scholarly journals Anxiety mouse model was constructed employing single intraperitoneal injection of m-Chlorophenpiperazine

2021 ◽  
Author(s):  
mai jia li ◽  
tian yuan Ye ◽  
dong mei Qi ◽  
xiao rui Cheng ◽  
xi jian Liu
Keyword(s):  
Mouse Model ◽  
Intraperitoneal Injection ◽  
Tail Flick ◽  
Icr Mice ◽  
Athletic Ability ◽  
Single Intraperitoneal Injection ◽  
Immobility Time ◽  
Significant Difference ◽  
Step Down ◽  
Light Side

Abstract Background Anxiety disorder is a common mental disorder. It is necessary to establish a rapid, stable and specific anxiety model to provide theoretical basis for further research on the pathogenesis of anxiety and drug development. Aim Establish a rapid, stable, specific anxiety model. Methods A single intraperitoneal injection of m-chlorophenylpipera-zine(mCPP) (1, 2, 4 mg/kg) was given to male ICR mice to establish an anxiety model, and the effects of mCPP on anxiety behavior, pain, athletic ability, passive avoidance response ability and depressive behavior of male ICR mice were evaluated. Results A single intraperitoneal injection of mCPP shortened time in open arms and decreased the percentage of time in open arms of mice in elevated plus-maze test, mCPP also shortened center zone distance and reduced the number of entries to central zone in open field test. Moreover, mCPP reduced head-dip counts and increased head-dip latency of mice in hole-board test. After administrated with a single intraperitoneal injection of mCPP for 24h, the mice showed no significant difference for the entry into the light side and the percentage of time in light side of light-dark box test. A single intraperitoneal injection of mCPP had no effects on tail flick latency, rotating time, number of errors and the step-down latency, the immobility time of mice in tail-flick test, rotarod test, step-down test and TST respectively. Conclusion A rapid, stable and specific anxiety mouse model can be constructed by using a single intraperitoneal injection of mCPP.

scholarly journals The role of bacteriophages in the complex treatment of peritonitis of appendicular origin (experimental study)

2017 ◽  
Vol 10 (4) ◽  
pp. 265-268
Author(s):  
Evgeny Mikhailovich Mokhov ◽  
Artem Mikhailovich Morozov ◽  
Victor Alekseevich Kadykov ◽  
Elshad Magomedovich Askerov ◽  
Nina Evgenievna Serova
Keyword(s):  
Surgical Treatment ◽  
Postoperative Complications ◽  
Acute Appendicitis ◽  
Intraperitoneal Injection ◽  
Abdominal Cavity ◽  
Experimental Studies ◽  
Morphological Data ◽  
White Rats ◽  
Single Intraperitoneal Injection ◽  
Significant Difference

Relevance: with the management of laparoscopic methods of surgical treatment of acute appendicitis, the problem of the occurrence of early postoperative complications has not changed at present, which makes it necessary to carry out preventive measures. Objective: to study the possibility of improving the results of surgical treatment of peritonitis, the most frequent complication of acute appendicitis, by reducing the number of postoperative complications of infectious genesis. Methods: Studies were performed on 47 non-linear white rats weighing 200-250 grams by modelling peritonitis using the biological model as an example, followed by antibiotic therapy and combination therapy using bacteriophages. To model peritonitis, the infection of the abdominal cavity with the E. coli strain 25922 was used. The laboratory animals were divided into 3 groups: the first group was control group, the second group received treatment in the form of a single intraperitoneal injection of Cefipime, the third group received treatment as a single intraperitoneal injection of the Sextapage. Results: the evaluation of the methods was carried out on the basis of the study of the clinical picture of the course of peritonitis in experimental animals, the data of pathomorphological and histological examination of the sectional peritoneum. As a result of experimental studies, there was no significant difference in the methods of perioperative prevention of complications of acute appendicitis, which makes it possible to perform monotherapy with bacteriophages. Phages in comparison with antibiotics have no less therapeutic efficacy. Conclusions: Thus, our experimental studies revealed completely satisfactory results of monotherapy of experimental peritonitis with a bacteriophage. According to the morphological data, the inflammatory process in the abdominal cavity is stopped by the phage fast enough and there is a tendency for a faster fading of the inflammation than in the treatment with antibiotics.

