scholarly journals Effect of Qingxin Kaiqiao Fang on Hippocampus mRNA Expression of the Inflammation-Related Genes IL-1β, GFAP, and Aβin an Alzheimer’s Disease Rat Model

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Dan-Dan Mao ◽  
Wen-Yu Yang ◽  
Yan Li ◽  
Jian-Wei Lin ◽  
Shi-Yu Gao ◽  
...  
Keyword(s):  
Rat Model ◽  
Particle Deposition ◽  
Therapeutic Potential ◽  
Interleukin 1 ◽  
Control Group ◽  
Model Group ◽  
Sprague Dawley ◽  
Amyloid A ◽  
Sprague Dawley Rats ◽  
High Doses

Objective. To investigate the effects of QKF on expression of amyloid-beta (Aβ), interleukin-1 beta (IL-1β), and glial fibrillary acidic protein (GFAP) using a rat model of AD.Materials and Methods. Fifty-six male Sprague-Dawley rats were randomly divided into seven groups (eight rats each): control group, sham-operated group, AD model group, groups of AD rats administered with low, medium, and high doses of QKF, and the donepezil group. AD was established by bilateral injection ofβ-amyloid (Aβ) 1–40 into the hippocampus. Two days after AD was established, drugs were administered by gavage. After 14 days of treatment, we used RT-PCR, Western blotting, and immunohistochemistry to measure the transcript expression and protein abundance of Aβ, IL-1β, and GFAP, and methenamine silver staining was used to detect amyloid protein particle deposition.Results. Compared to the control group, the rats from the AD model group showed significantly greater expression levels of Aβ, IL-1β, and GFAP. However, these differences in expression were abolished by treatment with QKF or donepezil.Conclusion. QKF possesses therapeutic potential against AD because it downregulated Aβ, IL-1β, and GFAP in the hippocampus of AD rats. Future studies should further examine the mechanisms through which QKF produces its effects and the consequences of long-term QKF administration.

Buprenorphine alleviation of pain does not compromise the rat monoarthritic pain model

2017 ◽  
Vol 16 (1) ◽  
pp. 167-167
Author(s):  
M.S. Berke ◽  
Klas S.P. Abelson
Keyword(s):  
Rat Model ◽  
Joint Stiffness ◽  
Positive Control ◽  
Negative Control ◽  
Pain Tolerance ◽  
Control Group ◽  
Mechanical Stimuli ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
A Minor

Abstract Aims This study investigated the effects of buprenorphine treatment on pain and welfare parameters and model specific parameters in a rat model of monoarthritis to eliminate unnecessary pain from this model. Methods 32 male Sprague Dawley rats were divided into four groups: (1) A negative control without arthritis receiving no analgesia. (2) A positive monoarthritic control group receiving no analgesia, but subcutaneous saline injections twice a day. (3) A positive control with monoarthritis receiving subcutaneous carprofen once a day and saline once a day. (4) A group with monoarthritis receiving subcutaneous buprenorphine twice a day. Monoarthritis was induced with an injection of 0.02 ml Complete Freund’s Adjuvant intra-articularly in the left tibiotarsal joint. Treatment with analgesia was initiated at day 15 and the rats were euthanized at day 23. Results The induced monoarthritis elicited a pronounced acute inflammation. Several parameters such as bodyweight, mobility, stance, joint-stiffness and lameness scores were affected. A marked mechanical hyperalgesia in the tarsal area was observed by Electronic Von Frey testing, but no severe compromise of the animal welfare was seen at any time. Signs of chronic development began to appear from day 10 after the monoarthritic induction. No significant change in serum cytokines and faecal corticosterone measurements was found after administration of buprenorphine. A minor decrease in body weight was seen, and a higher pain tolerance to mechanical stimuli was observed, indicating pain alleviation. The histological examination confirmed monoarthritic development in all monoarthritic rats and revealed periarticular lesions suggesting diffusion of adjuvant from intra-articular injection site to the periphery. Conclusions The study demonstrated that buprenorphine has an analgesic effect in the adjuvant induced monoarthritic rat model, without obvious interference with the development of arthritis.

