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Silibinin prevents amyloid beta peptide-induced memory impairment and oxidative stress in mice.
Br J Pharmacol. 2009 Aug; 157(7):1270-7.BJ

Abstract

BACKGROUND AND PURPOSE

Accumulated evidence suggests that oxidative stress is involved in amyloid beta (Abeta)-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 Abeta-induced neurotoxicity. In the present study, we examined the effect of silibinin on the memory impairment and accumulation of oxidative stress induced by Abeta(25-35) in mice.

EXPERIMENTAL APPROACH

Aggregated Abeta(25-35) (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 Abeta(25-35). Locomotor activity was evaluated 6 days after the Abeta(25-35) treatment, and cognitive function was evaluated in a Y-maze and novel object recognition tests 6-11 days after the Abeta(25-35) treatment. The levels of lipid peroxidation (malondialdehyde) and antioxidant (glutathione) in the hippocampus were measured 7 days after the Abeta(25-35) injection.

KEY RESULTS

Silibinin prevented the memory impairment induced by Abeta(25-35) in the Y-maze and novel object recognition tests. Repeated treatment with silibinin attenuated the Abeta(25-35)-induced accumulation of malondialdehyde and depletion of glutathione in the hippocampus.

CONCLUSIONS AND IMPLICATIONS

Silibinin prevents memory impairment and oxidative damage induced by Abeta(25-35) and may be a potential therapeutic agent for Alzheimer's disease.

Authors+Show Affiliations

Department of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, Meijo University, 150 Yagotoyama, Tempaku-ku, Nagoya, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19552690

Citation

Lu, P, et al. "Silibinin Prevents Amyloid Beta Peptide-induced Memory Impairment and Oxidative Stress in Mice." British Journal of Pharmacology, vol. 157, no. 7, 2009, pp. 1270-7.
Lu P, Mamiya T, Lu LL, et al. Silibinin prevents amyloid beta peptide-induced memory impairment and oxidative stress in mice. Br J Pharmacol. 2009;157(7):1270-7.
Lu, P., Mamiya, T., Lu, L. L., Mouri, A., Zou, L., Nagai, T., Hiramatsu, M., Ikejima, T., & Nabeshima, T. (2009). Silibinin prevents amyloid beta peptide-induced memory impairment and oxidative stress in mice. British Journal of Pharmacology, 157(7), 1270-7. https://doi.org/10.1111/j.1476-5381.2009.00295.x
Lu P, et al. Silibinin Prevents Amyloid Beta Peptide-induced Memory Impairment and Oxidative Stress in Mice. Br J Pharmacol. 2009;157(7):1270-7. PubMed PMID: 19552690.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Silibinin prevents amyloid beta peptide-induced memory impairment and oxidative stress in mice. AU - Lu,P, AU - Mamiya,T, AU - Lu,L L, AU - Mouri,A, AU - Zou,Lb, AU - Nagai,T, AU - Hiramatsu,M, AU - Ikejima,T, AU - Nabeshima,T, Y1 - 2009/06/22/ PY - 2009/6/26/entrez PY - 2009/6/26/pubmed PY - 2010/1/15/medline SP - 1270 EP - 7 JF - British journal of pharmacology JO - Br J Pharmacol VL - 157 IS - 7 N2 - BACKGROUND AND PURPOSE: Accumulated evidence suggests that oxidative stress is involved in amyloid beta (Abeta)-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 Abeta-induced neurotoxicity. In the present study, we examined the effect of silibinin on the memory impairment and accumulation of oxidative stress induced by Abeta(25-35) in mice. EXPERIMENTAL APPROACH: Aggregated Abeta(25-35) (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 Abeta(25-35). Locomotor activity was evaluated 6 days after the Abeta(25-35) treatment, and cognitive function was evaluated in a Y-maze and novel object recognition tests 6-11 days after the Abeta(25-35) treatment. The levels of lipid peroxidation (malondialdehyde) and antioxidant (glutathione) in the hippocampus were measured 7 days after the Abeta(25-35) injection. KEY RESULTS: Silibinin prevented the memory impairment induced by Abeta(25-35) in the Y-maze and novel object recognition tests. Repeated treatment with silibinin attenuated the Abeta(25-35)-induced accumulation of malondialdehyde and depletion of glutathione in the hippocampus. CONCLUSIONS AND IMPLICATIONS: Silibinin prevents memory impairment and oxidative damage induced by Abeta(25-35) and may be a potential therapeutic agent for Alzheimer's disease. SN - 1476-5381 UR - https://www.unboundmedicine.com/medline/citation/19552690/Silibinin_prevents_amyloid_beta_peptide_induced_memory_impairment_and_oxidative_stress_in_mice_ L2 - https://doi.org/10.1111/j.1476-5381.2009.00295.x DB - PRIME DP - Unbound Medicine ER -