scholarly journals Downregulation of nNOS and synthesis of PGs associated with endotoxin-induced delay in gastric emptying

2002 ◽  
Vol 283 (6) ◽  
pp. G1360-G1367 ◽  
Author(s):  
Sara Calatayud ◽  
Eugenia García-Zaragozá ◽  
Carlos Hernández ◽  
Elsa Quintana ◽  
Vicente Felipo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Emptying ◽  
Methyl Ester ◽  
Intraperitoneal Injection ◽  
Delayed Gastric Emptying ◽  
Single Intraperitoneal Injection ◽  
Inos Inhibitor ◽  
Oxide Synthase ◽  
Experimental Group ◽  
Inducible Nos

A single intraperitoneal injection of endotoxin (40 μg/kg) significantly delayed gastric emptying of a solid nutrient meal. Blockade of nitric oxide synthase (NOS) with 30 mg/kg ip N G-nitro-l-arginine methyl ester or 20 mg/kg ip 7-nitroindazole [neuronal NOS (nNOS) inhibitor] significantly delayed gastric emptying in control animals but failed to modify gastric emptying in endotoxin-treated rats. Administration of 2.5, 5, and 10 mg/kg ip N 6-iminoethyl-l-lysine [inducible NOS (iNOS) inhibitor] had no effect in either experimental group. Indomethacin (5 mg/kg sc), NS-398 (cyclooxygenase-2 inhibitor; 10 mg/kg ip), and dexamethasone (10 mg/kg sc) but not quinacrine (20 mg/kg ip) significantly prevented delay in gastric emptying induced by endotoxin but failed to modify gastric emptying in vehicle-treated animals. Ca2+-dependent NOS activity in the antrum pylorus of the stomach was diminished by endotoxin, whereas Ca2+-independent NOS activity was not changed. In addition, decreased nNOS mRNA and protein were observed in the antrum pylorus of endotoxin-treated rats. Our results suggest that downregulation of nNOS in the antrum pylorus of the stomach and synthesis of prostaglandins mediate the delay in gastric emptying of a solid nutrient meal induced by endotoxin.

Chemoprevention with Enalapril and Aspirin in Men1(+/T) Knockout Mouse Model

2018 ◽  
Vol 107 (3) ◽  
pp. 257-266 ◽  
Author(s):  
Jerena Manoharan ◽  
Volker Fendrich ◽  
Pietro Di Fazio ◽  
Carmen Bollmann ◽  
Silvia Roth ◽  
...  
Keyword(s):  
Mouse Model ◽  
Somatostatin Analogues ◽  
Control Group ◽  
Histopathological Analysis ◽  
Ki 67 ◽  
Chemopreventive Agents ◽  
Knockout Mouse Model ◽  
Angiotensin I Converting Enzyme ◽  
Significant Difference

