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DOI: 10.1055/s-0037-1608421
Quantitative analysis and biological efficacies regarding the neuroprotective and antineuroinflammatory actions of the herbal formula SCD-B-033
Publikationsverlauf
Publikationsdatum:
24. Oktober 2017 (online)
SCD-B-033 (B33) is a traditional herbal formula that comprises seven medicinal herbs and is broadly utilized to treat hypertension[1], dementia[2], and headache[3] in Korea, Japan, and China. However, the effects of B33 and its herbal components on neurodegenerative diseases in general have not been reported. The common cellular events of neurodegenerative diseases, such as Alzheimer's, Parkinson's, and Huntington's diseases, include neuronal cell death and neuroinflammation. In our study, we examined the inhibitory effects of B33 and its seven components on neuronal cell death and inflammation using HT22 hippocampal cells and BV-2 microglia, respectively. In HT22 cells that were damaged by hydrogen peroxide (H2O2) treatment, B33 significantly reversed cell viability compared with cells treated with H2O2 alone. Among its seven herbal components, Uncaria sinensis, Chrysanthemum morifolium, Zingiber officinale (ZO), Pinellia ternate (PT), Citrus unshiu (CU), and Poria cocos (PC) exhibited significant neuroprotective effects. In lipopolysaccharide-stimulated BV-2 cells, B33 significantly suppressed the production of the inflammatory cytokines tumor necrosis factor-alpha and interleukin-6, indicating the antineuroinflammatory activity of B33. In addition, the herbal extracts from ZO, Panax ginseng (PG), PT, CU, and PC, exhibited inhibitory effects on the inflammatory response in microglia. These data imply that the B33 effect on neurodegeneration occurs via coordination among its seven components. To establish a quality control for B33, a simultaneous analysis using five marker compounds identified hesperidin (37.892 ± 1.228 mg/g), a marker compound of CU, as a major compound of B33. Further investigation of the combinatorial activities of two or more marker compounds will be necessary to verify their antineurodegenerative regulatory mechanisms.
[1] Shimada Y, Yang Q, et al. Am J Chin Med 2003; 31: 79 – 85.
[2] Watanabe H, Zhao Q, et al. Pharmacol Biochem Behav 2003; 75: 635 – 643.
[3] Dohi K, Aruga T, et al. Headache 2004; 44: 375.