scholarly journals Association between Chronic Acetaminophen Exposure and Allergic Rhinitis in a Rat Model

2015 ◽  
Vol 6 (3) ◽  
pp. ar.2015.6.0131 ◽  
Author(s):  
Nadieska Caballero ◽  
Kevin C. Welch ◽  
Patrick S. Carpenter ◽  
Swati Mehrotra ◽  
Tom F. O'Connell ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Mast Cells ◽  
Rat Model ◽  
Group Versus ◽  
Inferior Turbinate ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Increased Risk ◽  
Hematoxylin And Eosin

Background Several population studies demonstrated an increased risk of allergic rhinitis in patients exposed to acetaminophen. However, no histologic studies have been conducted to assess the relationship between acetaminophen exposure and allergic rhinitis. Objective In this study, we investigated the association between chronic acetaminophen exposure and the development of allergic rhinitis in a rat model. Methods Ten female Sprague-Dawley rats were randomly assigned to either a control (n = 5) or an acetaminophen group (n = 5). The acetaminophen group received 200 mg/kg/day of acetaminophen suspended in yogurt via oral gavage for 120 days. The control group received only the yogurt vehicle. Allergic behavioral responses, including nose rub, eye rub, ear scratching, and neck and/or face scratching, were quantified. The rats were killed, and the noses were harvested. The portion of the nose, including the nasal septum and the inferior turbinates, was embedded in paraffin, sectioned, and stained with hematoxylin and eosin to quantify the inflammatory infiltrate. Results The average number of allergic responses per animal was 13.2 in the acetaminophen group versus 6.2 in the control group (p = 0.032). All the rats in the acetaminophen group (100%) had mast cells infiltrating the lamina propria of the inferior turbinate, whereas mast cells were detected in only 40% of the animals in the control group. The average number of mast cells per animal in the acetaminophen group was 134 versus 21 in the control group (p = 0.048). Conclusions Our study was the first to demonstrate a histologic association between chronic exposure to acetaminophen and rhinitis. Further research to elucidate the mechanism that underlies these findings is necessary.

scholarly journals The Effects of Trimetazidine and Sildenafil on Bilateral Cavernosal Nerve Injury Induced Oxidative Damage and Cavernosal Fibrosis in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Dogan Atilgan ◽  
Bekir S. Parlaktas ◽  
Nihat Uluocak ◽  
Fikret Erdemir ◽  
Fatma Markoc ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Oxidative Damage ◽  
Nerve Injury ◽  
Rat Model ◽  
Protein Carbonyl ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Collagen Density ◽  
Cavernosal Nerve

Aim. The aim of this study was to compare the effects of sildenafil and trimetazidine on bilateral cavernosal nerve injury-induced oxidative damage and fibrotic changes in cavernosal tissue in rat model.Material and Methods. A total of 32 male Sprague-Dawley rats were randomly divided into 4 groups; each group consist 8 rats (control, BCI, BCI + TMZ, and BCI + sildenafil groups). Tissue superoxide dismutase (SOD), malondialdehyde (MDA), and protein carbonyl (PC) levels were determined biochemically and distribution of cavernosal fibrosis density among groups was performed histopathologically.Results. Tissue SOD levels in BCI group were significantly lower than the control group (P<0.05). Tissue MDA and PC levels in BCI group were significantly higher than the control group (P<0.05). TMZ and sildenafil administration significantly increased tissue SOD levels (P<0.05) and reduced tissue MDA and PC levels (P<0.05). Histologically, the degree of cavernosal fibrosis and collagen density was higher in BCI group in comparison to control, TMZ-treated, and sildenafil-treated groups.Conclusion. BCI caused oxidative damage and increased cavernosal fibrosis in rat penis. TMZ and sildenafil treatment decreased oxidative damage and reduced the degree of fibrosis in penile tissue due to BCI.

