Ameliorating effects of HX106N, a water-soluble botanical formulation, on Aβ25-35-induced memory impairment and oxidative stress in mice

Biological and Pharmaceutical Bulletin

Volumn 37, Issue 6, 2014, Pages 954-960

  Lee, Doo Suk ^a   Choi, Jinyong ^a   Kim, Seon Hee ^b   Kim, Sunyoung ^a,b  

^a Seoul National University   (South Korea)

^b ViroMed Co Ltd   (South Korea)

Author keywords

Alzheimer's disease; Heme oxygenase 1; HX106N; Memory impairment; Oxidative stress

Indexed keywords

AMYLOID BETA PROTEIN[25-35]; ANTIOXIDANT; DONEPEZIL; HEME OXYGENASE 1; HX106N; INTERLEUKIN 1BETA; MESSENGER RNA; NEUROPROTECTIVE AGENT; PLANT EXTRACT; THIOBARBITURIC ACID REACTIVE SUBSTANCE; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG; AMYLOID BETA PROTEIN; AMYLOID BETA-PROTEIN (25-35); PEPTIDE FRAGMENT; WATER;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DIMOCARPUS LONGAN; DOSE RESPONSE; GASTRODIA ELATA; GENE EXPRESSION REGULATION; HO 1 GENE; LATENT PERIOD; LIPID PEROXIDATION; LIRIOPE PLATYPHYLLA; MALE; MAZE TEST; MEDICINAL PLANT; MEMORY DISORDER; MOUSE; NERVE CELL; NEUROPROTECTION; NEUROTOXICITY; NONHUMAN; OXIDATIVE STRESS; PASSIVE AVOIDANCE TEST; PROTEIN EXPRESSION; QUANTITATIVE ANALYSIS; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; SALVIA MILTIORRHIZA; TREATMENT DURATION; TREATMENT OUTCOME; WORKING MEMORY; ANIMAL; CELL LINE; CHEMICALLY INDUCED; CHEMISTRY; DRUG EFFECTS; HIPPOCAMPUS; INSTITUTE FOR CANCER RESEARCH MOUSE; INTRACEREBROVENTRICULAR DRUG ADMINISTRATION; ISOLATION AND PURIFICATION; MEMORY DISORDERS; METABOLISM; ORAL DRUG ADMINISTRATION; SOLUBILITY; TOXICITY;

ADMINISTRATION, ORAL; AMYLOID BETA-PEPTIDES; ANIMALS; CELL LINE; HIPPOCAMPUS; INJECTIONS, INTRAVENTRICULAR; LIPID PEROXIDATION; MALE; MAZE LEARNING; MEMORY DISORDERS; MICE, INBRED ICR; NEURONS; OXIDATIVE STRESS; PEPTIDE FRAGMENTS; PLANT EXTRACTS; PLANTS, MEDICINAL; SOLUBILITY; WATER;

EID: 84901834193     PISSN: 09186158     EISSN: 13475215     Source Type: Journal    
DOI: 10.1248/bpb.b13-00906     Document Type: Article

References (29)

