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Protective Effect of Pharmacological Preconditioning of Total Flavones of Abelmoschl Manihot on Cerebral Ischemic Reperfusion Injury in Rats
Author(s) -
Jiyue Wen,
Zhiwu Chen
Publication year - 2007
Publication title -
the american journal of chinese medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 63
eISSN - 1793-6853
pISSN - 0192-415X
DOI - 10.1142/s0192415x07005144
Subject(s) - nimodipine , medicine , reperfusion injury , ischemia , lactate dehydrogenase , nitric oxide synthase , pharmacology , cerebral infarction , anesthesia , nitric oxide , flavones , chemistry , biochemistry , enzyme , calcium , chromatography
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.

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