Ning Wang1, Li-Li Chang2. 1. Department of Gastroenterology No.1 Ward, ShiJiaZhuang No. 1 Hospital, Shijiazhuang 050011, China. 2. Department of Gastroenterology No.1 Ward, ShiJiaZhuang No. 1 Hospital, Shijiazhuang 050011, China. Electronic address: changlily_678@163.com.
Abstract
OBJECTIVE: To know the potential role of IKKα (an NF-κB noncanonical pathway) in gastric precancerous lesion via mediating Maspin. METHODS: Gastric cancer, precancerous lesion and control tissues (chronic non-atrophic gastritis) were collected for determining the expression of IKKα and Maspin by immunohistochemistry. Thereafter, gastric precancerous models were established and divided into the Control group, Model group and Model + shIKKα group. All rats were subjected to observe the pathological changes and ultramicro structure of the gastric mucosa by HE staining or electron microscope, and to measure the serum levels of inflammatory cytokines by ELISA, the expression of apoptosis-related proteins by immunohistochemistry, as well as the expression of IKKα and Maspin by quantitative real-time PCR and Western blotting. RESULTS: Precancerous lesion and gastric cancer tissues manifested significant upregulation of IKKα positive expression, concomitant with downregulation of the positive expression of Maspin, and these changes were more evident in the gastric cancer tissues. In comparison with the Control group, rats in the Model group had significant increases in serum levels of TNF-α, IL-1β, IL-6 and COX-2, with up-regulations of Bcl-2, CyclinD1, IKKα and p-IKKα, and down-regulations of Bax, Caspase-3 and Maspin. shIKKα treatment attenuate inflammation and apoptosis in gastric precancerous lesion (GPL) rat, with the downregulation of IKKα and p-IKKα, and upregulation of Maspin. CONCLUSION: Inhibiting IKKα, via upregulating Maspin, can mitigate the inflammation and promote cell apoptosis in precancerous rats, thereby delaying the development of the precancerous lesions.
OBJECTIVE: To know the potential role of IKKα (an NF-κB noncanonical pathway) in gastric precancerous lesion via mediating Maspin. METHODS:Gastric cancer, precancerous lesion and control tissues (chronic non-atrophic gastritis) were collected for determining the expression of IKKα and Maspin by immunohistochemistry. Thereafter, gastric precancerous models were established and divided into the Control group, Model group and Model + shIKKα group. All rats were subjected to observe the pathological changes and ultramicro structure of the gastric mucosa by HE staining or electron microscope, and to measure the serum levels of inflammatory cytokines by ELISA, the expression of apoptosis-related proteins by immunohistochemistry, as well as the expression of IKKα and Maspin by quantitative real-time PCR and Western blotting. RESULTS:Precancerous lesion and gastric cancer tissues manifested significant upregulation of IKKα positive expression, concomitant with downregulation of the positive expression of Maspin, and these changes were more evident in the gastric cancer tissues. In comparison with the Control group, rats in the Model group had significant increases in serum levels of TNF-α, IL-1β, IL-6 and COX-2, with up-regulations of Bcl-2, CyclinD1, IKKα and p-IKKα, and down-regulations of Bax, Caspase-3 and Maspin. shIKKα treatment attenuate inflammation and apoptosis in gastric precancerous lesion (GPL) rat, with the downregulation of IKKα and p-IKKα, and upregulation of Maspin. CONCLUSION: Inhibiting IKKα, via upregulating Maspin, can mitigate the inflammation and promote cell apoptosis in precancerous rats, thereby delaying the development of the precancerous lesions.