1. Selkoe DJ. Alzheimer's disease - a central role for amyloid. J. Neuropathol. Exp. Neurol., 53, 438-447 (1994).
2. Walsh DM, Selkoe DJ. Deciphering the molecular basis of memory failure in Alzheimer's disease. Neuron, 44, 181-193 (2004).
3. Schubert D, Behl C, Lesley R, Brack A, Dargusch R, Sagara Y, Kimura H. Amyloid peptides are toxic via a common oxidative mechanism. Proc. Natl. Acad. Sci. U.S.A., 92, 1989-1993 (1995).
4. Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, Cooper NR, Eikelenboom P, Emmerling M, Fiebich BL, Finch CE, Frautschy S, Griffin WST, Hampel H, Hull M, Landreth G, Lue LF, Mrak R, Mackenzie IR, McGeer PL, O'Banion MK, Pachter J, Pasinetti G, Plata-Salaman C, Rogers J, Rydel R, Shen Y, Streit W, Strohmeyer R, Tooyoma I, Van Muiswinkel FL, Veerhuis R, Walker D, Webster S, Wegrzyniak B, Wenk G, Wyss-Coray T, Grp NW. Inflammation and Alzheimer's disease. Neurobiol. Aging, 21, 383-421 (2000).
5. Mattson MP, Cheng B, Davis D, Bryant K, Lieberburg I, Rydel RE. beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity. J. Neurosci., 12, 376-389 (1992).
6. Ryter SW, Alam J, Choi AM. Heme oxygenase-1/carbon monoxide: from basic science to therapeutic applications. Physiol. Rev., 86, 583-650 (2006).
7. Schipper HM, Cissé S, Stopa EG. Expression of heme oxygenase-1 in the senescent and Alzheimer's diseased Brain. Ann. Neurol., 37, 758-768 (1995).
8. Castellani R, Smith MA, Richey PL, Perry G. Glycoxidation and oxidative stress in Parkinson's disease and diffuse Lewy body disease. Brain Res., 737, 195-200 (1996).
9. Chen K, Gunter K, Maines MD. Neurons overexpressing heme oxygenase-1 resist oxidative stress-mediated cell death. J. Neurochem., 75, 304-313 (2000).
10. Le WD, Xie WJ, Appel SH. Protective role of heme oxygenase-1 in oxidative stress-induced neuronal injury. J. Neurosci. Res., 56, 652-658 (1999).
11. Hung SY, Liou HC, Kang KH, Wu RM, Wen CC, Fu WM. Overexpression of heme oxygenase-1 protects dopaminergic neurons against l-methyl-4-phenylpyridinium- induced neurotoxicity. Mol. Pharmacol, 74, 1564-1575 (2008).
12. Park SJ, Park DH, Kim DH, Lee S, Yoon BH, Jung WY, Lee KT, Cheong JH, Ryu JH. The memory-enhancing effects of Euphoria longan fruit extract in mice. J. Ethnopharmacol., 128, 160-165 (2010).
13. Kang B, Ko E, No S, Park Y, Seo B, Seo Y. Herbology. Younlimsa, Seoul (2000).
14. Park J, Lee C. The encyclopedia of medicinal plants. Shinilbooks, Seoul, pp. 363-364 (2000).
15. Hur J, Lee P, Moon E, Kang I, Kim SH, Oh MS, Kim SY. Neurite outgrowth induced by spicatoside A, a steroidal saponin, via the tyrosine kinase A receptor pathway. Eur. J. Pharmacol, 620, 9-15 (2009).
16. Zhao G-R, Xiang Z-J, Ye T-X, Yuan Y-J, Guo Z-X. Antioxidant activities of Salvia miltiorrhiza and Panax notoginseng. Food Chem., 99, 767-774 (2006).
17. Kim JS, Narula AS, Jobin C. Salvia miltiorrhiza water-soluble extract, but not its constituent salvianolic acid B, abrogates LPS-induced NF-kappa B signalling in intestinal epithelial cells. Clin. Exp. Immunol., 141, 288-297 (2005).
18. Kim HJ, Moon KD, Oh SY, Kim SP, Lee SR. Ether fraction of methanol extracts of Gastrodia elata, a traditional medicinal herb, protects against kainic acid-induced neuronal damage in the mouse hippocampus. Neurosci. Lett., 314, 65-68 (2001).
19. Maurice T, Lockhart BP, Privat A. Amnesia induced in mice by centrally administered beta-amyloid peptides involves cholinergic dysfunction. Brain Res., 706, 181-193 (1996).
20. Arya M, Shergill IS, Williamson M, Gommersall L, Arya N, Patel HRH. Basic principles of real-time quantitative PCR. Expert Rev. Mol. Diagn., 5, 209-219 (2005).
21. Näslund J, Haroutunian V, Mohs R, Davis KL, Davies P, Greengard P, Buxbaum JD. Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline. JAMA, 283, 1571-1577 (2000).
22. Yamada K, Nabeshima T. Animal models of Alzheimer's disease and evaluation of anti-dementia drugs. Pharmacol. Ther., 88, 93-113 (2000).
23. Butterfield DA, Castegna A, Lauderback CM, Drake J. Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death. Neurobiol. Aging, 23, 655-664 (2002).
24. Wang Q, Wu J, Rowan MJ, Anwyl R. beta-Amyloid inhibition of long-term potentiation is mediated via tumor necrosis factor. Eur. J. Neurosci., 22, 2827-2832 (2005).
25. Schmid AW, Lynch MA, Herron CE. The effects of IL-1 receptor antagonist on beta amyloid mediated depression of LTP in the rat CA1 in vivo. Hippocampus, 19, 670-676 (2009).
26. Minogue AM, Schmid AW, Fogarty MP, Moore AC, Campbell VA, Herron CE, Lynch MA. Activation of the c-Jun N-terminal kinase signaling cascade mediates the effect of amyloid-beta on long term potentiation and cell death in hippocampus: a role for interleukin-1beta? J. Biol. Chem., 278, 27971-27980 (2003).
27. Medeiros R, Prediger RD, Passos GF, Pandolfo P, Duarte FS, Franco JL, Dafre AL, Di Giunta G, Figueiredo CP, Takahashi RN, Campos MM, Calixto JB. Connecting TNF-alpha signaling pathways to iNOS expression in a mouse model of Alzheimer's disease: relevance for the behavioral and synaptic deficits induced by amyloid beta protein. J. Neurosci., 27, 5394-5404 (2007).
28. Tan S, Schubert D, Maher P. Oxytosis: A novel form of programmed cell death. Curr. Top. Med. Chem., 1, 497-506 (2001).
29. Cuadrado A, Rojo AI. Heme oxygenase-1 as a therapeutic target in neurodegenerative diseases and brain infections. Curr. Pharm. Des., 14, 429-442 (2008).