Pancreatic neuroendocrine neoplasias (pNEN) are the most common cause of death in adult patients with multiple endocrine neoplasia type 1 (MEN1). So far, only few chemopreventive strategies (e.g., with somatostatin analogues) have been evaluated for MEN1 associated pNENs. In this experimental study on 75 Men1(+/T) knockout mice, the effect of aspirin (n = 25) and an inhibitor of angiotensin-I converting enzyme (enalapril, n = 25) compared to controls (n = 25) were evaluated as single chemopreventive strategies for pNENs after 6, 9, 12, 15, and 18 months. After each study period, mice were sacrificed and the resected pancreata were evaluated by histopathological analysis, immunostaining, and real-time PCR. PNEN size and number was measured. Aspirin and enalapril lead to a pNEN size reduction of 80% (167,518 vs. 838,876 µm2, p < 0.001) and 79% (174,758 vs. 838,876 µm2, p < 0.001) compared to controls. Furthermore, aspirin and enalapril treatment resulted in a significant reduction of the number of pNENs by 33%, (p = 0.04) and 41% (p = 0.002) respectively. The apoptosis marker caspase 3 revealed a higher positive expression in pNEN of treated Men1(+/T) mice. Immunostaining of VEGF in pNEN detected a downregulation of its expression in treated Men1(+/T) mice compared to the control group. REL A transcript was significantly downregulated in 18-months treated enalapril Men1(+/T) mice, but not in aspirin-treated Men1(+/T) mice. There was no significant difference in the Ki-67 index. Using a transgenic mouse model that imitates human MEN1, this study provides first evidence that aspirin and enalapril are effective chemopreventive agents that aid in the progression of pNENs.

scholarly journals Dipeptide mimetic of the bdnf loop 4 possesses analgetic activity

2019 ◽  
Vol 485 (3) ◽  
pp. 366-369
Author(s):  
T. A. Gudasheva ◽  
M. A. Konstantinopolsky ◽  
A. V. Tarasiuk ◽  
L. G. Kolik ◽  
S. B. Seredenin
Keyword(s):  
Analgesic Activity ◽  
Neurotrophic Factor ◽  
Intraperitoneal Injection ◽  
Brain Derived Neurotrophic Factor ◽  
Tail Flick ◽  
Hot Plate ◽  
The Brain

Previously, we synthesized a dimeric dipeptide mimetic of the brain-derived neurotrophic factor (BDNF) loop 4, GSB-106, which, similarly to BDNF, activated TrkB, PI3K/AKT, and MAPK/ERK. When administered systemically, it exhibited neuroprotective, antidepressant, and antidiabetic activities and stimulated neurogenesis and synaptogenesis. In this study, we established that GSB-106 also exhibits the analgesic activity, typical for BDNF, which was revealed in rats in hot plate and tail flick tests 0.5–48 h after intraperitoneal injection at doses of 0.1 and 1 mg/kg.

scholarly journals The Effect of Herniarin on Spatial Working Memory, Pain Threshold, and Oxidative Stress in Ischemic Hypoperfusion Model in Rats

2021 ◽  
Vol 7 (1) ◽  
pp. 42-50
Author(s):  
Zahra Nazari Barchestani ◽  
◽  
Maryam Rafieirad ◽  
Keyword(s):  
Oxidative Stress ◽  
Pain Threshold ◽  
Male Rats ◽  
Control Group ◽  
Tail Flick ◽  
Pain Thresholds ◽  
Ischemic Group ◽  
Significant Difference ◽  
The Brain ◽  
And Oxidative Stress

Background: Ischemia causes severe neuronal damage and induces oxidative stress, memory impairment, and reduces pain threshold. Herniarin is a powerful antioxidant. Objectives: This study aimed to evaluate the effect of herniarin on memory, pain, and oxidative stress in an ischemia model in male rats. Materials & Methods: In this study, 50 male rats were divided into 5 groups of control, sham, ischemic, and two other ischemic groups, which received herniarin at doses of 150 and 300 mg/kg by gavage for 14 days. Behavioral tests were performed by shuttle box, and Y-maze and pain tests were performed by Tail-Flick test. Then, the rats’ brains were extracted to evaluate lipid peroxidation and measure the levels of thiol and Glutathione Peroxidase (GPX) in the hippocampus and striatum tissues. The results were expressed as Mean±SEM and then analyzed using suitable statistical methods of ANOVA and least significant difference post-hoc test in SPSS V. 20. Results: Herniarin significantly increased the avoidance memory, spatial memory, and pain thresholds of ischemic rats at different concentrations (P<0.001). Besides, the amount of malondialdehyde (MDA) and thiol in the ischemic group increased significantly in comparison to the control group (P<0.001). Also, in the ischemic group, GPX (P<0.001) significantly decreased. Decreased MDA (P<0.001) and thiol (P<0.001) and increased GPX levels were observed with herniarin administration (P<0.01). Conclusion: According to this study’s results, herniarin can remove free radicals and oxidant substances from the brain. Thus, it improves memory and pain thresholds in the brain hypoperfusion ischemia model.

