Effect of basic fibroblast growth factor on focal ischemic injury and antioxidant enzyme activities
Abstract
AIM:
To explore the effect of basic fibroblast growth factor (bFGF) on focal cerebral ischemic injury and antioxidant enzyme activities.
METHODS:
Rats underwent 24-h middle cerebral artery occlusion by intraluminal suture. Infarction volume was shown with staining and quantitated by image analysis system. Neurologic deficit scores were determined with a 0-5 grade scale. Antioxidant enzyme activities of forebrains were detected.
RESULTS:
bFGF (45 micrograms.kg-1.h-1 i.v. for 3 h, started 5 min after the onset of ischemia) showed potent neuroprotective effects. Infarction volumes were decreased from 272 mm3 +/- 22 mm3 (saline-treated) to 201 mm3 +/- 30 mm3 (bFGF-treated). Neurologic deficit scores were decreased from 3.6 +/- 1.5 (saline-treated) to 2.3 +/- 1.6 (bFGF-treated). Focal cerebral ischemia induced an increase in the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), but a decrease in the level of glutathione s-transferase (GSH-ST). Treatment of bFGF further increased the CAT activity but had no effect on the activities of SOD, GSH-PX, and GSH-ST.
CONCLUSION:
bFGF has a neuroprotective effect against focal cerebral ischemic injury. The elevation of CAT activity by bFGF may be involved in this effect.
Keywords:
To explore the effect of basic fibroblast growth factor (bFGF) on focal cerebral ischemic injury and antioxidant enzyme activities.
METHODS:
Rats underwent 24-h middle cerebral artery occlusion by intraluminal suture. Infarction volume was shown with staining and quantitated by image analysis system. Neurologic deficit scores were determined with a 0-5 grade scale. Antioxidant enzyme activities of forebrains were detected.
RESULTS:
bFGF (45 micrograms.kg-1.h-1 i.v. for 3 h, started 5 min after the onset of ischemia) showed potent neuroprotective effects. Infarction volumes were decreased from 272 mm3 +/- 22 mm3 (saline-treated) to 201 mm3 +/- 30 mm3 (bFGF-treated). Neurologic deficit scores were decreased from 3.6 +/- 1.5 (saline-treated) to 2.3 +/- 1.6 (bFGF-treated). Focal cerebral ischemia induced an increase in the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), but a decrease in the level of glutathione s-transferase (GSH-ST). Treatment of bFGF further increased the CAT activity but had no effect on the activities of SOD, GSH-PX, and GSH-ST.
CONCLUSION:
bFGF has a neuroprotective effect against focal cerebral ischemic injury. The elevation of CAT activity by bFGF may be involved in this effect.