Abstract
Purpose: To explore the effects of Xinwei granule (XWG) on low-grade gastric intraepithelial neoplasia (LGIN) and the underlying mechanisms.
 Methods: To establish LGIN model, Wistar rats were treated with N-methyl-N'-nitrosoguanidine for 3 months. LGIN model rats were randomly grouped into five groups (n = 15), viz, negative control (NC), normal saline (NS) group, Xinwei granule (XWG) group, Weifuchun tablet (WFCT) group, and vatacoenayme tablet (VT) group. Normal rats (n = 17) served as negative control. Histological evaluation of gastric mucosa was undertaken using hematoxylin and eosin staining. Quantitative realtime polymerase chain reaction (qRT-PCR), western blot, and immunohistochemical assays were performed to determine mRNA expressions, protein expression, and the distribution of cyclin D1, kruppel-like factor 4 (KLF4), and p21-WAF1-CIP1, respectively.
 Results: Compared with LGIN group, the body weight of the rats increased in XWG, WFCT, and VT groups. The pathological characteristics of LGIN group were alleviated by XWG, WFCT and VT treatments. The positive expression of cyclin D1 was enhanced in LGIN group, but reduced in XWG, WFCT and VT groups. The expression levels of KLF4 and p21-WAF1-CIP1, upstream regulators of cyclin D1 reduced in LGIN groups. However, administration of XWG, WFCT and VT strengthened the expressions of KLF4 and p21-WAF1-CIP1. More importantly, the protective effects of XWG against LGIN were superior to those of WFCT and VT.
 Conclusion: Xinwei granules alleviate LGIN in vivo by inhibiting cyclin D1 expression and enhancing KLF4 and p21-WAF1-CIP1 expression.
Highlights
Gastric intraepithelial neoplasia (GIN) is a precancerous lesion of gastric cancer
There were only two cases in the Xinwei granule (XWG) group, four cases in the Weifuchun tablet (WFCT) group, and four cases in the vatacoenayme tablet (VT) group, indicating that the degree of low-grade gastric intraepithelial neoplasia (LGIN) was mitigated by XWG, WFCT, and VT
In contrast to the normal saline (NS) group, treatment with XWG, WFCT, or VT relieved the pathological changes in LGIN
Summary
Gastric intraepithelial neoplasia (GIN) is a precancerous lesion of gastric cancer. Uncontrolled cell cycle progression can lead to carcinogenesis and the growth of human cancers [4,5]. Cell cycle progression is modulated by cyclin-dependent kinases [6]. Cyclin D1 is an important cell cycle regulator, which plays a role in human cancer progression [7,8,9]. Kruppel-like factor 4 (KLF4), a tumor regulator can modulate the expression of cyclin D1 [11]. Disruption of KLF4 [13] and p21-WAF1CIP1 [14] expression has been observed in gastric cancer. Investigating the expression of cyclin D1, KLF4, and p21-WAF1CIP1 may be beneficial for understanding the mechanisms of LGIN development
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