叶酸治疗萎缩性胃炎并改变P16蛋白表达

Effect of folic acid on atrophic gastritis and expression of P16 protein

目的:研究叶酸干预萎缩性胃炎后的黏膜改变、P16蛋白表达变化及p16基因甲基化状态．方法:根据胃镜及病理结果确诊为萎缩性胃炎的患者56例,随机分为叶酸治疗组(n=28) 和非叶酸治疗组(n=28),治疗前后观察临床症状、血浆叶酸水平、黏膜病理、P16蛋白表达变化,并采用甲基化敏感的内切酶酶切后 PCR法检测p16基因甲基化状态．结果:叶酸治疗组临床症状缓解快而持久,患者血浆叶酸水平升高(47．98±2．68 μg／L vs 14.37±3．56 μg／L,P<0．01),病理改变逆转(有效率:80．8％vs39．3％,P<0．01),P16蛋白表达增强,有效率达61．6％(P<0．01),而p16基因甲基化状态两组在治疗前后均正常．结论:萎缩性胃炎的发生与叶酸缺乏有关,叶酸治疗可以提高血浆叶酸水平,有效改善临床症状,一定程度上逆转胃黏膜的萎缩、肠化和不典型增生,能提高P16蛋白表达．萎缩性胃炎中不存在甲基化异常．

AIM： To study the mucosal changes, P16 protein expression and p16 gene methylation status in atrophic gastritis after treatment of folic acid （FA）. METHODS： Fifty-six patients, who were diagnosed with gastroendoscopy and pathological examination, were randomly assigned into FA and non-FA treatment group （control）. Before and after treatment, the clinical symptoms of the patients, the levels of plasma FA, and the expression of P16 protein were observed. Meanwhile, the methylation status of p16 gene was detected by methylation specific polymerase chain reaction （MSP）. RESULTS： After treatment with FA, The clinical symptoms of patients alleviated rapidly and lasted a longer period in FA group. Meanwhile, the level of plasma FA was significantly increased （47.98 ± 2.68 μg/L vs 14.37 ± 3.56 μg/L, P 〈 0.01）. The pathological changes were notably improved and the efficacy rate was 80.8% in FA group, which was markedly higher than that in the controls （39.3%, P 〈 0.01）. The expression of P16 protein was increased with a rate of 61.6% （P 〈 0.01） in comparison with that of control group. The methlytion status of p16 gene was normal in both groups before and after treatment. CONCLUSION： Lack of FA plays an important role in the pathogenesis of atrophic gastritis. FA treatment can elevate the plasma FA level, improve the clinical symptoms, and reverse the pathological changes to some extent. No aberrant methylation exists in atrophic gastritis.