scholarly journals Beneficial Effect of Continuous Normobaric Hypoxia on Ventricular Dilatation in Rats With Post-Infarction Heart Failure

2016 ◽  
pp. 867-870 ◽  
Author(s):  
J. HRDLIČKA ◽  
J. NECKÁŘ ◽  
F. PAPOUŠEK ◽  
J. VAŠINOVÁ ◽  
P. ALÁNOVÁ ◽  
...  
Keyword(s):  
Heart Failure ◽  
Prolonged Exposure ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coronary Artery Occlusion ◽  
Normobaric Hypoxia ◽  
Male Rats ◽  
Ventricular Dilatation ◽  
Sham Operation ◽  
Therapeutic Effects

Adaptation to continuous normobaric hypoxia (CNH) protects the heart against ischemia/reperfusion injury but much less is known about its potential therapeutic effects. The aim of this study was to find out whether post-infarction exposure to CNH can attenuate the progression of heart failure. Ten-week-old male rats underwent myocardial infarction (MI) or sham operation. MI was induced by 60-min coronary artery occlusion. Seven days post-MI, the rats were randomly assigned to two groups: i) sedentary controls kept at room air and ii) rats exposed to CNH (12 % O2, 3 weeks). Echocardiographic examination of the left ventricle (LV) was performed 3 days before surgery and 7, 14 and 28 days post-MI. MI resulted in a gradual increase in LV end-diastolic diameter (LVDd) compared to sham-operated animals. Fractional shortening (FS) decreased from 42.8 % before MI to 15.1 % on day 28 post-MI. CNH significantly attenuated ventricular dilatation without affecting scar area and FS. Our data suggest that prolonged exposure to CNH has certain potential to attenuate the progression of unfavorable changes in ventricular geometry induced by MI in rats.

scholarly journals Electroacupuncture Ameliorates Cerebral Ischemia-Reperfusion Injury by Regulation of Autophagy and Apoptosis

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Shi Shu ◽  
Chun-Ming Li ◽  
Yan-Li You ◽  
Xiao-Lu Qian ◽  
Shuang Zhou ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Neurological Deficit ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Beclin 1 ◽  
Male Rats ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Sham Operation Group

Background. The therapeutic mechanisms of cerebral ischemia treatment by acupuncture are yet not well addressed.Objective. We investigated the effects of electroacupuncture (EA) at GV26 observing the expression of autophagy-related proteins Beclin-1 and LC3B and proportion of apoptotic cells and Bcl-2 positive cells in MCAO/R model rats.Methods. Sprague-Dawley (SD) male rats were randomly assigned to 7 groups: model groups (M6h, M24h, and M72h), EA treatment groups (T6h, T24h, and T72h), and sham operation group (S). Neurological deficit and cerebral infarction volume were measured to assess the improvement effect, while the expression of Beclin-1 and LC3B and proportion of Tunel-positive and Bcl-2 positive cells were examined to explore EA effect on autophagy and apoptosis.Results. EA significantly decreased neurological deficit scores and the volume of cerebral infarction. Beclin-1 was significantly decreased in T24h, while LC3B-II/LC3B-I ratio markedly reduced in 6th hour. EA groups markedly reduced the number of Tunel positive cells, especially in T24h. Meanwhile, the number of Bcl-2 positive cells obviously increased after EA treatment, especially in T6h and T24h.Conclusions. The alleviation of inadequate autophagy and apoptosis may be a key mechanism involved in the reflex regulation of EA at GV26 to treat cerebral ischemia.

scholarly journals The Effect of Erythropoietin on Ischemia/Reperfusion Injury after Testicular Torsion/Detorsion: A Randomized Experimental Study

ISRN Urology ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Fahimeh Kazemi Rashed ◽  
Babollah Ghasemi ◽  
Hamid Deldade Mogaddam ◽  
Mehran Mesgari
Keyword(s):  
Testicular Torsion ◽  
Ischemia Reperfusion Injury ◽  
Protective Efficacy ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Sham Operation ◽  
Scoring Method ◽  
Group Vi ◽  
Sham Operation Group ◽  
Group I

