Limits...
Effects of the antioxidant sulforaphane on hyperlocomotion and prepulse inhibition deficits in mice after phencyclidine administration.

Shirai Y, Fujita Y, Hashimoto K - Clin Psychopharmacol Neurosci (2012)

Bottom Line: This study was undertaken to examine the effects of the potent antioxidant sulforaphane (SFN), found in cruciferous vegetables, on behavioral abnormalities (e.g., hyperlocomotion and prepulse inhibition [PPI] deficits) in mice after a single administration of the N-methyl-D-aspartate (NMDA)-receptor antagonist phencyclidine (PCP).These results suggest that SFN has antipsychotic activity in an animal model of schizophrenia.Therefore, it is likely that SFN may be a potential therapeutic drug for schizophrenia.

View Article: PubMed Central - PubMed

Affiliation: Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan.

ABSTRACT

Objective: Accumulating evidence suggests that oxidative stress plays a role in the pathophysiology of schizophrenia and that the potent antioxidants may be potential therapeutic drugs for schizophrenia. This study was undertaken to examine the effects of the potent antioxidant sulforaphane (SFN), found in cruciferous vegetables, on behavioral abnormalities (e.g., hyperlocomotion and prepulse inhibition [PPI] deficits) in mice after a single administration of the N-methyl-D-aspartate (NMDA)-receptor antagonist phencyclidine (PCP).

Methods: Effects of SFN (3, 10, and 30 mg/kg, intraperitoneally [i.p.]) on hyperlocomotion and PPI deficits in the adult male ddY mice after administration of PCP (3.0 mg/kg, subcutaneously [s.c.]) were examined.

Results: Administration of SFN (30 mg/kg, intraperitoneally [i.p.]), but not low doses (3 and 10 mg/kg, i.p.), significantly attenuated hyperlocomotion in mice after PCP administration (3.0 mg/kg, subcutaneously [s.c.]). Furthermore, administration of SFN (3, 10, and 30 mg/kg, i.p.) attenuated the PPI deficits in mice after PCP administration (3.0 mg/kg, s.c.) in a dose-dependent manner.

Conclusion: These results suggest that SFN has antipsychotic activity in an animal model of schizophrenia. Therefore, it is likely that SFN may be a potential therapeutic drug for schizophrenia.

No MeSH data available.


Related in: MedlinePlus

Effect of sulforaphane (SFN) on phencyclidine (PCP)-induced prepulse inhibition deficits in mice. Thirty minutes after a single intraperitoneally administration of vehicle (10 ml/kg), or SFN (3.0, 10 or 30 mg/kg), PCP (3 mg/kg) or vehicle (10 ml/kg) was administered subcutaneously to the mice. Each value is the mean±standard error of the mean (n=17-21 per group). PPI, prepulse inhibition. *p<0.05, ***p<0.01 as compared with the vehicle+PCP treated group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3569145&req=5

Figure 3: Effect of sulforaphane (SFN) on phencyclidine (PCP)-induced prepulse inhibition deficits in mice. Thirty minutes after a single intraperitoneally administration of vehicle (10 ml/kg), or SFN (3.0, 10 or 30 mg/kg), PCP (3 mg/kg) or vehicle (10 ml/kg) was administered subcutaneously to the mice. Each value is the mean±standard error of the mean (n=17-21 per group). PPI, prepulse inhibition. *p<0.05, ***p<0.01 as compared with the vehicle+PCP treated group.

Mentions: Fig. 2 shows the effects of SFN (3.0, 10, or 30 mg/kg) on PCP (3.0 mg/kg)-induced PPI deficits in mice. The MANOVA analysis of all PPI data revealed a significant effect (Wilks lambda=0.500; p<0.001). Subsequent ANOVA analyses revealed significant differences (p<0.001) for all dB groups (69, 73, 77, and 81 dB). A post hoc analysis indicated a significant (p<0.001) difference in PPI deficits between the vehicle and vehicle+PCP (3.0 mg/kg) groups at all dB levels (Fig. 3). Pretreatment with SFN (3.0, 10, or 30 mg/kg) attenuated PCP-induced PPI deficits in a dose-dependent manner. A high SFN dose (30 mg/kg) significantly attenuated PCP-induced PPI deficits at 73 and 81 dB (Fig. 3). In contrast, PPI in mice after SFN administration (30 mg/kg) alone was similar to that in control mice (Fig. 3).