scholarly journals Lack of synergistic nephrotoxicity between vancomycin and piperacillin/tazobactam in a rat model and a confirmatory cellular model

2020 ◽  
Vol 75 (5) ◽  
pp. 1228-1236 ◽  
Author(s):  
Gwendolyn M Pais ◽  
Jiajun Liu ◽  
Sean N Avedissian ◽  
Danielle Hiner ◽  
Theodoros Xanthos ◽  
...  
Keyword(s):  
Rat Model ◽  
Kidney Injury ◽  
Cellular Injury ◽  
Cellular Model ◽  
Sprague Dawley ◽  
Injury Score ◽  
Sprague Dawley Rats ◽  
High Doses ◽  
Vancomycin Group ◽  
Synergistic Toxicity

Abstract Background Vancomycin and piperacillin/tazobactam are reported in clinical studies to increase acute kidney injury (AKI). However, no clinical study has demonstrated synergistic toxicity, only that serum creatinine increases. Objectives To clarify the potential for synergistic toxicity between vancomycin, piperacillin/tazobactam and vancomycin + piperacillin/tazobactam treatments by quantifying kidney injury in a translational rat model of AKI and using cell studies. Methods (i) Male Sprague–Dawley rats (n = 32) received saline, vancomycin 150 mg/kg/day intravenously, piperacillin/tazobactam 1400 mg/kg/day intraperitoneally or vancomycin + piperacillin/tazobactam for 3 days. Urinary biomarkers and histopathology were analysed. (ii) Cellular injury was assessed in NRK-52E cells using alamarBlue®. Results Urinary output increased from Day −1 to Day 1 with vancomycin but only after Day 2 for vancomycin + piperacillin/tazobactam-treated rats. Plasma creatinine was elevated from baseline with vancomycin by Day 2 and only by Day 4 for vancomycin + piperacillin/tazobactam. Urinary KIM-1 and clusterin were increased with vancomycin from Day 1 versus controls (P &lt; 0.001) and only on Day 3 with vancomycin + piperacillin/tazobactam (P &lt; 0.001, KIM-1; P &lt; 0.05, clusterin). The histopathology injury score was elevated only in the vancomycin group when compared with piperacillin/tazobactam as a control (P = 0.04) and generally not so with vancomycin + piperacillin/tazobactam. In NRK-52E cells, vancomycin induced cell death with high doses (IC50 48.76 mg/mL) but piperacillin/tazobactam did not, and vancomycin + piperacillin/tazobactam was similar to vancomycin. Conclusions All groups treated with vancomycin demonstrated AKI; however, vancomycin + piperacillin/tazobactam was not worse than vancomycin. Histopathology suggested that piperacillin/tazobactam did not worsen vancomycin-induced AKI and may even be protective.

scholarly journals Acupotomy Alleviates Energy Crisis at Rat Myofascial Trigger Points

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yi Zhang ◽  
Ning-Yu Du ◽  
Chen Chen ◽  
Tong Wang ◽  
Li-Juan Wang ◽  
...  
Keyword(s):  
High Performance ◽  
Trigger Points ◽  
Control Group ◽  
Model Group ◽  
Sprague Dawley ◽  
Myofascial Trigger Points ◽  
Sprague Dawley Rats ◽  
Lower Treatment ◽  
Lidocaine Injection ◽  
Mechanical Pain Thresholds

