Rg3-enriched Korean Red Ginseng extract inhibits blood-brain barrier disruption in an animal model of multiple sclerosis by modulating expression of NADPH oxidase 2 and 4
| Autor: | Seung-Yeol Nah, Byung-Joon Chang, Jun-Gyo In, Young Hyun Lee, Min Jung Lee, Jinhee Oh, Jong Hee Choi, Ik-Hyun Cho |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Chronic experimental autoimmune encephalomyelitis Rg3-enriched Korean Red Ginseng extract Pharmacology Blood–brain barrier Biochemistry Genetics and Molecular Biology (miscellaneous) Neuroprotection 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Blood-brain barrier NADPH oxidase biology Experimental autoimmune encephalomyelitis Botany NOX4 medicine.disease Nitric oxide synthase 030104 developmental biology medicine.anatomical_structure Complementary and alternative medicine chemistry QK1-989 030220 oncology & carcinogenesis Apocynin biology.protein Nicotinamide adenine dinucleotide phosphate Research Article Biotechnology |
| Zdroj: | Journal of Ginseng Research Journal of Ginseng Research, Vol 45, Iss 3, Pp 433-441 (2021) |
| ISSN: | 1226-8453 |
| Popis: | Background Multiple sclerosis (MS) and its animal model, the experimental autoimmune encephalomyelitis (EAE), are primarily characterized as dysfunction of the blood-brain barrier (BBB). Ginsenoside-Rg3-enriched Korean red ginseng extract (Rg3-KRGE) is known to exert neuroprotective, anti-inflammatory, and anti-oxidative effects on neurological disorders. However, effects of Rg3-KRGE in EAE remain unclear. Methods Here, we investigated whether Rg3-KRGE may improve the symptoms and pathological features of myelin oligodendroglial glycoprotein (MOG)35-55 peptide – induced chronic EAE mice through improving the integrity of the BBB. Results Rg3-KRGE decreased EAE score and spinal demyelination. Rg3-KRGE inhibited Evan's blue dye leakage in spinal cord, suppressed increases of adhesion molecule platelet endothelial cell adhesion molecule-1, extracellular matrix proteins fibronection, and matrix metallopeptidase-9, and prevented decreases of tight junction proteins zonula occludens-1, claudin-3, and claudin-5 in spinal cord following EAE induction. Rg3-KRGE repressed increases of proinflammatory transcripts cyclooxygenase-2, inducible nitric oxide synthase, interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-alpha, but enhanced expression levels of anti-inflammatory transcripts arginase-1 and IL-10 in the spinal cord following EAE induction. Rg3-KRGE inhibited the expression of oxidative stress markers (MitoSOX and 4-hydroxynonenal), the enhancement of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and NOX4, and NADPH activity in the spinal cord of chronic EAE mice. Furthermore, apocynin, a NOX inhibitor, mimicked beneficial effects of Rg3-KRGE in chronic EAE mice. Conclusion Our findings suggest that Rg3-KRGE might alleviate behavioral symptoms and pathological features of MS by improving BBB integrity through modulation of NOX2/4 expression. |
| Databáze: | OpenAIRE |
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