Abstract
BackgroundBerberine, an isoquinoline derivative alkaloid, has a wide range of pharmacological properties and is considered to have anti-inflammatory and neuroprotective effects. However, there are no reports about the effects and mechanisms of berberine in experimental autoimmune encephalomyelitis (EAE), an established model of multiple sclerosis (MS).Methodology/Principal FindingsFemale C57 BL/6 mice immunized with myelin oligodendrocyte glycoprotein 35–55 amino acid peptide were treated with berberine at the day of disease onset and medication was administered daily until mice were sacrificed. Blood–brain barrier (BBB) permeability and the alteration of matrix metalloproteinase-2 (MMP-2, 72 kDa) and matrix metalloproteinase-9 (MMP-9, 92 kDa) in the brain and cerebrospinal fluid (CSF) of EAE mice were detected by quantitative measurement for Evan's blue (EB) content, Western blot and gelatin zymography respectively. The results showed that berberine attenuated clinical and pathological parameters of EAE, reduced the permeability of BBB, inhibited the activity and expression of MMP-9 but not MMP-2 in the CSF and brain of EAE mice.Conclusions/SignificanceThese findings suggest that berberine is effective to attenuate the clinical severity of EAE in C57 BL/6 mice by reducing the permeability of BBB, decreasing the expression and activity of MMP-9, and decreasing the inflammatory infiltration. We think that berberine might be a potential therapeutic agent for MS.
Highlights
Multiple Sclerosis (MS) is a chronic inflammatory demyelinating autoimmune disease of the central nervous system (CNS) which classically exhibits a relapsing- remitting course with increasing neurological sequelae [1]
It has been reported that berberine could play its anti-inflammatory effects through inhibiting the production of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6) and monocyte chemoattractant protein 1 (MCP-1), suppressing cyclooxygenase-2 (COX-2) expression, retarding prostaglandin E2 (PGE2) production and exudates formation, and down-regulating the expression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) through mitogen-activated protein kinase (MAPK) and nuclear factor-kB (NF-kB) signaling pathways [7,13,14,15]
We further investigated the permeability of blood–brain barrier (BBB) and the alteration of matrix metalloproteinases (MMPs)-2 (72 kDa) and MMP-9 (92 kDa) in the cerebrospinal fluid (CSF) and the brain of EAE mice
Summary
Multiple Sclerosis (MS) is a chronic inflammatory demyelinating autoimmune disease of the central nervous system (CNS) which classically exhibits a relapsing- remitting course with increasing neurological sequelae [1]. Berberine is an isoquinoline derivative alkaloid isolated from many medicinal herbs, such as Hydrastis canadensis (goldenseal), Cortex phellodendri (Huangbai) and Rhizoma coptidis (Huanglian) [6]. It is frequently utilized in proprietary Chinese herbal drugs to treat inflammation, especially in the oral cavity [7]. An isoquinoline derivative alkaloid, has a wide range of pharmacological properties and is considered to have anti-inflammatory and neuroprotective effects. There are no reports about the effects and mechanisms of berberine in experimental autoimmune encephalomyelitis (EAE), an established model of multiple sclerosis (MS)
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