Abstract WP138: Jiedu Tongluo Injection, a Chinese Herbal Extract Complex Prescription, Protects Cerebral Ischemia/Reperfusion by Modulating Inflammatory Cascade
Background: The pathological and physiological mechanism of cerebral ischemia/reperfusion (I/R) is considered to be related to energy metabolism failure, excitotoxicity, free radicals, Ca2+ overload, and platelet activation, et al. In recent years, it is proved that inflammatory cascade plays an important role in I/R damage. Jiedu Tongluo injection (JDTL) is a compound prescription comprising of Geniposide (50 mg/ml), Panax Notoginseng Saponins (180 mg/ml), and Scutellarin (8 mg/ml), which are extracted from Chinese herb medicine. Several previous researches have proved that JDTL can inhibit experimental thrombosis and platelet aggregation significantly. We assessed the hypothesis that JDTL could ameliorate cerebral ischemia/reperfusion injury in rats by modulating inflammatory cascade.
Methods: One hundred and twenty SD rats (4 months old, 250±20g) were subjected to middle cerebral artery occlusion for 2 hours followed by 24 hours reperfusion or sham operation. Vehicle, JDTL (4 ml/kg, 2 ml/kg, and 1 ml/kg respectively) were injected 15 minutes after ischemia. Neurobehavioral tests were conducted 1, 4, and 24 hours after reperfusion. Infarct size, adhesion molecule, inflammatory molecule, and transcription factors were measured at 24 hours after reperfusion.
Results: JDTL 4 ml/kg and 2 ml/kg significantly ameliorated the neurobehavioral impairment (p<0.05) and decreased infarct size compared to vehicle (p<0.05). The result of ELISA showed that JDTL 4 ml/kg and 2 ml/kg down-regulated the expression of adhesion molecule (ICAM-1, VCAM-1 and E-selectin) and inflammatory factors (IL-1β, IL-6 and TNF-α) in the brain compared to vehicle (p<0.05). JDTL 4 ml/kg and 2 ml/kg also reduced the expression of NF-κB, p38, and p44/42 detected by immunohistology staining (p<0.05) and western blot (p<0.05).
Conclusion: JDTL has a protective effect on rats after I/R injury by decreasing infarct size, down-regulating the expression of adhesion molecules, inflammatory factors, transcription factors and inhibiting MAPK pathway.
- © 2012 by American Heart Association, Inc.