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Journal of Ethnopharmacology 2015-Sep

Anti-ulcerogenic effect of Zuojin Pill against ethanol-induced acute gastric lesion in animal models.

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Пријави се / Пријави се
Веза се чува у привремену меморију
Jing Wang
Tianzhu Zhang
Lingpeng Zhu
Chunhua Ma
Shumin Wang

Кључне речи

Апстрактан

BACKGROUND

Zuojin Pill (ZJP), a traditional Chinese medicinal decoction, contains two herbal drugs: Coptis chinensis Franch. and Tetradium ruticarpum (A. Juss.) Hartley in the ratio of 6:1 (w/w). In this study, ZJP was evaluated for its gastroprotective potential against mucosal lesions induced by ethanol in mice.

METHODS

50 mice were assigned to 5 groups: groups 1 and 2 were given distilled water orally. Group 3 was administered omeprazole 20mg/kg, groups 4 and 5 were given ZJP (1g/kg, 2g/kg, respectively). After an additional hour, the mice in groups 2-5 received ethanol (0.2ml/kg) orally while group 1 received distilled water instead. Mice were killed after 4h and their serum and stomachs subjected to further studies. The superoxidase dismutase (SOD) activities and malondialdehyde (MDA) level in serum were assayed by SOD and MDA kits, respectively. The myeloperoxidase (MPO) activities in stomachs were assayed by MPO kit. The levels of inflammatory mediators including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in serum were assayed by enzyme-linked immunosorbent assay method (ELISA). Pathological changes were observed by hematoxylin-eosin (HE) staining. The levels of nuclear factor-кBp65 (NF-кBp65), P-NF-кBp65, P-IкBα, IкBα, P-IKKα, IKKα, P-IKKβ, IKKβ in stomachs were assayed by western blot.

RESULTS

The data showed that treatment with the ZJP markedly attenuated MPO, MDA, TNF-α, IL-6, IL-1βand increased SOD; and ZJP also decreased protein levels of P-NF-кBp65, P-IкBα, P-IKKαand P-IKKβin gastric stomachs.

CONCLUSIONS

It was concluded that ZJP may represents a potential therapeutic option to reduce the risk of gastric ulceration and the gastroprotective activity of ZJP might contribute in adjusting the inflammatory cytokine by regulating the NF-кB signaling pathway.

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