郑州大学学报（医学版）
鄭州大學學報（醫學版）
정주대학학보（의학판）
JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES)
2013年
6期
769-772
,共4页
韩俊%王彬%马珂%闫昱博%董开源%刘芳娥
韓俊%王彬%馬珂%閆昱博%董開源%劉芳娥
한준%왕빈%마가%염욱박%동개원%류방아
褪黑素%睡眠剥夺%胃黏膜溃疡%还原型谷胱甘肽%丙二醛%前列腺素E2%大鼠
褪黑素%睡眠剝奪%胃黏膜潰瘍%還原型穀胱甘肽%丙二醛%前列腺素E2%大鼠
퇴흑소%수면박탈%위점막궤양%환원형곡광감태%병이철%전렬선소E2%대서
melatonin%sleep deprivation%gastric mucosal lesion%reduced glutathione hormone%malondialdehyde%pros-taglandin E2%rat
目的：研究褪黑素对睡眠剥夺大鼠胃黏膜损伤的保护作用及机制。方法：将24只SD大鼠采用随机数字表法分为3组，分别为对照组（生理盐水腹腔注射）、模型组（生理盐水腹腔注射＋睡眠剥夺）和实验组（15 mg/kg褪黑素腹腔注射＋睡眠剥夺）。采用小平台水环境法建立大鼠睡眠剥夺模型，睡眠剥夺前大鼠适应环境7 d，从适应环境开始至睡眠剥夺期间继续给药。睡眠剥夺72 h后用相应试剂盒检测各组大鼠血清丙二醛（ MDA）、还原型谷胱甘肽（GSH）及前列腺素E2（PEG2）含量。观察胃黏膜组织病理损伤情况并进行胃黏膜损伤指数测定。结果：3组大鼠血清MDA、GSH、PEG2及胃黏膜损伤指数比较，差异均有统计学意义（ F＝9．441、9．667、9．747、486．804，P均＜0．05）。与对照组比较，模型组胃黏膜损伤指数升高（P＜0．05），血清MDA和PEG2含量升高、GSH含量降低（P均＜0．05）；与模型组比较，实验组胃黏膜损伤指数降低（P＜0．05），血清MDA和PEG2含量降低、GSH含量升高（P均＜0．05）。结论：褪黑素可通过降低血清MDA和升高GSH减轻睡眠剥夺造成的胃黏膜损伤。
目的：研究褪黑素對睡眠剝奪大鼠胃黏膜損傷的保護作用及機製。方法：將24隻SD大鼠採用隨機數字錶法分為3組，分彆為對照組（生理鹽水腹腔註射）、模型組（生理鹽水腹腔註射＋睡眠剝奪）和實驗組（15 mg/kg褪黑素腹腔註射＋睡眠剝奪）。採用小平檯水環境法建立大鼠睡眠剝奪模型，睡眠剝奪前大鼠適應環境7 d，從適應環境開始至睡眠剝奪期間繼續給藥。睡眠剝奪72 h後用相應試劑盒檢測各組大鼠血清丙二醛（ MDA）、還原型穀胱甘肽（GSH）及前列腺素E2（PEG2）含量。觀察胃黏膜組織病理損傷情況併進行胃黏膜損傷指數測定。結果：3組大鼠血清MDA、GSH、PEG2及胃黏膜損傷指數比較，差異均有統計學意義（ F＝9．441、9．667、9．747、486．804，P均＜0．05）。與對照組比較，模型組胃黏膜損傷指數升高（P＜0．05），血清MDA和PEG2含量升高、GSH含量降低（P均＜0．05）；與模型組比較，實驗組胃黏膜損傷指數降低（P＜0．05），血清MDA和PEG2含量降低、GSH含量升高（P均＜0．05）。結論：褪黑素可通過降低血清MDA和升高GSH減輕睡眠剝奪造成的胃黏膜損傷。
목적：연구퇴흑소대수면박탈대서위점막손상적보호작용급궤제。방법：장24지SD대서채용수궤수자표법분위3조，분별위대조조（생리염수복강주사）、모형조（생리염수복강주사＋수면박탈）화실험조（15 mg/kg퇴흑소복강주사＋수면박탈）。채용소평태수배경법건립대서수면박탈모형，수면박탈전대서괄응배경7 d，종괄응배경개시지수면박탈기간계속급약。수면박탈72 h후용상응시제합검측각조대서혈청병이철（ MDA）、환원형곡광감태（GSH）급전렬선소E2（PEG2）함량。관찰위점막조직병리손상정황병진행위점막손상지수측정。결과：3조대서혈청MDA、GSH、PEG2급위점막손상지수비교，차이균유통계학의의（ F＝9．441、9．667、9．747、486．804，P균＜0．05）。여대조조비교，모형조위점막손상지수승고（P＜0．05），혈청MDA화PEG2함량승고、GSH함량강저（P균＜0．05）；여모형조비교，실험조위점막손상지수강저（P＜0．05），혈청MDA화PEG2함량강저、GSH함량승고（P균＜0．05）。결론：퇴흑소가통과강저혈청MDA화승고GSH감경수면박탈조성적위점막손상。
Aim:To study the protective effects of melatonin on gastric mucosal lesions in rats induced by sleep depri-vation and the mechanism .Methods:A total of 24 SD rats were randomly allocated into 3 groups:the control group ( intra-peritoneal injection of normal saline ) , the model group ( sleep deprivation+intraperitoneal injection of normal saline ) and the experimental group (sleep deprivation +intraperitoneal injection of 15 mg/kg melatonin).The rats in the model group and the experimental group were set up sleep deprivation model with a small platform of water situation .The rats adapted to the situation for 7 days before sleep deprivation , and injection was kept during acclimation and the sleep deprivation days . After 72 h sleep deprivation, malondialdehyde(MDA), prostaglandin E2(PGE2) and reduced glutathione hormone(GSH) contents in serum of the rats in each group were determined , the pathological gastric mucosal lesions were observed , and gastric mucosal ulcer index was determined .Results:The contents of MDA, GSH, and PEG2 in serum and gastric muco-sal ulcer index among the three groups had statistical difference (F=9.441, 9.667, 9.747, 486.804, P<0.05).Com-pared with the control group, in the model group the gastric mucosal ulcer index increased significantly (P<0.05),the contents of MDA and PGE2 in serum increased and GSH decreased significantly (P<0.05).Compared with the model group, in the experimental group the gastric mucosal ulcer index decreased significantly (P<0.05),the contents of MDA and PGE2 in serum decreased and GSH increased significantly (P<0.05).Conclusion:Melatonin could alleviate the gas-tric injury caused by sleep deprivation .The mechanism maybe involve its inhibiting the increase of MDA as well as the pro-motion of the increase of GSH .