scholarly journals Mouse Model of Loeys–Dietz Syndrome Shows Elevated Susceptibility to Periodontitis via Alterations in Transforming Growth Factor-Beta Signaling

2021 ◽  
Vol 12 ◽  
Author(s):  
Satoru Yamada ◽  
Kenichiro Tsushima ◽  
Masaki Kinoshita ◽  
Hiromi Sakashita ◽  
Tetsuhiro Kajikawa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Bone Loss ◽  
Mouse Model ◽  
Mrna Expression ◽  
Missense Mutation ◽  
Transforming Growth Factor ◽  
Alveolar Bone ◽  
Elastic Fibers ◽  
Periodontal Tissues ◽  
Significant Difference

Loeys–Dietz syndrome (LDS) is a syndromic connective tissue disorder caused by a heterozygous missense mutation in genes that encode transforming growth factor (TGF)-β receptor (TGFBR) 1 and 2. We encountered a patient with LDS, who had severe periodontal tissue destruction indicative of aggressive periodontitis. The patient had a missense mutation in the glycine and serine-rich domain of TGFBR1 exon 3. This G-to-T mutation at base 563 converted glycine to valine. We established an LDS model knock-in mouse that recapitulated the LDS phenotype. Homozygosity of the mutation caused embryonic lethality and heterozygous knock-in mice showed distorted and ruptured elastic fibers in the aorta at 24 weeks of age and died earlier than wildtype (WT) mice. We stimulated mouse embryonic fibroblasts (MEFs) from the knock-in mouse with TGF-β and examined their responses. The knock-in MEFs showed downregulated Serpine 1 mRNA expression and phosphorylation of Smad2 to TGF-β compared with WT MEFs. To clarify the influence of TGF-β signaling abnormalities on the pathogenesis or progression of periodontitis, we performed pathomolecular analysis of the knock-in mouse. There were no structural differences in periodontal tissues between WT and LDS model mice at 6 or 24 weeks of age. Micro-computed tomography revealed no significant difference in alveolar bone resorption between WT and knock-in mice at 6 or 24 weeks of age. However, TGF-β-related gene expression was increased significantly in periodontal tissues of the knock-in mouse compared with WT mice. Next, we assessed a mouse periodontitis model in which periodontal bone loss was induced by oral inoculation with the bacterial strain Porphyromonas gingivalis W83. After inoculation, we collected alveolar bone and carried out morphometric analysis. P. gingivalis-induced alveolar bone loss was significantly greater in LDS model mice than in WT mice. Peritoneal macrophages isolated from Tgfbr1G188V/+ mice showed upregulation of inflammatory cytokine mRNA expression induced by P. gingivalis lipopolysaccharide compared with WT macrophages. In this study, we established an LDS mouse model and demonstrated that LDS model mice had elevated susceptibility to P. gingivalis-induced periodontitis, probably through TGF-β signal dysfunction. This suggests that TGF-β signaling abnormalities accelerate the pathogenesis or progression of periodontitis.

