Objective To explore the correlation between intestinal mucosal immune barrier and pathogenesis of pigment gallstone and its possible mechanism.Methods Eighty guinea pigs were randomly divided into control group(group CON),pigment gallstone group(group PS),and intestinal mucosal protection group(group GLN).The guinea pigs were fed with normal diet in group CON,pigment gallstonein during diet in group PS,and glutamine-supplemented diet in group GLN for 8 weeks.The guinea pig model of pigment gallstone was established.The incidence of pigment gallstone was detected.The morphology of intestinal mucosa was observed,and the numbers of CD3~+T cell,CD40~+B cell,and IgA~+ plasma cell were counted.Results The incidence of pigment gallstone was significantly higher in group PS than in groups GLN and CON(P＜0.05).Compared with group CON,the intestinal wall was significant thinner and represented obvious signs of inflammation in group PS,and the numbers of CD3~+ T cell,CD40~+ B cell,and IgA~+ plasma cell significantly decreased(CD3~+ T cell,21.8±2.5 vs 11.1±3.4,P＜0.01;CD 40~+B cell,12.9±2.0 vs 10.7±3.6,P＜0.01;IgA~+ plasma cell,12.4±3.4 vs 10.7±3.5,P＜0.01).The signs of inflammation were less severe in group GLN than in group PS.There were significant differences in the numbers of CD3~+ T cell,CD40~+ B cell,and IgA~+plasma cell between groups GLN and PS.Conclusion Intestinal barrier dysfunction,including mechanical barrier and immune barrier,is involved in the formation of pigment gallstone.Glutamine has proved to improve the function of intestinal mucosal barrier and decrease the incidence of pigment gallstone.

As one of the most common malignant tumors, lung cancer poses a serious threat to human life and health. The platinum-based drug cisplatin (DDP) is used as the first-line treatment for lung cancer. The poor prognosis of lung cancer is mostly due to developed resistance to cisplatin, which poses a serious treatment challenge. The mechanism of cisplatin resistance is complex and unclear. Numerous studies have shown that DNA methylation plays a crucial role in the emergence of lung cancer cisplatin resistance. DNA hypermethylation results in the deactivation of numerous drug resistance genes and tumor suppressor genes through a change in chromatin conformation. Finding new therapeutic targets and indicators to predict the therapeutic effect can be aided by elucidating the complex mechanism. In order to discover novel strategies to overcome cisplatin resistance in lung cancer, this paper discusses DNA methylation-mediated cisplatin resistance and offers an overview of current demethylation procedures.
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Humans ; Antineoplastic Agents/therapeutic use* ; Cell Line, Tumor ; Cisplatin/therapeutic use* ; DNA Methylation ; Drug Resistance, Neoplasm/genetics* ; Gene Expression Regulation, Neoplastic ; Lung Neoplasms/pathology*