This study was conducted to investigate the protective effect of erythropoietin (EPO) on ischemia/reperfusion related changes after testicular torsion/detorsion. In a randomized experimental trial 30 male rats were randomly allocated into six equal groups of five rats each. Group I (orchiectomy for histopathologic examination), group II (sham operation), group III (torsion for 2 hours, and ischemia/detorsion for 24 hours, and orchiectomy); group IV (torsion for 2 hours, ischemia/detorsion for 24 hours with erythropoietin injection then orchiectomy), group V (torsion for 2 hours and detorsion and EPO injection and orchiectomy 1 week later, group VI (torsion for 2 hours/detorsion and orchiectomy 1 week later). Two groups (groups 4 and 5) received different protocols of erythropoietin administration after testicular torsion/distortion. other groups were not receiving erythropoietin. Johnsen’s spermatogenesis scoring method and Cosentino’s histologic staging method were used to assess main outcome measures of the study. After the experimentation, Johnsen’s score in EPO Groups was statistically different from the score in some groups not receiving erythropoietin. Cosentino’s score in EPO groups was statistically different from the score in all groups not receiving erythropoietin. Neovascularization, vascular necrosis, vascular congestion, edema, hemorrhage, and acute inflammation were observed in some groups. This study shows short-term protective efficacy of erythropoietin on rat testicular injury after ischemia/reperfusion.

Hawthorn: Potential Roles in Cardiovascular Disease

2005 ◽  
Vol 33 (01) ◽  
pp. 1-10 ◽  
Author(s):  
Wei-Tien Chang ◽  
Jenny Dao ◽  
Zuo-Hui Shao
Keyword(s):  
Heart Failure ◽  
New York ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nyha Class ◽  
Heart Association ◽  
Prospective Clinical Study ◽  
Therapeutic Effects ◽  
Pharmacological Mechanism ◽  
Beneficial Effects

Hawthorn (Crataegus) may play a role in the prevention and treatment of cardiovascular diseases such as hypertension, hyperlipidemia, and in particular, congestive heart failure. Evidence is accumulating that hawthorn may induce anti-ischemia/reperfusion-injury, anti-arrhythmic, hypolipidemic and hypotensive effects. These beneficial effects may in part be due to the presence of antioxidant flavonoid components. While a number of studies have been performed to evaluate the clinical efficacy of hawthorn, an international, multi-center, prospective clinical study including a large number of New York Heart Association (NYHA) class II/III heart failure patients is ongoing to test hawthorn's long-term therapeutic effects. Further clinical trials as well as pharmacokinetic and mechanistic studies are needed to explore and confirm its effectiveness, safety and pharmacological mechanism.

Effects of 3-aminobenzamide on unilateral testicular ischemia–reperfusion injury: What is the role of PARP inhibition?

2010 ◽  
Vol 88 (12) ◽  
pp. 1123-1129 ◽  
Author(s):  
Askin Hekimoglu ◽  
Zehra Kurcer ◽  
Faruk Aral ◽  
Fusun Baba ◽  
Ahmet Atessahin ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Sperm Quality ◽  
Ischemia Reperfusion ◽  
Sperm Concentration ◽  
Adenosine Diphosphate ◽  
Male Rats ◽  
Parp Inhibition ◽  
Therapeutic Effects ◽  
Sperm Analysis ◽  
Testicular Ischemia

The therapeutic effects of poly(adenosine diphosphate-ribose) polymerase inhibition by 3-aminobenzamide (3-AB) were investigated in testicular ischemia–reperfusion (I/R) injury, using sperm analysis and histopathological and biochemical examinations, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities and reduced glutathione (GSH) levels. Male rats were divided into 3 groups: sham (n = 12), I/R (n = 12), and I/R with 3-AB (I/R–3-AB) (n = 12). The left testicular artery was occluded for 1 h, followed by 24 h (for biochemical and histopathological examinations) and 30 days (for sperm analysis) of reperfusion. 3-AB treatment intraperitoneally 10 min prior to and 1 h after reperfusion increased the I/R-induced decrease in sperm motility in both testes and reduced the increased abnormal sperm rates in the ipsilateral testis. However, 3-AB treatment failed to prevent the I/R-induced decrease in sperm concentration in both testes. SOD and CAT activities did not change in any group. GSH-Px activity and GSH levels were increased by I/R. 3-AB treatment reversed the I/R-induced increase in GSH-Px activity, similar to the level in sham rats, but did not alter GSH levels. 3-AB treatment significantly increased the I/R-induced decrease in histopathologic score. In conclusion, 3-AB treatment has potential biochemical and histopathological benefits beyond improving sperm quality and may have the potential to decrease damage from testicular torsion.