Effects of the antioxidant sulforaphane on hyperlocomotion and prepulse inhibition deficits in mice after phencyclidine administration.

Shirai Y, Fujita Y, Hashimoto K - Clin Psychopharmacol Neurosci (2012)

Effect of sulforaphane (SFN) on phencyclidine (PCP)-induced prepulse inhibition deficits in mice. Thirty minutes after a single intraperitoneally administration of vehicle (10 ml/kg), or SFN (3.0, 10 or 30 mg/kg), PCP (3 mg/kg) or vehicle (10 ml/kg) was administered subcutaneously to the mice. Each value is the mean±standard error of the mean (n=17-21 per group). PPI, prepulse inhibition. *p<0.05, ***p<0.01 as compared with the vehicle+PCP treated group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3569145&req=5

Figure 3: Effect of sulforaphane (SFN) on phencyclidine (PCP)-induced prepulse inhibition deficits in mice. Thirty minutes after a single intraperitoneally administration of vehicle (10 ml/kg), or SFN (3.0, 10 or 30 mg/kg), PCP (3 mg/kg) or vehicle (10 ml/kg) was administered subcutaneously to the mice. Each value is the mean±standard error of the mean (n=17-21 per group). PPI, prepulse inhibition. *p<0.05, ***p<0.01 as compared with the vehicle+PCP treated group.
Mentions: Fig. 2 shows the effects of SFN (3.0, 10, or 30 mg/kg) on PCP (3.0 mg/kg)-induced PPI deficits in mice. The MANOVA analysis of all PPI data revealed a significant effect (Wilks lambda=0.500; p<0.001). Subsequent ANOVA analyses revealed significant differences (p<0.001) for all dB groups (69, 73, 77, and 81 dB). A post hoc analysis indicated a significant (p<0.001) difference in PPI deficits between the vehicle and vehicle+PCP (3.0 mg/kg) groups at all dB levels (Fig. 3). Pretreatment with SFN (3.0, 10, or 30 mg/kg) attenuated PCP-induced PPI deficits in a dose-dependent manner. A high SFN dose (30 mg/kg) significantly attenuated PCP-induced PPI deficits at 73 and 81 dB (Fig. 3). In contrast, PPI in mice after SFN administration (30 mg/kg) alone was similar to that in control mice (Fig. 3).

Bottom Line: This study was undertaken to examine the effects of the potent antioxidant sulforaphane (SFN), found in cruciferous vegetables, on behavioral abnormalities (e.g., hyperlocomotion and prepulse inhibition [PPI] deficits) in mice after a single administration of the N-methyl-D-aspartate (NMDA)-receptor antagonist phencyclidine (PCP).These results suggest that SFN has antipsychotic activity in an animal model of schizophrenia.Therefore, it is likely that SFN may be a potential therapeutic drug for schizophrenia.

View Article: PubMed Central - PubMed

Affiliation: Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan.

ABSTRACT

Objective: Accumulating evidence suggests that oxidative stress plays a role in the pathophysiology of schizophrenia and that the potent antioxidants may be potential therapeutic drugs for schizophrenia. This study was undertaken to examine the effects of the potent antioxidant sulforaphane (SFN), found in cruciferous vegetables, on behavioral abnormalities (e.g., hyperlocomotion and prepulse inhibition [PPI] deficits) in mice after a single administration of the N-methyl-D-aspartate (NMDA)-receptor antagonist phencyclidine (PCP).

Methods: Effects of SFN (3, 10, and 30 mg/kg, intraperitoneally [i.p.]) on hyperlocomotion and PPI deficits in the adult male ddY mice after administration of PCP (3.0 mg/kg, subcutaneously [s.c.]) were examined.

Results: Administration of SFN (30 mg/kg, intraperitoneally [i.p.]), but not low doses (3 and 10 mg/kg, i.p.), significantly attenuated hyperlocomotion in mice after PCP administration (3.0 mg/kg, subcutaneously [s.c.]). Furthermore, administration of SFN (3, 10, and 30 mg/kg, i.p.) attenuated the PPI deficits in mice after PCP administration (3.0 mg/kg, s.c.) in a dose-dependent manner.

Conclusion: These results suggest that SFN has antipsychotic activity in an animal model of schizophrenia. Therefore, it is likely that SFN may be a potential therapeutic drug for schizophrenia.

No MeSH data available.


Related in: MedlinePlus