The aim of this study was to determine the effects of acupotomy on energy crises in rat trigger points (TrPs) by measuring mechanical pain thresholds (MPTs) and levels of acetylcholinesterase (AChE), free sarcoplasmic calcium (Ca2+), adenosine 5′-triphosphate (ATP), adenosine 5′-monophosphate (AMP), substance P (SP), and calcitonin gene-related peptide (CGRP) in rat muscle TrP tissue. Male Sprague Dawley rats (n = 32) were randomly divided into four groups: control, TrP, acupotomy, and lidocaine injection. Enzyme-linked immunosorbent assays were used to measure AChE, and free sarcoplasmic Ca2+ concentrations were determined by fluorescent staining with Fura-2 AM; high-performance liquid chromatography was used to measure ATP and AMP, and SP and CGRP were evaluated by immunohistochemistry. Compared with the control group, free sarcoplasmic Ca2+, AMP, SP, and CGRP were higher in the model group, while MPT, AChE, and ATP were lower. Treatment with acupotomy or lidocaine injection reduced free sarcoplasmic Ca2+, SP, and CGRP and increased MPTs and AChE levels compared with the model group. However, only acupotomy also led to decreased AMP and increased ATP levels relative to the model group. We conclude that acupotomy can alleviate energy crises at TrPs.

Chronotropic, Inotropic and Dromotropic Parameters of the Heart and Oxidative Stress in Rats Receiving High Doses of Fructose

2019 ◽  
Vol 8 ◽  
pp. 1250
Author(s):  
Esmat Radmanesh ◽  
Mahin Dianat ◽  
Narges Atefipour
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Drinking Water ◽  
Control Group ◽  
Free Access ◽  
Qtc Interval ◽  
Sprague Dawley ◽  
Cvd Risk ◽  
Sprague Dawley Rats ◽  
High Doses

Background: Many risk factors, including nutritional ones, contribute to cardiovascular diseases (CVDs). Increased fructose consumption, for example, can lead to an increase in CVD risk factors, i.e. an increase in blood lipids and the development of insulin resistance. Materials and Methods: In the present study, Sprague Dawley rats were divided into two groups:  control group (free access to tap drinking water for seven weeks), and a group that received fructose 10% in drinking water for seven weeks, (n ═8 per each group). In all groups, before starting the test period and seven weeks after it, electrocardiogram was recorded by Power lab system. Unpaired t-test and two-way ANOVA were used for data analysis. Also, oxidative stress parameters were measured. Results: In the group received high doses of fructose, a significant reduction (P <0.05) was observed in the PR interval (P<0.001) and a significant increase (P<0.05) in the QTc interval. However, there was no significant change in the RR interval and the voltage of the QRS complex. A significant decrease in catalase, superoxide dismutase and glutathione peroxidase (P<0.05) and a significant increase (P<0.05) in malondialdehyde and lactate dehydrogenase were observed in the group that received fructose in comparison with the control group at the end of the experiment. Conclusion: According to our results, the chance of arrhythmias in the rats receiving high doses of fructose was possibly due to the increased oxidative stress in the healthy rats. [GMJ.2019;8:e1250]

scholarly journals Cardioprotective effect of lithium chloride on a rat model of myocardial infarction

2019 ◽  
Vol 23 (2) ◽  
pp. 43 ◽  
Author(s):  
O. A. Grebenchikov ◽  
A. V. Lobanov ◽  
E. R. Shayhutdinova ◽  
A. N. Kuzovlev ◽  
A. V. Ershov ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Lithium Chloride ◽  
Rat Model ◽  
Conflict Of Interest ◽  
Chloride Solution ◽  
Glycogen Synthase ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Lithium Chloride Solution