A single intraperitoneal injection of bovine fetuin-A attenuates bone resorption in a murine calvarial model of particle-induced osteolysis

Bone ◽  
2017 ◽  
Vol 105 ◽  
pp. 262-268 ◽  
Author(s):  
Heidrun Jablonski ◽  
Christina Polan ◽  
Christian Wedemeyer ◽  
Gero Hilken ◽  
Rüdiger Schlepper ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Intraperitoneal Injection ◽  
Fetuin A ◽  
Single Intraperitoneal Injection

Neuroprotection by glucagon: role of gluconeogenesis

2011 ◽  
Vol 114 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Rami Abu Fanne ◽  
Taher Nassar ◽  
Achinoam Mazuz ◽  
Otailah Waked ◽  
Samuel N. Heyman ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Amino Acid ◽  
Intraperitoneal Injection ◽  
Neuroprotective Effect ◽  
Closed Head Injury ◽  
Lesion Size ◽  
Hepatic Uptake ◽  
Glucose Levels ◽  
Single Intraperitoneal Injection ◽  
Amino Acid Glutamate

Object The severity of neurological impairment following traumatic brain injury (TBI) is exacerbated by several endogenous processes, including hyperglycemia, hypotension, and the generation of glutamate. However, in addition to controlling hyperglycemia, insulin has pleiotropic effects on tissue metabolism, which include reducing the concentration of the neurotoxic amino acid glutamate, making it unclear whether insulin's beneficial effects are attributable to the establishment of euglycemia per se. In the present study, the authors asked if reducing glutamate via approaches that do not lower glucose levels would improve neurological outcome following TBI. Methods Glucagon activates gluconeogenesis by increasing the hepatic uptake of amino acids such as glutamate and facilitating their conversion to glucose. Glucagon was administered as a single intraperitoneal injection before or after closed head injury (CHI). Neurological function, brain histological features, blood glutamate and glucose levels, and CSF glutamate concentrations were measured. Results A single intraperitoneal injection of glucagon (25 μg) into mice 10 minutes before or after CHI reduced lesion size by about 60% (p < 0.0001) and accelerated neurological recovery. The neuroprotective effect of glucagon was related to gluconeogenesis by decreasing the concentration of the neuroexcitatory amino acid glutamate in the circulation from 207 ± 32.1 μmol/L in untreated mice to 101.11 ± 21.6 μmol/L in treated mice (p < 0.001); a similar effect occurred in the CSF. The neuroprotective effect of glucagon was seen notwithstanding the attendant increase in blood glucose, the final substrate of gluconeogenesis. Conclusions Glucagon exerts a marked neuroprotective effect post-TBI by decreasing CNS glutamate. Glucagon was beneficial despite increasing blood glucose. Favorable effects also occurred when glucagon was given prior to TBI, suggesting its involvement in the preconditioning process. Thus, glucagon may be of value in providing neuroprotection when administered after TBI or prior to certain neurosurgical or cardiac interventions in which the incidence of perioperative ischemia is high.

Duration of Availability of Tritiated Thymidine Following Intraperitoneal Injection

1968 ◽  
Vol 3 (1) ◽  
pp. 89-93
Author(s):  
W. K. BLENKINSOPP
Keyword(s):  
Cell Division ◽  
Intraperitoneal Injection ◽  
Deoxyribonucleic Acid ◽  
Direct Evidence ◽  
Tritiated Thymidine ◽  
Indirect Evidence ◽  
Acid Synthesis ◽  
Single Intraperitoneal Injection ◽  
Deoxyribonucleic Acid Synthesis

Much indirect evidence supports the assumption that tritiated thymidine does not label cells which enter the deoxyribonucleic acid synthesis phase (S) more than 1 h after injection. Direct evidence confirming this assumption was obtained by counting labelled epithelial nuclei in mice killed 1, 4 or 6 h after a single intraperitoneal injection of [3H]thymidine; colchicine was used to prevent the increase in number of labelled nuclei which would otherwise have occurred because of cell division. The proportion of cells labelled was the same at 1 h as at 4 or 6 h after injection of [3H]thymidine. Nuclei were regarded as labelled if they were overlaid by 4 grains or more; comparison of nuclear and background labelling indicated that nuclei overlaid by 3 grains or less represented background labelling.

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