Objective: To explore the protective effects of intranasal (IN) dosing of nerve growth factor (NGF) on brain injury induced by organophosphorus compounds (OP) in rats.
Methods: The OP-treated Sprague-Dawley rats received an intraperitoneal injection of atropine sulphate and pralidoxime at 1 min after intoxication. Then NGF or saline was dosed via the olfactory pathway. All rats were sacrificed 24 hours after OP exposure. Damaged nerve cells were estimated on corpus striatum strained with hematoxylin-eosin (H&E) method. And the activity of acetylcholinesterase (AchE) and the concentrations of malondialdehyde (MDA) and reduced glutathione hormone (GSH) in corpus striatum were measured by colorimetric method.
Results: As assessed by H&E staining, a large number of degenerated and necrotic nerve cells were observed in corpus striatum in rats from in IN saline group. But in IN NGF group, the number of degenerated neurons was smaller than in IN NS group. Following OP exposure, the activity of AchE decreased in corpus striatum in both IN saline and IN NGF groups (0.46 ± 0.11 vs 0.35 ± 0.09 U/mg prot). No significant differences existed between two groups. But the concentrations of MDA in corpus striatum of IN NGF group rats reduced markedly by 25.14% (4.02 ± 0.85 vs 5.37 ± 1.33 nmol/mg prot) and the level of GSH increased sharply by 15.73% (52.82 ± 2.80 vs 45.64 ± 4.88 mg/g prot) as compared with IN saline group (P < 0.05).
Conclusion: Intranasal dosing of NGF may improve neuropathology and protect rats against OP-induced oxidative damage in corpus striatum.