner. Reverse tolerance, similar to the reoccurrence of schizophrenic symptoms, was observed as a fixed stereotypy associated with loss of ICSS. These abnormal phenomena were suppressed by pretreatment with haloperidol. In the present study, the combination of ICSS and locomotor trace affected by chronic MAP treatment was proposed as an animal model of schizophrenia and as a useful technique for gauging the effect of neuroleptics.Key words: self-stimulation, anhedonia, stereotypy, reverse tolerance, animal disease model, schizophrenia, methamphetamine.

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Botulinum Toxin Type A Intralesional Monotherapy for Treating Human Hypertrophic Scar in a Dose-dependent Manner: in an Animal Model

Journal of Plastic Reconstructive & Aesthetic Surgery ◽

10.1016/j.bjps.2021.03.062 ◽

2021 ◽

Author(s):

Yawei Li ◽

Xiaofeng Shan ◽

Qianying Mao ◽

Ruolan Xiang ◽

Zhigang Cai

Keyword(s):

Animal Model ◽

Botulinum Toxin ◽

Hypertrophic Scar ◽

Botulinum Toxin Type A ◽

Type A ◽

Botulinum Toxin Type ◽

Dependent Manner ◽

Dose Dependent

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Effect of hCMSCs and liraglutide combination in ALI through cAMP/PKAc/β-catenin signaling pathway

Stem Cell Research & Therapy ◽

10.1186/s13287-019-1492-6 ◽

2020 ◽

Vol 11 (1) ◽

Cited By ~ 7

Author(s):

Yun Feng ◽

Linlin Wang ◽

Xiaoying Ma ◽

Xiaotong Yang ◽

Ocholi Don ◽

...

Keyword(s):

Animal Model ◽

Western Blot ◽

Lavage Fluid ◽

Dependent Manner ◽

Chorionic Villi ◽

Airway Injury ◽

Camp Pathway ◽

Injury Model ◽

Glucagon Like Peptide 1 ◽

Dose Dependent

Abstract Background ALI/ARDS is the major cause of acute respiratory failure in critically ill patients. As human chorionic villi-derived MSCs (hCMSCs) could attenuate ALI in the airway injury model, and liraglutide, glucagon-like peptide 1 (GLP-1) agonist, possesses anti-inflammatory and proliferation promotion functions, we proposed to probe the potential combinatory effect of hCMSCs and liraglutide on ALI. Methods We examined the time- and dose-dependent manner of GLP-1R, SPC, Ang-1, and FGF-10 with LPS via western blot and qRT-PCR. Western blot and chromatin immunoprecipitation assay detected the effects of liraglutide on GLP-1R, SPC, Ang-1, and FGF-10 through PKAc/β-catenin pathway and cAMP pathway. In the ALI animal model, we detected the effects of MSC and liraglutide combination on ALI symptoms by H&E staining, western blot, ELISA assays, calculating wet-to-dry ratio of the lung tissue, and counting neutrophils, leukocytes, and macrophages in mouse bronchoalveolar lavage fluid (BALF). Results The data demonstrated that LPS reduced hCMSC proliferation and GLP-1R, SPC, Ang-1, and FGF-10 levels in a dose- and time-dependent manner. Liraglutide significantly dampened the reduction of GLP-1R, SPC, Ang-1, and FGF-10 and reversed the effect of LPS on hCMSCs, which could be regulated by GLP-1R and its downstream cAMP/PKAc/β-catenin-TCF4 signaling. Combination of hCMSCs with liraglutide showed more therapeutic efficacy than liraglutide alone in reducing LPS-induced ALI in the animal model. Conclusions These results reveal that the combination of hCMSCs and liraglutide might be an effective strategy for ALI treatment.

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ANTI-DIABETIC EFFECT OF A NOVEL NANO POLYMER OF THYMOL IN STREPTOZOTOCIN-INDUCED DIABETIC WISTAR RATS

International Journal of Applied Pharmaceutics ◽

10.22159/ijap.2019v11i5.34205 ◽

2019 ◽

pp. 81-89

Author(s):

ELAHE KARIMI ◽

SHAHRYAR ABBASI ◽

ALI AIDY ◽

HORI GHANEIALVAR ◽

SHAHRAM MOHAMMADPOUR ◽

...

Keyword(s):

Animal Model ◽

Biochemical Parameters ◽

Wistar Rats ◽

Liver Enzymes ◽

Serum Glucose ◽

Diabetic Rats ◽

Dependent Manner ◽

Elisa Kit ◽

Blood Biochemical ◽

Dose Dependent

Objective: The aim of this study was to evaluate the effect of thymol and thymol nano polymer on the blood biochemical parameters and anti-diabetic activity in Streptozotocin (STZ)-induced diabetic rats. Methods: The synthesized nano polymer (NP) was characterized by using different spectroscopy methods, such as IR, HNMR and CNMR. Loading and releasing of thymol were investigated by HPLC. Eleven groups of the Streptozotocin-induced diabetic and normal rats (overall 110 males) were tested through various biochemical factors such as: serum glucose, insulin, liver function-related enzymes including ALT, AST, ALP and bilirubin by ELISA kit methods. Results: It has shown that thymol nano polymer is desirable for transferring drug. The amount of thymol loaded on NP estimated at 43±2.5 %. Then, 65% of the loaded drug was released. LD50 for thymol and thymol nano polymer were 435 and 583 mg/kg, respectively. thymol nano polymer at doses of 30, 60 and 90 mg/kg, in a dose-dependent manner, reduced blood glucose, increased insulin levels, and controlled liver enzymes ALT, AST, ALP and bilirubin in the STZ-induced diabetic rats. Conclusion: The use of thymol nano polymer appears to be a new aspect concerning to protect diabetes-induced damage in the animal model.

