scholarly journals Study of the protective effect of ischemic and pharmacological preconditioning on hepatic ischemic reperfusion injury induced in rats

JGH Open ◽  
2017 ◽  
Vol 1 (3) ◽  
pp. 105-111 ◽  
Author(s):  
Afaf S Osman ◽  
Ahmed H Osman ◽  
Mahmoud M Kamel
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Pharmacological Preconditioning

scholarly journals Protective Effect of Pharmacological Preconditioning of Total Flavones of Abelmoschl Manihot on Cerebral Ischemic Reperfusion Injury in Rats

2007 ◽  
Vol 35 (04) ◽  
pp. 653-661 ◽  
Author(s):  
Ji-Yue Wen ◽  
Zhi-Wu Chen
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inos Mrna ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Infarction Volume ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion ◽  
Pharmacological Preconditioning

The present study was to investigate the effect of pharmacological preconditioning of total flavones of Abelmoschl Manihot (TFA) on cerebral ischemic reperfusion injury in rats. Rat cerebral ischemia/reperfusion injury was induced by occluding the right middle cerebral artery (MCA). The infarct size was determined by staining with 2,3,5-triphenyl tetrazalium chloride (TTC). The serum malonaldehyde (MDA), nitric oxide (NO) and lactate dehydrogenase (LDH) levels were measured by using spectrophotometry; Inducible NO synthase (iNOS) mRNA expression was detected by RT-PCR method. The percentage of cerebral infarction volume was 28.1 ± 0.8 in the model group, while TFA or nimodipine (Nim) pretreatment 36 hours prior to the ischemic insult significantly decreased the infarction volume. Increases of serum LDH activity and MDA level were observed after ischemia/reperfusion, but these changes were inhibited in rats pretreated with either TFA (20, 40, 80, 160 mg/kg) or Nim, indicating a delayed protective effect of TFA preconditioning on cerebral ischemic reperfusion injury. In addition, the serum NO level and the cerebral iNOS mRNA were up-regulated, suggesting a possible mechanism for the protective effect of TFA pretreatment on cerebral ischemic reperfusion injury.

Protective effect of bradykinin antagonist Hoe-140 during in vivo myocardial ischemic-reperfusion injury in the cat

2003 ◽  
Vol 115 (3) ◽  
pp. 211-218 ◽  
Author(s):  
Rashmi Kumari ◽  
Mohua Maulik ◽  
Subhash Chandra Manchanda ◽  
Subir Kumar Maulik
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Bradykinin Antagonist ◽  
Hoe 140

scholarly journals PROTECTIVE EFFECT OF ETHANOLIC EXTRACT FROM THE ROOT OF ARGYREIA SPECIOSA AGAINST GLOBAL CEREBRAL ISCHEMIC REPERFUSION INJURY IN RATS

2018 ◽  
Vol 8 (6) ◽  
pp. 8-15
Author(s):  
Bhagat Singh Jaiswal ◽  
Mukul Tailang
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Ethanolic Extract ◽  
Cerebral Stroke ◽  
Sham Control ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Group I ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Reperfusion

Cerebral stroke is the principal reason of death without effective treatment in the world and recognized as the common cause of disability. Argyreia speciosa (Linn.f.) (Convolvulaceae, Synonyms: Argyreia nervosa) is widely distributed plant species in India. It is commonly known as Elephant creeper and Vryddhadaru. A. speciosa is a very valuable plant in the Ayurvedic system. In 'Rasayan' drug it has been used for the treatment of various neurological diseases. Its root taste is bitter and having the multiple uses like as a brain tonic, nootropic, anti-anxiety and anticonvulsant activity. The current study, plan to investigate the neuroprotective effect of ethanolic extract of A. speciosa root (ASEE) in a validate rat model of stroke known as global cerebral ischemic reperfusion injury (GCIRI). We divided 36 male Wistar rats to six experimental groups (n= 6). The group-I considered as sham control (no GCIRI), Group-II saline treated GCIRI, Group-III, IV, and V received ASEE (100, 200 and 400 mg/kg, p.o.) for 7 days prior to the induction of GCIRI while Group-VI termed as standard and it received quercetin (20 mg/kg, i.p.) 30 min prior induction of GCIRI. GCIRI produced the significant neurological deficit, sensorimotor dysfunction, decrease neurobehavioral parameters, increased cerebral infarction area and brain edema as compared with sham control rats. Seven days of pretreatment with ASEE markedly attenuates all the changes caused by GCIRI to the normal level. Our results proved that ASEE possess the protective effect on GCIRI induced stroke and aforementioned neuroprotection may be due to its antioxidant and anti-inflammatory property. Keywords: Brain stroke, BCCAO, Antioxidants, Neuroprotection, Argyreia speciosa

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