title: Bombycis excrementum reduces amyloid-β oligomer-induced memory impairments, neurodegeneration, and neuroinflammation in mice.
abstract: Alzheimer's disease (AD) is the most common cause of progressive dementia and is characterized by memory impairments, neuronal death, and neuroinflammation. AD-related pathophysiology is caused primarily by the presence of amyloid-β oligomers (AβO). Recently, an increased focus has been directed toward natural compounds or medicinal extracts for the treatment of AD. Extracts from Bombycis excrementum (BE), which is composed of various bioactive constituents and mulberry leaves (the preferred food of silkworms), have been shown to possess anti-inflammatory, anti-diabetic, and anti-oxidative effects. Additionally, mulberry leaves exert anti-amyloidogenic action and neuroprotective effects against Aβ peptides but it is unknown whether BE has a therapeutic effect on AD-related pathologies. Therefore, the present study examined whether BE inhibits AβO-induced memory loss, neuronal death, and inflammation. Behavioral tests revealed that BE significantly ameliorated AβO-induced memory impairments and inhibited AβO-induced neuronal loss in cultured cells and the brains of mice. BE also significantly inhibited microgliosis and astrogliosis following intra-hippocampal AβO injections in mice. Furthermore, BE significantly attenuated the release of nitric oxide from microglia and reduced AβO-induced S100-β cytokine release from activated astrocytes. These results suggest that BE may be a candidate agent for the treatment of AD.
authors.affiliation: School of Medicine, Kyung Hee University, Dongdaemun-gu, Seoul, Republic of Korea.
authors.forename: Minho
authors.initials: M
authors.lastname: Moon
authors.affiliation: College of Pharmacy, Kyung Hee University, Dongdaemun-gu, Seoul, Republic of Korea Department of Life and Nanopharmaceutical Science and Kyung Hee East-West Pharmaceutical Research Institute, Kyung Hee University, Dongdaemun-gu, Seoul, Republic of Korea.
authors.forename: Jin Gyu
authors.initials: JG
authors.lastname: Choi
authors.affiliation: College of Pharmacy, Gachon University, Incheon, Republic of Korea.
authors.forename: Sun Yeou
authors.initials: SY
authors.lastname: Kim
authors.affiliation: College of Pharmacy, Kyung Hee University, Dongdaemun-gu, Seoul, Republic of Korea Department of Life and Nanopharmaceutical Science and Kyung Hee East-West Pharmaceutical Research Institute, Kyung Hee University, Dongdaemun-gu, Seoul, Republic of Korea.
authors.forename: Myung Sook
authors.initials: MS
authors.lastname: Oh
mesh_terms: D016229:Amyloid beta-Peptides; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D001253:Astrocytes / Q000187:drug effects / Q000502:physiology; D012831:Bombyx; D001921:Brain / Q000187:drug effects / Q000503:physiopathology; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D002460:Cell Line; D005243:Feces; D005911:Gliosis / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008569:Memory Disorders / Q000188:drug therapy* / Q000503:physiopathology; D051379:Mice; D008813:Mice, Inbred ICR; D017628:Microglia / Q000187:drug effects / Q000502:physiology; D031625:Morus / Q000378:metabolism; D019636:Neurodegenerative Diseases / Q000188:drug therapy* / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D018696:Neuroprotective Agents / Q000008:administration & dosage*; D016716:PC12 Cells; D011897:Random Allocation; D051381:Rats
chemical_list: D016229:Amyloid beta-Peptides; D000893:Anti-Inflammatory Agents; D018696:Neuroprotective Agents
keywords: Alzheimer's disease; Bombycis excrementum; amyloid-β oligomer; cognitive impairment; neuroinflammation; neuronal death; silkworm droppings