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Dose-dependent effects of almitrine on hemodynamics and gas exchange in an animal model of acute lung injury

Intensive Care Medicine ◽

10.1007/s001340051178 ◽

2000 ◽

Vol 26 (4) ◽

pp. 434-441 ◽

Cited By ~ 10

Author(s):

A. Sommerer ◽

U. Kaisers ◽

R. Dembinski ◽

H. P. Bubser ◽

K. J. Falke ◽

...

Keyword(s):

Animal Model ◽

Acute Lung Injury ◽

Gas Exchange ◽

Lung Injury ◽

Dose Dependent

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Inhibition of murine erythroid colony formation in vitro by interferon gamma and correction by interferon receptor immunoadhesin

Blood ◽

10.1182/blood.v83.4.911.bloodjournal834911 ◽

1994 ◽

Vol 83 (4) ◽

pp. 911-915 ◽

Cited By ~ 1

Author(s):

RT Jr Means ◽

SB Krantz ◽

J Luna ◽

SA Marsters ◽

A Ashkenazi

Keyword(s):

Animal Model ◽

Interferon Gamma ◽

Colony Formation ◽

Interleukin 1 ◽

Inhibitory Effect ◽

Dependent Manner ◽

Ifn Gamma ◽

Dose Dependent

It has been previously reported that inhibition of human erythroid colony-forming units (CFU-E) in vitro by interleukin-1 (IL-1) is an indirect effect, occurring through the production of interferon gamma (IFN gamma). IFN gamma, in turn, inhibits CFU-E colony formation directly, and its inhibitory effect can be overcome by exposure to high concentrations of erythropoietin (EPO). To develop an in vitro animal model for investigating inhibition of erythropoiesis by IFN gamma, the effects of recombinant murine (rm) IFN gamma on highly purified CFU-E from the spleens of mice infected with the anemia strain of the Friend virus (FVA) were studied. rmIFN gamma inhibited CFU-E colony formation in a dose-dependent manner. This inhibition occurred with large (> or = 8 cell) colonies only; smaller colonies were not affected. The inhibitory effect was corrected to 72% of control by high EPO concentrations of 64 U/mL. Murine CFU-E were then cultured with rmIFN gamma in the presence of a soluble murine IFN gamma receptor fused to the hinge and Fc domains of the human IgG1 heavy chain (mIFN gamma R-IgG). Inhibition of CFU-E colony formation by rmIFN gamma (100 U/mL) was corrected by mIFN gamma R-IgG in a dose-dependent manner, with an approximate IC50 of 0.05 nmol/L, and complete or near complete correction at 0.5 nmol/L. Similarly, a human IFN gamma R-IgG greatly reduced the inhibitory effect of recombinant human IFN gamma on human CFU-E. These experiments provide an in vitro animal model for studying the inhibitory effects of IFN gamma on erythropoiesis and indicate that IFN gamma R-IgG may be a useful agent for reducing the toxicity of IFN gamma in vivo.

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AN IN VIVO MODEL FOR TESTING INHIBITION OF ARGININE-INDUCED INSULIN AND GLUCAGON RELEASE BY SOMATOSTATIN ANALOGS

Acta Endocrinologica ◽

10.1530/acta.0.0860833 ◽

1977 ◽

Vol 86 (4) ◽

pp. 833-841 ◽

Cited By ~ 11

Author(s):

Ariel Gordin ◽

Chester Meyers ◽

Akira Arimura ◽

David H. Coy ◽

Andrew V. Schally

Keyword(s):

Animal Model ◽

Somatostatin Analogs ◽

Insulin Level ◽

In Vivo Model ◽

Dependent Manner ◽

Glucagon Release ◽

Plasma Glucagon ◽

Quantitative Manner ◽

Dose Dependent

ABSTRACT An animal model for testing the in vivo potency of somatostatin analogs in inhibiting the release of insulin and glucagon is described. The secretion of these pancreatic hormones was stimulated in rat by infusion of arginine. The plasma insulin level increased almost to a maximum after an infusion of 10 min, while plasma glucagon rose more slowly, reaching its maximum only after a 30 min infusion. Concomitant infusion of graded doses of somatostatin (2.5, 10, 40 and 160 μg/100 g BW) for 30 min inhibited both insulin and glucagon release in a dose-dependent manner, enabling us to test somatostatin analogs for insulin and glucagon-suppressive activity in a semi-quantitative manner. Using this animal model, 3 analogs of somatostatin, [D-Cys14]-, [Ala2, D-Cys14]- and [D-Trp8, D-Cys14]somatostatin were tested in a 4-point assay. They all showed dissociated activity in inhibiting the secretion of glucagon more than that of insulin.

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