Abstract
Dendrobium officinale is a herb in traditional Chinese medicine where D. officinale polysaccharides (DOP) are the main active ingredient. This study aimed at evaluating DOP efficiency at inhibiting 1-Methyl-2-nitro-1-nitrosoguanidine (MNNG) induced precancerous lesions of gastric cancer (PLGC) in rats through the Wnt/b-catenin pathway and analyzing the variations of serum endogenous metabolites. PLGC was established in male Sprague-Dawley (SD) rats by administering 150 μg/mL MNNG in drinking water for 7 months and giving 0.1 mL of 10% NaCl once weekly during the initial 20 weeks. Treatment with DOP inhibited the progress of PLGC through decreasing the expression of β-catenin by immunohistochemical analysis. The futher study indicated DOP downregulated gene expression of Wnt2β, Gsk3β, PCNA, CyclinD1, and β-catenin, as well as protein expression of Wnt2β, PCNA, and β-catenin. On the other hand, there were nine endogenous metabolites identified after the DOP treatment. Among these, the most significant one is betaine because of its strong antioxidant activity, leading to an anti-tumor effect. DOP can inhibit MNNG-induced PLGC models via regulating Wnt/β-catenin pathway and by changing endogenous metabolites.
Highlights
Gastric cancer is a common malignant digestive tract tumor, with the latest report showing that its incidence at 5.7% and its mortality at 8.2% in the world [1]
Precancerous lesions of gastric cancer (PLGC) is the most important phase in the progression of gastric cancer, in that it presents the best opportunity for inhibiting tumor progression [2,3]
It is well documented that the Wnt pathway is constitutively activated and beta-catenin accumulation is changed in the progression of the gastric tumorigenesis
Summary
Gastric cancer is a common malignant digestive tract tumor, with the latest report showing that its incidence at 5.7% and its mortality at 8.2% in the world [1]. Precancerous lesions of gastric cancer (PLGC) is the most important phase in the progression of gastric cancer, in that it presents the best opportunity for inhibiting tumor progression [2,3]. The Wnt pathway is one of the most important signaling pathways involved in gastric carcinogenesis. It is well documented that the Wnt pathway is constitutively activated and beta-catenin accumulation is changed in the progression of the gastric tumorigenesis. The Wnt pathway is recognized as a useful pathway to examine the relationship between gastric tumorigenesis and drug effects, as well as to explain the mechanism of its preventive effect [4,5].
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