Bardoxolone Ameliorates Cerebral Ischemia/ Reperfusion Injury in Male Rats

2019 ◽  
Vol 22 (04) ◽  
pp. 122-130
Author(s):  
Rihab H Al-Mudhaffer ◽  
Laith M Abbas Al-Huseini ◽  
Saif M Hassan ◽  
Najah R Hadi
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

scholarly journals Propofol attenuates lung ischemia/reperfusion injury though the involvement of the MALAT1/microRNA-144/GSK3β axis

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Jian-Ping Zhang ◽  
Wei-Jing Zhang ◽  
Miao Yang ◽  
Hua Fang
Keyword(s):  
Cell Apoptosis ◽  
Ischemia Reperfusion Injury ◽  
Glycogen Synthase ◽  
Ischemia Reperfusion ◽  
Inflammatory Factors ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Loss Of Function

Abstract Background Propofol, an intravenous anesthetic, was proven to protect against lung ischemia/reperfusion (I/R) injury. However, the detailed mechanism of Propofol in lung I/R injury is still elusive. This study was designed to explore the therapeutic effects of Propofol, both in vivo and in vitro, on lung I/R injury and the underlying mechanisms related to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA-144 (miR-144)/glycogen synthase kinase-3β (GSK3β). Methods C57BL/6 mice were used to establish a lung I/R injury model while pulmonary microvascular endothelial cells (PMVECs) were constructed as hypoxia/reperfusion (H/R) cellular model, both of which were performed with Propofol treatment. Gain- or loss-of-function approaches were subsequently employed, followed by observation of cell apoptosis in lung tissues and evaluation of proliferative and apoptotic capabilities in H/R cells. Meanwhile, the inflammatory factors, autophagosomes, and autophagy-related proteins were measured. Results Our experimental data revealed that Propofol treatment could decrease the elevated expression of MALAT1 following I/R injury or H/R induction, indicating its protection against lung I/R injury. Additionally, overexpressing MALAT1 or GSK3β promoted the activation of autophagosomes, proinflammatory factor release, and cell apoptosis, suggesting that overexpressing MALAT1 or GSK3β may reverse the protective effects of Propofol against lung I/R injury. MALAT1 was identified to negatively regulate miR-144 to upregulate the GSK3β expression. Conclusion Overall, our study demonstrated that Propofol played a protective role in lung I/R injury by suppressing autophagy and decreasing release of inflammatory factors, with the possible involvement of the MALAT1/miR-144/GSK3β axis.

scholarly journals The protective effects of pomegranate extracts against renal ischemia-reperfusion injury in male rats

2014 ◽  
Vol 6 (1) ◽  
pp. 46 ◽  
Author(s):  
AhmetA Sancaktutar ◽  
MehmetN Bodakci ◽  
NamıkK Hatipoglu ◽  
Kemal Basarılı ◽  
Haluk Soylemez ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Male Rats ◽  
Protective Effects ◽  
Renal Ischemia Reperfusion Injury

Abstract 428: Pharmacologic and Activated Fibroblast-specific Gβγ-GRK2 Inhibition is Protective Following Ischemia Reperfusion Injury

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Joshua G Travers ◽  
Fadia A Kamal ◽  
Michelle L Nieman ◽  
Michelle A Sargent ◽  
Jeffery D Molkentin ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Function ◽  
Reperfusion Injury ◽  
G Protein ◽  
Knockout Mice ◽  
Ischemia Reperfusion Injury ◽  
Interstitial Fibrosis ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Ventricular Compliance

Heart failure is a devastating disease characterized by chamber remodeling, interstitial fibrosis and reduced ventricular compliance. Cardiac fibroblasts are responsible for extracellular matrix homeostasis, however upon injury or pathologic stimulation, these cells transform to a myofibroblast phenotype and play a fundamental role in myocardial fibrosis and remodeling. Chronic sympathetic overstimulation induces excess signaling through G protein βγ subunits and ultimately the pathologic activation of G protein-coupled receptor kinase 2 (GRK2). We hypothesized that Gβγ-GRK2 inhibition plays an important role in the cardiac fibroblast to attenuate pathologic myofibroblast activation and cardiac remodeling. To investigate this hypothesis, mice were subjected to ischemia/reperfusion (I/R) injury and treated with the small molecule Gβγ-GRK2 inhibitor gallein. While animals receiving vehicle demonstrated a reduction in overall cardiac function as measured by echocardiography, mice treated with gallein exhibited nearly complete preservation of cardiac function and reduced fibrotic scar formation. We next sought to establish the cell specificity of this compound by treating inducible cardiomyocyte- and activated fibroblast-specific GRK2 knockout mice post-I/R. Although we observed modest restoration in cardiac function in cardiomyocyte-specific GRK2 null mice, treatment of these mice with gallein resulted in further protection against myocardial dysfunction following injury, suggesting a functional role in other cardiac cell types, including fibroblasts. Activated fibroblast-specific GRK2 knockout mice were also subjected to ischemia/reperfusion injury; these animals displayed preserved myocardial function and reduced collagen deposition compared to littermate controls following injury. Furthermore, systemic Gβγ-GRK2 inhibition by gallein did not appear to confer further protection over activated fibroblast-specific GRK2 ablation alone. In summary, these findings suggest a potential therapeutic role for Gβγ-GRK2 inhibition in limiting pathologic myofibroblast activation, interstitial fibrosis and heart failure progression.

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