AI Article Synopsis
- Korean Red Ginseng's nonsaponin fraction (NSF) is studied for its potential gastroprotective effects, particularly in combating inflammation.
- The study utilized various methods to analyze the effects of NSF on COX-1 levels and assessed its protective abilities in mouse models experiencing gastritis and colitis.
- Results indicated that NSF enhances COX-1 expression without toxicity and successfully alleviates gastrointestinal inflammation symptoms in the tested models.
Article Abstract
Background: Korean Red Ginseng is known to exhibit immune-enhancing and anti-inflammatory properties. The immune-enhancing effects of the nonsaponin fraction (NSF) of Korean Red Ginseng have been studied in many reports. However, the gastroprotective effect of this fraction is not fully understood. In this study, we demonstrate the activities of NSF for gastrointestinal protection and its related critical factor.
Methods: The and regulatory functions of NSF on cyclooxygenase-1 (COX-1) messenger RNA and protein levels were examined by reverse transcription polymerase chain reaction and immunoblotting analyses. Gastroprotective effects of NSF were investigated by histological score, gastric juice pH, and myeloperoxidase activity on indomethacin-induced, cold stress-induced, and acetylsalicylic acid-induced gastritis and dextran sulfate sodium-induced colitis in mouse models.
Results: NSF did not show cytotoxicity, and it increased COX-1 messenger RNA expression and protein levels in RAW264.7 cells. This upregulation was also observed in colitis and gastritis models. In addition, NSF treatment in mice ameliorated the symptoms of gastrointestinal inflammation, including histological score, colon length, gastric juice pH, gastric wall thickness, and myeloperoxidase activity.
Conclusion: These results suggest that NSF has gastroprotective effects on gastritis and colitis in mouse models through COX-1 upregulation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7322762 | PMC |
| http://dx.doi.org/10.1016/j.jgr.2019.11.001 | DOI Listing |
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