Erschienen in:
01.12.2014 | Original Article
Protective Effects of Garlic Extract, PMK-S005, Against Nonsteroidal Anti-inflammatory Drugs–Induced Acute Gastric Damage in Rats
verfasst von:
Yoon Jeong Choi, Nayoung Kim, Ju Yup Lee, Ryoung Hee Nam, Hyun Chang, Ji Hyung Seo, Kyu Keun Kang, Hee Jin Kim, Yun Jin Choi, Hye Seung Lee, Dong Ho Lee
Erschienen in:
Digestive Diseases and Sciences
|
Ausgabe 12/2014
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Abstract
Background
PMK-S005 is synthetic s-allyl-l-cysteine (SAC), a sulfur-containing amino acid, which was initially isolated from garlic. The antioxidant and anti-inflammation activities of SAC have been demonstrated in diverse experimental animal models.
Aims
The purpose of this study was to investigate the gastroprotective effects of PMK-S005 against NSAIDs-induced acute gastric damage in rats.
Methods
Eight-week SD rats were pretreated with PMK-S005 (1, 5, or 10 mg/kg) or rebamipide (50 mg/kg) 1 h before administration of NSAIDs including aspirin (200 mg/kg), diclofenac (80 mg/kg), and indomethacin (40 mg/kg). After 4 h, the gross ulcer index, histological index, and gastric mucus level were determined. Myeloperoxidase (MPO), TNF-α, IL-1β, PGE2, and LTB4 levels were estimated in the gastric mucosal tissue by ELISA. Protein expressions of cPLA2, COX-1, and COX-2 were assessed by Western blot analysis.
Results
Pretreatment with PMK-S005 significantly attenuated the NSAIDs-induced gastric damage and increased the gastric mucus level. In addition, PMK-S005 attenuated increases in MPO, TNF-α, and IL-1β production. The expressions of cPLA2 and COX-2 induced by NSAIDs were decreased by PMK-S005 pretreatment. PMK-S005 did not cause suppression of PGE2 synthesis induced by NSAIDs, but LTB4 production was significantly suppressed by PMK-S005. The effects of PMK-S005 were consistently maximized at a concentration of 5 mg/kg, which were frequently superior to those of rebamipide.
Conclusions
These results strongly suggest that PMK-S005 can be a useful gastroprotective agent against acute gastric mucosal damage by suppressing proinflammatory cytokines, down-regulating cPLA2, COX-2 and LTB4 expression, and increasing the synthesis of mucus.