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 ◽  
...  

<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>

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 723-723
Author(s):  
Qing-Feng Tao ◽  
Diego Martinez vasquez ◽  
Ricardo Rocha ◽  
Gordon H Williams ◽  
Gail K Adler

P165 Aldosterone through its interaction with the mineralocorticoid receptor (MR) plays a critical role in the development of hypertension and cardiovascular injury (CVI). Normally, MR is protected by 11β-hydroxysteroid dehydrogenase (11β-HSD) which inactivates glucocorticoids preventing their binding to MR. We hypothesis that if activation of MR by either aldosterone or glucocorticoids induces hypertension and CVI, then the inhibition of 11β-HSD with glycyrrhizin (GA), a natural inhibitor of 11β-HSD, should induce damage similar to that observed with aldosterone. Sprague-Dawley rats were uninephrectomized, and treated for 4 weeks with 1% NaCl (in drinking water) for the control group, 1% NaCl + aldosterone infusion (0.75 μg/h), or 1% NaCl + GA (3.5 g/l in drinking water). After 4 weeks, aldosterone and GA caused significant increases in blood pressure compared to control rats ([mean ± SEM] 211± 9, 205 ± 12, 120 ± 9 mmHg, respectively, p<0.001). Both aldosterone- and GA-treated rats had a significant increase in proteinuria (152.2 ± 8.7 and 107.7 ± 19.5 mg/d, respectively) versus controls (51.2 ± 9.5 mg/d). There was a significant increase (p<0.001) in heart to body weight ratio in the rats treated with aldosterone or GA compared with control (3.92 ± 0.10, 3.98 ± 0.88, and 3.24 ± 0.92 mg/g, respectively). Hearts of GA and aldosterone treated rats showed similar histological changes consisting of biventricular myocardial necrosis and fibrinoid necrosis of small coronary arteries and arterioles. These data suggests that in rodents activation of MR by either aldosterone or corticosterone leads to severe hypertension, vascular injury, proteinuria and myocardial infarction. Thus, 11β-HSD plays an important role in protecting the organism from injury.


2017 ◽  
Vol 16 (1) ◽  
pp. 167-167
Author(s):  
M.S. Berke ◽  
Klas S.P. Abelson

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.


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 ◽  
...  

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.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Dan-Dan Mao ◽  
Wen-Yu Yang ◽  
Yan Li ◽  
Jian-Wei Lin ◽  
Shi-Yu Gao ◽  
...  

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.


2007 ◽  
Vol 102 (3) ◽  
pp. 1123-1129 ◽  
Author(s):  
David Jegger ◽  
Ajit S. Mallik ◽  
Mohammed Nasratullah ◽  
Xavier Jeanrenaud ◽  
Rafaela da Silva ◽  
...  

It has been suggested that the shape of the normalized time-varying elastance curve [En( tn)] is conserved in different cardiac pathologies. We hypothesize, however, that the En( tn) differs quantitatively after myocardial infarction (MI). Sprague-Dawley rats ( n = 9) were anesthetized, and the left anterior descending coronary artery was ligated to provoke the MI. A sham-operated control group (CTRL) ( n = 10) was treated without the MI. Two months later, a conductance catheter was inserted into the left ventricle (LV). The LV pressure and volume were measured and the En( tn) derived. Slopes of En( tn) during the preejection period (αPEP), ejection period (αEP), and their ratio (β = αEP/αPEP) were calculated, together with the characteristic decay time during isovolumic relaxation (τ) and the normalized elastance at end diastole (Eminn). MI provoked significant LV chamber dilatation, thus a loss in cardiac output (−33%), ejection fraction (−40%), and stroke volume (−30%) ( P < 0.05). Also, it caused significant calcium increase (17-fold), fibrosis (2-fold), and LV hypertrophy. End-systolic elastance dropped from 0.66 ± 0.31 mmHg/μl (CTRL) to 0.34 ± 0.11 mmHg/μl (MI) ( P < 0.05). Normalized elastance was significantly reduced in the MI group during the preejection, ejection, and diastolic periods ( P < 0.05). The slope of En( tn) during the αPEPand β were significantly altered after MI ( P < 0.05). Furthermore, τ and end-diastolic Eminnwere both significantly augmented in the MI group. We conclude that the En( tn) differs quantitatively in all phases of the heart cycle, between normal and hearts post-MI. This should be considered when utilizing the single-beat concept.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Dogan Atilgan ◽  
Bekir S. Parlaktas ◽  
Nihat Uluocak ◽  
Fikret Erdemir ◽  
Fatma Markoc ◽  
...  

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.


2018 ◽  
Vol 6 (2) ◽  
pp. 14-19
Author(s):  
Mahmoud Abdelaziz Kora ◽  
Yassin Salah Yassin ◽  
Ahmed Mohamed Zahran ◽  
Ahmed Ragheb ◽  
Safwa Othman Abdellatif ◽  
...  

