Vitamin C supplementation does not protect L‐gulono‐γ‐lactone oxidase‐deficient mice from Helicobacter pylori‐induced gastritis and gastric premalignancy
Vitamin C supplementation does not protect L‐gulono‐γ‐lactone oxidase‐deficient mice from Helicobacter pylori‐induced gastritis and gastric premalignancy
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补充维生素 C 并不能保护 L-古洛糖酸-γ-内酯氧化酶缺陷小鼠免受幽门螺杆菌引起的胃炎和胃癌前病变
DOI：
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发表时间：
2007
影响因子：
6.4
通讯作者：
J. Fox
中科院分区：
文献类型：
--
作者：
Chung;Xiang‐Dong Wang;K. Chien;Z. Ge;B. Rickman;A. Rogers;A. Varró;M. Whary;T. Wang;J. Fox
In human studies, low vitamin C intake has been associated with more severe Helicobacter pylori gastritis and a higher incidence of gastric cancer. However, vitamin C supplementation has not been definitively shown to protect against gastric cancer. Using vitamin C‐deficient B6.129P2‐Gulotm1Umc/mmcd (gulo−/−) mice lacking L‐gulono‐γ‐lactone oxidase, we compared gastric lesions and Th1 immune responses in H. pylori‐infected gulo−/− mice supplemented with low (33 mg/L) or high (3,300 mg/L) vitamin C in drinking water for 16 or 32 weeks. Vitamin C levels in plasma and gastric tissue correlated with the vitamin C supplementation levels in gulo−/− mice. H. pylori infection resulted in comparable gastritis and premalignant lesions in wildtype C57BL/6 and gulo−/− mice supplemented with high vitamin C, but lesions were less severe in gulo−/− mice supplemented with low vitamin C at 32 weeks post infection. The reduced gastric lesions in infected gulo−/− mice supplemented with low vitamin C correlated with reduced Th1‐associated IgG2c, gastric IFN‐γ and TNF‐α mRNA and higher H. pylori colonization levels. These results in the H. pylori‐infected gulo−/− mouse model suggest that although supplementation with a high level of vitamin C achieved physiologically normal vitamin C levels in plasma and gastric tissue, this dose of vitamin C did not protect gulo−/− mice from H. pylori‐induced premalignant gastric lesions. In addition, less severe gastric lesions in H.pylori infected gulo−/− mice supplemented with low vitamin C correlated with an attenuated Th1 inflammatory response. © 2007 Wiley‐Liss, Inc.
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影响因子：
29.4
作者：
Mohammadi, M;Nedrud, J;Czinn, SJ
通讯作者：
Czinn, SJ
影响因子：
11.2
作者：
J. Fox;C. Dangler;N. Taylor;Amy King;T. Koh;T. Wang
通讯作者：
J. Fox;C. Dangler;N. Taylor;Amy King;T. Koh;T. Wang
影响因子：
7.4
作者：
Baldwin, JC;Karthikeyan, AS;Raghothama, KG
通讯作者：
Raghothama, KG
影响因子：
11.2
作者：
Rogers, AB;Taylor, NS;Fox, JG
通讯作者：
Fox, JG
影响因子：
11.2
作者：
E. Mannick;L. Bravo;G. Zarama;J. Realpe;X.‐J. Zhang;B. Ruiz;E. Fontham;R. Mera;M. Miller;P. Correa
通讯作者：
E. Mannick;L. Bravo;G. Zarama;J. Realpe;X.‐J. Zhang;B. Ruiz;E. Fontham;R. Mera;M. Miller;P. Correa