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

Author:

Li Qiu-yue1,Yang Peng-hui1,Huang Xin1,Li Xin-long1,Luo Min-yi1,Xiao Bi-juan1,Zhao Zi-ming2,Li Si-yi345ORCID,Pan Hua-feng1ORCID

Affiliation:

1. Guangzhou University of Chinese Medicine, Guangzhou 510405, China

2. 2Guangdong Provincial Second Hospital of Traditional Chinese Medicine (Guangdong Provincial Engineering Technology Research Institute of Traditional Chinese Medicine), Guangzhou 510095, China

3. 3Joint Laboratory for Translational Cancer Research of Chinese Medicine of the Ministry of Education of the People’s Republic of China, Guangzhou 510405, China

4. International Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510405, China

5. Dongguan Institute of Guangzhou University of Chinese Medicine, Dongguan 523808, China

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.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Complementary and alternative medicine

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