 Background: Management of acute kidney injury is still facing a big problem. It is only dependent up till now on supportive measures, like fluid resuscitation and renal replacement therapy. No current drug therapy has been approved for the treatment of acute kidney injury. Acute kidney injury situations in a lot of cases can be predicted so, finding a drug for AKI will really benefit many patients. The pathophysiology of AKI is complex and many signaling pathways are involved in it. The Glycogen synthase kinase 3B enzyme is an important member in some of these pathways. The effect of its inhibition by the FDA approved drug, lithium on AKI is still under study.Material & Methods: The current study was conducted on28 Male Sprague–Dawley rats. We classified the rats into groups. We induced acute kidney injury to rats with cisplatin. We administered lithium chloride to treat AKI in comparison with saline treatment. We have done renal functions and histopathological examinations to all rats enrolled in our study.Results: Single intraperitoneal injection of cisplatin (5 mg/kg) in rat induced acute kidney injury. The effect of lithium chloride treatment with dose (80 mg/kg) on serum creatinine and blood urea levels showed significant regression in the rising of serum creatinine and blood urea in lithium chloride treated rats in comparison to saline-treated rats. Pathological pictures and scores demonstrated an improvement in lithium chloride treated rats than saline-treated but results were not significant.Conclusion:Administration of lithium may be a promising treatment for acute kidney injury.Journal of Nobel Medical CollegeVolume 6, Number 2, Issue 11 (July-December, 2017) Page:14-19


2017 ◽  
Vol 35 (6) ◽  
pp. 445-451 ◽  
Author(s):  
Hui Zhang ◽  
Jiao-Jiao Lü ◽  
Qiang-Min Huang ◽  
Lin Liu ◽  
Qing-Guang Liu ◽  
...  

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.


2016 ◽  
Vol 34 (3) ◽  
pp. 194-200 ◽  
Author(s):  
Xianwei Zhu ◽  
Zhibin Liu ◽  
Hongyan Qu ◽  
Wenmin Niu ◽  
Li Gao ◽  
...  

Background Electroacupuncture (EA) is used clinically for the treatment of constipation. Serotonin (5-hydroxytryptamine, 5-HT) plays an important role in colonic motility; however it is unknown whether alterations in colonic 5-HT are associated with EA. In this study, the effect and mechanism of EA at acupuncture points LI11 and ST37 were examined using a cold saline-induced rat model of constipation. Methods A rat constipation model was induced by cold saline gavage in 24 Sprague-Dawley rats. A further six rats were included as a Control group. The constipated rats were divided into four groups (n=6 each): a Constipation group that remained untreated; a Constipation+LI11 group that received EA at LI11; a Constipation+ST37 groups that received EA at ST37; and a Constipation+LI11+ST37 group that received EA at both LI11 and ST37. After EA treatment, faecal water content, defaecation frequency, and gastrointestinal (GI) transit were measured, as well as the expression of tryptophan hydroxylase (TPH) in colonic tissues (by Western blot analysis) and 5-HT in both faeces and colonic tissues (by ELISA). Results All three EA-treated groups demonstrated significant improvements in faecal water content, defaecation frequency and GI transit (p<0.05). In addition, TPH and 5-HT expression were both increased by EA at LI11 and/or ST37 (p<0.05). There were no significant differences between the three EA groups for any outcomes. Conclusions EA at LI11 and/or ST37 had a positive effect on objective markers of constipation in a rat model. In addition, EA increased 5-HT and TPH in the colonic tissues.


Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2409 ◽  
Author(s):  
Tubagus Bahtiar Rusbana ◽  
Afifah Zahra Agista ◽  
Wahyu Dwi Saputra ◽  
Yusuke Ohsaki ◽  
Kouichi Watanabe ◽  
...  

Fermented rice bran (FRB), a prospective supplement, has been proven to ameliorate certain medical conditions. However, its nutraceutical effect on muscle atrophy has never been investigated. The present study aimed to evaluate the effect of FRB on muscle atrophy in a streptozotocin (STZ)-induced diabetic rat model. Three groups of Sprague-Dawley rats, namely the control, STZ, and FRB groups, were treated as follows. The diabetic groups (STZ and FRB) were injected intraperitoneally with STZ (40 mg/kg BW), whereas the control group was injected with the vehicle. The STZ and control groups were fed the AIN93M diet, and the FRB group was fed 10% of FRB based on the AIN93M diet. The diabetic groups had reduced muscle size compared to the control group; however, these changes were alleviated in the FRB group. Moreover, the FRB group had a significantly lower expression of FBXO32/Atrogin-1 and TRIM63/MuRF1 (p < 0.05) due to blocked NF-κB activation. In conclusion, the anti-inflammatory effect of FRB may be beneficial for ameliorating muscle atrophy in diabetic conditions.


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