<p><strong>Aim.</strong> To investigate the cardioprotective effect of lithium chloride in vivo on a rat model of myocardial infarction.<br /><strong>Methods.</strong> Twelve male Sprague-Dawley rats were randomly divided into two groups of six, with both groups modelling cardiac ischaemia and subsequent reperfusion. At the start of reperfusion, 30 mg/kg of 4.2% lithium chloride solution was intravenously administered via a catheter to the test group and 0.5 ml/kg of saline solution was administered to the comparison group. A control group comprised sham-operated rats that were not injected with any drugs other than anaesthesia during making skin incision. At the end of each experiment, the total area of the risk zone and areas of the infarction zone and left ventricle were calculated for each animal using a double-staining technique with 2% methylene blue and 1% triphenyltetrazolium chloride. A further series of experiments using 15 male Sprague-Dawley rats (third group) was performed to assess the protein content of glycogen synthase-3β in myocardial tissue. The method was similar to that for the earlier experiments; however, at the end of the experiments, the hearts were removed and homogenised, following which the concentration of glycogen synthase-3β was determined using electrophoresis.<br /><strong>Results.</strong> The group treated with lithium chloride showed a significant decrease in the area of the infarction zone compared with the group treated with saline. The difference in the indices between the two groups was &gt;26% (p &lt; 0.05).<br /><strong>Conclusion.</strong> This study demonstrated that 30 mg/kg of 4.2% lithium chloride solution, administered at the onset of reperfusion, exerted a protective effect on cardiomyocytes in a rat model of myocardial infarction by reducing the area of the infarction zone compared with that in the control group. This effect was probably mediated by an almost two-fold increase in the content of the phosphorylated form of glycogen synthase-3β in the myocardium.</p><p>Received 23 June 2019. Revised 6 August 2019. Accepted 7 August 2019.</p><p><strong>Funding:</strong> The study did not have sponsorship.</p><p><strong>Conflict of interest:</strong> Authors declare no conflict of interest.</p><p><strong>Author contributions</strong> <br />Conception and study design: A.N. Kuzovlev<br />Data collection and analysis: O.A. Grebenchikov<br />Statistical analysis: A.V. Ershov<br />Drafting the article: A.V. Lobanov, E.R. Shayhutdinova<br />Critical revision of the article: V.V. Likhvantsev<br />All authors approved final version to be published.<br /><br /></p>

Gastrodin attenuates lithium-pilocarpine-induced epilepsy by activating AMPK-mediated PPARα in a juvenile rat model

2021 ◽  
Author(s):  
Yanfei Yang ◽  
Yabin Li ◽  
Jinli Han ◽  
Yanfen Wang
Keyword(s):  
Morris Water Maze ◽  
Rat Model ◽  
Neurological Disease ◽  
Water Maze ◽  
Therapeutic Potential ◽  
Pediatric Epilepsy ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Electroencephalogram Eeg ◽  
Histological Staining

Abstract Gastrodin has shown the potential as an anticonvulsant. Epilepsy is a neurological disease with significant effects in children. In the current study, the therapeutic potential of gastrodin in handling pediatric epilepsy was explored by focusing on AMPK/PPARα pathway. Three-week-old Sprague-Dawley rats were subjected to lithium-pilocarpine method to induce epileptic symptoms and then administrated with gastrodin. The effects of gastrodin on rats were firstly assessed using electroencephalogram (EEG) recording, Racine classification, Morris water maze (MWM) test, and histological staining. The levels of BDNF and NGF, and the activity of AMPK/PPARα were measured. Based on the results of EEG, behavior analyses, and histological staining, epileptic symptoms were significantly alleviated by gastrodin. Moreover, the administration of gastrodin also suppressed the levels of BDNF and NGF, and activated AMPK/PPARα pathway. In conclusion, our results demonstrated that gastrodin contributed to the alleviation of pediatric epilepsy by activating AMPK/PPARα signaling transduction.

scholarly journals Histopathological Nature of Myofascial Trigger Points at Different Stages of Recovery from Injury in a Rat Model

2017 ◽  
Vol 35 (6) ◽  
pp. 445-451 ◽  
Author(s):  
Hui Zhang ◽  
Jiao-Jiao Lü ◽  
Qiang-Min Huang ◽  
Lin Liu ◽  
Qing-Guang Liu ◽  
...  
Keyword(s):  
Rat Model ◽  
Large Diameter ◽  
Trigger Points ◽  
Control Group ◽  
Sprague Dawley ◽  
Myofascial Trigger Points ◽  
Sprague Dawley Rats ◽  
Longitudinal View ◽  
Recovery Times ◽  
Electron Microscopes

