Gastric Mucosa Pathology in Rats with Precancerous Lesions of Gastric Cancer with Spleen Deficiency and Blood Stasis

Abstract

Objective. This research aimed at better understanding the histopathological development of precancerous lesions of gastric cancer (PLGC) and organelle ultrastructure changes. Methods. Sprague-Dawley rats were randomly assigned to the model and control groups. Model rats drank N-methyl-N′-nitro-N-nitrosoguanidine solution, while control rats drank pure water ad libitum. At 1, 3, 5, 6, and 8 months after the start of feeding, eight rats were randomly chosen from each group, and gastric mucosa tissues were removed for histopathological analysis. H&E staining was applied to analyze the pathological histological structure of the rat gastric mucosa via a light microscope, and the ultrastructural changes were observed via a transmission electron microscope. Results. Gastric mucosal pathologies of model rats such as mucosal atrophy, intestinal metaplasia, inflammatory lesions, and even intraepithelial neoplasia deteriorated over time. The endoplasmic reticulum gap widened, the mitochondrial endothelial cristae were disrupted, the nuclear membrane thickened, and chromatin condensed with heterotypic alterations in the main and parietal cells. Additionally, endothelial cell enlargement and thickening of the microvascular intima were seen. Conclusion. Our research showed that the PLGC progression of rats is correlated with the pathological alteration axis of “normal gastric mucosa-gastric mucosa inflammatory changes-intestinal metaplasia with mild dysplasia-moderate to severe dysplasia.” Ultrastructure analysis of model rats is compatible with the structural changes in the gastric mucosa with spleen deficiency and blood stasis. The pathological evolutionary axis and ultrastructural analysis are helpful for evaluating potential novel herbal therapies for PLGC.

Research progress on etiology, pathogenesis and treatment of gastric precancerous lesions

“…At present, modern medicine is relatively single in the treatment of PLGC, and its treatment methods are mostly symptomatic treatment, such as oral proton pump inhibitors: omeprazole, lansoprazole or pantoprazole; Gastric mucosal protector: aluminum magnesium carbonate chewable tablets, aluminum magnesium turbid liquid or colloidal pectin bismuth and so on. Or it may be treated by eradicating Helicobacter pylori, but the treatment effect is not satisfactory due to drug resistance and other problems [3]. Endoscopic submucosal dissection is an endoscopic resection that has emerged in recent years, which uses high-frequency electric surgery to completely remove diseased tissue, and its surgical safety is high, and some patients have incomplete resection of individual lesions, metastasis, and complications such as perforation and bleeding will occur [4].…”