Abstract
Background and purpose: Accumulated evidence suggests that oxidative stress is involved in amyloid b (Ab)-induced cognitive dysfunction. Silibinin (silybin), a flavonoid derived from the herb milk thistle (Silybum marianum), has been shown to have antioxidative properties; however, it remains unclear whether silibinin improves Ab-induced neurotoxicity. In the present study, we examined the effect of silibinin on the memory impairment and accumulation of oxidative stress induced by Ab25-35 in mice. Experimental approach: Aggregated Ab25-35 (3 nmol) was intracerebroventricularly administered to mice. Treatment with silibinin (2, 20 and 200 mg-kg-1, once a day, p.o.) was started immediately after the injection of Ab25-35. Locomotor activity was evaluated 6 days after the Ab25-35 treatment, and cognitive function was evaluated in a Y-maze and novel object recognition tests 6-11 days after the Ab25-35 treatment. The levels of lipid peroxidation (malondialdehyde) and antioxidant (glutathione) in the hippocampus were measured 7 days after the Ab25-35 injection. Key results: Silibinin prevented the memory impairment induced by Ab25-35 in the Y-maze and novel object recognition tests. Repeated treatment with silibinin attenuated the Ab25-35-induced accumulation of malondialdehyde and depletion of glutathione in the hippocampus. Conclusions and implications: Silibinin prevents memory impairment and oxidative damage induced by Ab25-35 and may be a potential therapeutic agent for Alzheimer's disease.
| Original language | English |
|---|---|
| Pages (from-to) | 1270-1277 |
| Number of pages | 8 |
| Journal | British Journal of Pharmacology |
| Volume | 157 |
| Issue number | 7 |
| DOIs | |
| Publication status | Published - 29-10-2009 |
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All Science Journal Classification (ASJC) codes
- Pharmacology
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Silibinin prevents amyloid b peptide-induced memory impairment and oxidative stress in mice. / Lu, P.; Mamiya, T.; Lu, L. L.; Mouri, Akihiro; Zou, L. B.; Nagai, T.; Hiramatsu, M.; Ikejima, T.; Nabeshima, Toshitaka.
In: British Journal of Pharmacology, Vol. 157, No. 7, 29.10.2009, p. 1270-1277.Research output: Contribution to journal › Article
TY - JOUR
T1 - Silibinin prevents amyloid b peptide-induced memory impairment and oxidative stress in mice
AU - Lu, P.
AU - Mamiya, T.
AU - Lu, L. L.
AU - Mouri, Akihiro
AU - Zou, L. B.
AU - Nagai, T.
AU - Hiramatsu, M.
AU - Ikejima, T.
AU - Nabeshima, Toshitaka
PY - 2009/10/29
Y1 - 2009/10/29
N2 - Background and purpose: Accumulated evidence suggests that oxidative stress is involved in amyloid b (Ab)-induced cognitive dysfunction. Silibinin (silybin), a flavonoid derived from the herb milk thistle (Silybum marianum), has been shown to have antioxidative properties; however, it remains unclear whether silibinin improves Ab-induced neurotoxicity. In the present study, we examined the effect of silibinin on the memory impairment and accumulation of oxidative stress induced by Ab25-35 in mice. Experimental approach: Aggregated Ab25-35 (3 nmol) was intracerebroventricularly administered to mice. Treatment with silibinin (2, 20 and 200 mg-kg-1, once a day, p.o.) was started immediately after the injection of Ab25-35. Locomotor activity was evaluated 6 days after the Ab25-35 treatment, and cognitive function was evaluated in a Y-maze and novel object recognition tests 6-11 days after the Ab25-35 treatment. The levels of lipid peroxidation (malondialdehyde) and antioxidant (glutathione) in the hippocampus were measured 7 days after the Ab25-35 injection. Key results: Silibinin prevented the memory impairment induced by Ab25-35 in the Y-maze and novel object recognition tests. Repeated treatment with silibinin attenuated the Ab25-35-induced accumulation of malondialdehyde and depletion of glutathione in the hippocampus. Conclusions and implications: Silibinin prevents memory impairment and oxidative damage induced by Ab25-35 and may be a potential therapeutic agent for Alzheimer's disease.
AB - Background and purpose: Accumulated evidence suggests that oxidative stress is involved in amyloid b (Ab)-induced cognitive dysfunction. Silibinin (silybin), a flavonoid derived from the herb milk thistle (Silybum marianum), has been shown to have antioxidative properties; however, it remains unclear whether silibinin improves Ab-induced neurotoxicity. In the present study, we examined the effect of silibinin on the memory impairment and accumulation of oxidative stress induced by Ab25-35 in mice. Experimental approach: Aggregated Ab25-35 (3 nmol) was intracerebroventricularly administered to mice. Treatment with silibinin (2, 20 and 200 mg-kg-1, once a day, p.o.) was started immediately after the injection of Ab25-35. Locomotor activity was evaluated 6 days after the Ab25-35 treatment, and cognitive function was evaluated in a Y-maze and novel object recognition tests 6-11 days after the Ab25-35 treatment. The levels of lipid peroxidation (malondialdehyde) and antioxidant (glutathione) in the hippocampus were measured 7 days after the Ab25-35 injection. Key results: Silibinin prevented the memory impairment induced by Ab25-35 in the Y-maze and novel object recognition tests. Repeated treatment with silibinin attenuated the Ab25-35-induced accumulation of malondialdehyde and depletion of glutathione in the hippocampus. Conclusions and implications: Silibinin prevents memory impairment and oxidative damage induced by Ab25-35 and may be a potential therapeutic agent for Alzheimer's disease.
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UR - http://www.scopus.com/inward/citedby.url?scp=70349337734&partnerID=8YFLogxK
U2 - 10.1111/j.1476-5381.2009.00295.x
DO - 10.1111/j.1476-5381.2009.00295.x
M3 - Article
C2 - 19552690
AN - SCOPUS:70349337734
VL - 157
SP - 1270
EP - 1277
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
SN - 0007-1188
IS - 7
ER -