Objective To investigate the histopathological nature of myofascial trigger points (MTrPs) or spots (MTrSs) at different stages of recovery from injury in a rat model. Methods Forty Sprague–Dawley rats were randomly divided into two groups: a control group (CG) and experimental group (EG). The CG was further randomly subdivided into CG1 and CG2 subgroups. The CG2 was used for palpating the taut band and CG1 as a blank. EG was subdivided into three groups according to recovery times: 4 weeks (4W), 8 weeks (8W) and 12 weeks (12W); these groups consisted of eight rats each. All CG rats received no intervention, whereas the intervention in EG rats was by a blunt strike to the vastus medialis and eccentric exercise for 8 weeks. The taut bands with spontaneous electrical activity were then detected in the muscle to guide a muscle biopsy. The histopathological findings were investigated under optical and electron microscopes in all groups. Results Under optical microscopy, the differently augmented sizes of round fibres (contracture knots) with deep staining in the transverse section and fusiform shapes in a longitudinal view were clearly seen in CG2 and EGs with a large diameter; the number of contracture knots was significantly more in EGs than in CGs. Under an electron microscope, the mitochondria in EGs significantly decreased with abnormal structures. The sarcomeres were significantly shortened in the 8W and 12W EGs. Conclusion An injury can cause activation of MTrSs in a muscle and an activated level of MTrPs depending on the number of contracture knots in muscle with impaired energy production.

scholarly journals Urinary biomarker and histopathological evaluation of vancomycin and piperacillin-tazobactam nephrotoxicity in comparison with vancomycin in a rat model and a confirmatory cellular model

2019 ◽  
Author(s):  
Gwendolyn M. Pais ◽  
Jiajun Liu ◽  
Sean N. Avedissian ◽  
Theodoros Xanthos ◽  
Athanasios Chalkias ◽  
...  
Keyword(s):  
Rat Model ◽  
Rat Kidney ◽  
Hospital Setting ◽  
Kidney Injury ◽  
Sprague Dawley ◽  
Drug Dosing ◽  
Viability Assay ◽  
Sprague Dawley Rats ◽  
Kidney Epithelial Cell ◽  
High Doses

AbstractIntroductionVancomycin and piperacillin tazobactam (VAN+TZP) are two of the most commonly utilized antibiotics in the hospital setting and are reported in clinical studies to increase acute kidney injury (AKI). However, no clinical study has demonstrated that synergistic toxicity occurs, only that serum creatinine (SCr) increases with VAN+TZP. The purpose of this study was to assess biologic plausibility by quantifying kidney injury between VAN, TZP, and VAN+TZP treatments using a translational rat model of AKI and rat kidney epithelial cell studies.Methods(i) Male Sprague-Dawley rats (n=32) received either saline, VAN 150 mg/kg/day intravenously, TZP 1400 mg/kg/day via intraperitoneal injection, or VAN+TZP. Animals were placed in metabolic cages pre-study and on drug dosing days 1-3. Urinary biomarkers and histopathology were analyzed. (ii) Cellular injury of VAN+TZP was assessed in serum-deprived rat kidney cells (NRK-52E) using an alamarBlue® viability assay. Cells were incubated with antibiotics VAN, TZP, cefepime, and gentamicin alone or combined with the same drugs plus VAN 1 mg/mL.ResultsIn the VAN-treated rats, urinary KIM-1 and clusterin were increased on days 1, 2, and 3 compared to controls (P<0.001). Elevations were seen only after 3 days of treatment with VAN+TZP (P<0.001 KIM-1, P<0.05 clusterin). Histopathology was only elevated in the VAN group when compared to TZP as a control (P=0.04). Results were consistent across biomarkers and histopathology suggesting that adding TZP did not worsen VAN induced AKI and may even be protective. In NRK-52E cells, VAN alone caused moderate cell death with high doses (IC5048.76 mg/mL). TZP alone did not cause cellular death under the same conditions. VAN+TZP was not different from VAN alone in NRK-52E cells (P>0.2).ConclusionsVAN+TZP does not cause more kidney injury than VAN alone in a rat model of VIKI or in rat kidney epithelial cells.

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