Digestive diseases and sciences · 2008
Intravenous injection of micafungin counteracts Candida albicans-induced aggravation of duodenal ulcers caused by cysteamine in rats.
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Nakamura Tetsuya, Yoshida Masashi, Kitagawa Yuko, Jin Longxue, Ishikawa Hideki, Kameyama Kaori, Wakabayashi Go, Tanabe Minoru, Kawachi Shigeyuki, Shinoda Masahiro, Saikawa Yoshiro, Wada Norihito, Kubota Tetsuro, Kumai Koichiro, Sano Katsuko, Kitajima Masaki
Аннотация
BACKGROUND: We have reported previously that Candida albicans is involved in the pathogenesis of peptic ulcer perforation; it was shown that C. albicans aggravated the severity of duodenal ulceration and increased the rate of perforation. We considered it incumbent upon us to ascertain whether C. albicans is a virulence factor involved in peptic ulcer perforation. In the present study, we administered an antifungal drug (micafungin) intravenously to rats that had received intragastric (i.g.) administration of C. albicans and cysteamine, in order to examine that micafungin could counteract the C. albicans-aggravation of duodenal ulcers.
METHODS: Cysteamine was administered thrice on day 1 to male Wistar rats. C. albicans was administered to the animals 1 h before, and 12 and 24 h after the first administration of cysteamine. Micafungin (n = 22) or saline (n = 24) was administered 12, 24, and 48 h after the administration of cysteamine.
RESULTS: The area of the duodenal ulcers was also significantly smaller in the micafungin group (P < 0.05). In addition, the survival rate of the rats was significantly higher in the micafungin group (P < 0.05). While in the control group, the ulcer base was found to be colonized by C. albicans, there was no evidence of the presence of C. albicans in the micafungin group.
CONCLUSION: It was shown that intravenous injection of micafungin counteracted the aggravation by C. albicans of cysteamine-induced duodenal ulcers in rats. This finding supports the concept that C. albicans is an aggravating factor for peptic ulcers.
METHODS: Cysteamine was administered thrice on day 1 to male Wistar rats. C. albicans was administered to the animals 1 h before, and 12 and 24 h after the first administration of cysteamine. Micafungin (n = 22) or saline (n = 24) was administered 12, 24, and 48 h after the administration of cysteamine.
RESULTS: The area of the duodenal ulcers was also significantly smaller in the micafungin group (P < 0.05). In addition, the survival rate of the rats was significantly higher in the micafungin group (P < 0.05). While in the control group, the ulcer base was found to be colonized by C. albicans, there was no evidence of the presence of C. albicans in the micafungin group.
CONCLUSION: It was shown that intravenous injection of micafungin counteracted the aggravation by C. albicans of cysteamine-induced duodenal ulcers in rats. This finding supports the concept that C. albicans is an aggravating factor for peptic ulcers.