The pharmacologically active components of oxytropis falcata bungereduce ischemic-reperfusion injury in the rat heart

2016 ◽  
Author(s):  
Dejun Zhang ◽  
Ruofei Jiang ◽  
Eun-Kyung Hong ◽  
Guosheng Tan ◽  
Dianxiang Lu ◽  
...  
Keyword(s):  
Ethyl Acetate ◽  
Reperfusion Injury ◽  
Pathological Change ◽  
Total Flavonoids ◽  
Active Components ◽  
Ischemic Reperfusion Injury ◽  
Rat Serum ◽  
Ischemic Reperfusion ◽  
Pharmacologically Active ◽  
Ethyl Acetate Extracts

Oxytropis falcata is used as the main material to prepare various Tibetan traditional medicine, which its activity was reported that anti-inflammation and analgesia. Flavonoids is the chemical basis for the anti-inflammatory and anti-oxidant efficacy. The influence of total flavonoids of Tibetan herb O. falcata on myocardial ischemic-reperfusion injury was investigated using ethanol, chloroform, and ethyl acetate extracts. Rats were pretreated with different concentrations of the extract for 7 days. The model of myocardial ischemic-reperfusion injury was established by ligating the left anterior descending (LAD) artery in the heart. Following reperfusion for 40 minutes, the enzyme activity of creatine kinase (CK), lactic acid dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px), and the concentration of malondialdehyde (MDA) in the rat serum were measured. The ultrastructural pathological change was observed under transmission electron microscopy (TEM). The serum levels of CK, LDH, and MDA were reduced, and the activity of SOD and GSH-Px were increased significantly, by chloroform and ethyl acetate extracts (P Less Than 0.01, PP Less Than 0.05). The ultrastructural pathological change in myocardial ischemic-reperfusion injury was alleviated by both extracts. The major components in chloroform extract were 7-hydroxy-flavonone and 2',4'-dihydroxy chalcone. 7-Hydroxy-flavanon naringenine naringetol and 2',4'-dihydroxy chalcone were the major components in ethyl acetate extract. Total flavonoids of Tibetan herb O. falcata might alleviate myocardial ischemic-reperfusion injury.

The Effect of C1 Esterase Inhibitor on Ischemic Reperfusion Injury in Rat Epigastric Skin Flaps: Preliminary Results

2014 ◽  
Vol 30 (S 01) ◽  
Author(s):  
Inmaculada Jurado ◽  
Alberto Rodríguez ◽  
Carmen Vázquez ◽  
Víctor Velasco ◽  
Víctor Turrión ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Skin Flaps ◽  
Ischemic Reperfusion Injury ◽  
Preliminary Results ◽  
C1 Esterase Inhibitor ◽  
Ischemic Reperfusion ◽  
Esterase Inhibitor

Myocardial Ischemic-reperfusion Injury in a Rat Model of Metabolic Syndrome

Obesity ◽  
2008 ◽  
Vol 16 (10) ◽  
pp. 2253-2258 ◽  
Author(s):  
Mahmood S. Mozaffari ◽  
Stephen W. Schaffer
Keyword(s):  
Metabolic Syndrome ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

scholarly journals Role of NAD(P)H Oxidase- and Mitochondria-Derived Reactive Oxygen Species in Cardioprotection of Ischemic Reperfusion Injury by Angiotensin II

Hypertension ◽  
2005 ◽  
Vol 45 (5) ◽  
pp. 860-866 ◽  
Author(s):  
Shoji Kimura ◽  
Guo-Xing Zhang ◽  
Akira Nishiyama ◽  
Takatomi Shokoji ◽  
Li Yao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Reperfusion Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

Abstract 90: Diabetes Impairs Post-stroke Cerebrovascular Plasticity And Long-term Functional Recovery.

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Roshini Prakash ◽  
Weiguo Li ◽  
Zhi Qu ◽  
Susan C Fagan ◽  
Adviye Ergul
Keyword(s):  
Cognitive Decline ◽  
Reperfusion Injury ◽  
Functional Recovery ◽  
Diabetic Rats ◽  
Neurological Deficits ◽  
Ischemic Reperfusion Injury ◽  
Post Stroke ◽  
Ischemic Reperfusion ◽  
Sensorimotor Recovery ◽  
The Impact

Background: Stroke associated with pre-existing diabetes worsens ischemic injury and impairs recovery. We have previously shown that type-2-diabetic rats subjected to cerebral ischemic reperfusion injury develop hemorrhagic transformation (HT) and greater neurological deficits. These diabetic rats also exhibit enhanced dysfunctional cerebral neovascularization that increases the risk of bleeding post-stroke. However, our knowledge of vascular and functional plasticity during the recovery phase of diabetic stroke is limited. This study tested the hypothesis that post-stroke neovascularization is impaired in diabetes and this is associated with poor sensorimotor and cognitive outcomes. Methods: Reparative neovascularization was assessed in the lesional and non-lesional areas in diabetic rats after 14 days of ischemic reperfusion injury. 3-dimensional reconstruction of the FITC stained vasculature were obtained by confocal microscopy and stereological parameters including vascular volume and surface area were measured. Astrogliosis was also determined by GFAP staining. The relative rates of sensorimotor recovery, cognitive decline and spontaneous activity were assessed. Results: Diabetes impairs reparative neovascularization in the lesional areas compared to control rats. Astroglial swelling and reactivity was pronounced in diabetic stroke compared to control stroke. Rate of sensorimotor recovery was significantly slower in diabetic stroke compared to the controls. Diabetes also exacerbated anxiety-like symptoms and cognitive decline post-stroke relative to control. Conclusion: Diabetes impairs post-stroke reparative neovascularization and impedes functional recovery. The impact of glycemic control on poor recovery in this critical period needs to be tested. N=6-8 * p≤ 0.05, ** p≤ 0.005

Double-Negative αβ T cells: A Novel Player in Lung Ischemic-Reperfusion Injury

2018 ◽  
Vol 37 (4) ◽  
pp. S221
Author(s):  
J. Hsu ◽  
A. Krishnan ◽  
S. Lee ◽  
J.M. Dodd-o ◽  
B. Kim ◽  
...  
Keyword(s):  
T Cells ◽  
Reperfusion Injury ◽  
Double Negative ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Αβ T Cells
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