CAJ | 학술논문

目的研究正加速度(+Gz)暴露下急性胃黏膜损伤大鼠血浆热休克蛋白70 (HSP70)的含量变化及还原型谷胱甘肽(GSH)对其的影响及相应的保护机制.方法 40只雄性SD大鼠计算机随机分为4组:无水乙醇对照组,+5 Gz值暴露组,+10 Gz值暴露组,GSH保护组,各10只.GSH保护组适应性喂养7d后,连续3d腹腔注射GSH.4组均于10d后禁食24 h,禁水12 h,用无水乙醇(0.4 ml/100 g)灌胃lh后,无水乙醇对照组不受加速度作用,+5 Gz值暴露组于+5 Gz值、后2组于+ 10 Gz值下分别连续暴露3 min.每组下离心机后立即予戊巴比妥麻醉,腹主动脉取血,并取大鼠胃组织,观察各组胃黏膜损伤情况,按GUTH法计算胃黏膜损伤指数,并用放免法检测血浆中HSP70的含量.结果 (1)各组大鼠胃黏膜在肉眼观察下均有损伤,经GSH预处理后胃黏膜损伤程度明显减轻,无水乙醇对照组胃黏膜损伤较轻,+5 Gz值暴露组损伤较无水乙醇对照组重[胃黏膜损伤指数为25.4(14.0 ～ 30.0)比10.0(9.2 ～13.9),P=0.001];+10 Gz值暴露组胃黏膜损伤最重,肉眼可见胃黏膜弥漫性充血、水肿,伴糜烂、大面积出血斑、黏膜皱襞平坦,胃黏膜损伤指数[47.2(41.5 ～60.1)]明显高于前两组(均P＜0.01);GSH保护组胃黏膜损伤最轻,胃黏膜损伤指数[9.5(7.5 ～ 14.1)]明显低于+ 10 Gz值暴露组(P＜0.01).(2) +5 Gz值暴露组血浆中HSP70的含量与无水乙醇对照组差异无统计学意义[均为(6.5±0.5) ng/ml,P=0.897];+10 Gz值暴露组[(5.9±0.5) ng/ml]明显低于前两组(P =0.018、0.014)和GSH保护组[(7.0±0.5)ng/ml,P＜0.01].结论 +Gz暴露可引起急性胃黏膜损伤大鼠血浆中HSP70的含量变化,高+Gz值暴露可降低其含量,加重胃黏膜损伤;还原型谷胱甘肽可提高+ Gz暴露大鼠血浆中HSP70的含量,降低胃黏膜损伤.
목적 연구정가속도(+Gz)폭로하급성위점막손상대서혈장열휴극단백70 (HSP70)적함량변화급환원형곡광감태(GSH)대기적영향급상응적보호궤제.방법 40지웅성SD대서계산궤수궤분위4조:무수을순대조조,+5 Gz치폭로조,+10 Gz치폭로조,GSH보호조,각10지.GSH보호조괄응성위양7d후,련속3d복강주사GSH.4조균우10d후금식24 h,금수12 h,용무수을순(0.4 ml/100 g)관위lh후,무수을순대조조불수가속도작용,+5 Gz치폭로조우+5 Gz치、후2조우+ 10 Gz치하분별련속폭로3 min.매조하리심궤후립즉여무파비타마취,복주동맥취혈,병취대서위조직,관찰각조위점막손상정황,안GUTH법계산위점막손상지수,병용방면법검측혈장중HSP70적함량.결과 (1)각조대서위점막재육안관찰하균유손상,경GSH예처리후위점막손상정도명현감경,무수을순대조조위점막손상교경,+5 Gz치폭로조손상교무수을순대조조중[위점막손상지수위25.4(14.0 ～ 30.0)비10.0(9.2 ～13.9),P=0.001];+10 Gz치폭로조위점막손상최중,육안가견위점막미만성충혈、수종,반미란、대면적출혈반、점막추벽평탄,위점막손상지수[47.2(41.5 ～60.1)]명현고우전량조(균P＜0.01);GSH보호조위점막손상최경,위점막손상지수[9.5(7.5 ～ 14.1)]명현저우+ 10 Gz치폭로조(P＜0.01).(2) +5 Gz치폭로조혈장중HSP70적함량여무수을순대조조차이무통계학의의[균위(6.5±0.5) ng/ml,P=0.897];+10 Gz치폭로조[(5.9±0.5) ng/ml]명현저우전량조(P =0.018、0.014)화GSH보호조[(7.0±0.5)ng/ml,P＜0.01].결론 +Gz폭로가인기급성위점막손상대서혈장중HSP70적함량변화,고+Gz치폭로가강저기함량,가중위점막손상;환원형곡광감태가제고+ Gz폭로대서혈장중HSP70적함량,강저위점막손상.
Objective To explore the change of plasma heat shock protein 70 (HSP70) in rats exposed to acute gastric mucosal injury under the condition of positive acceleration (+ Gz) and elucidate the effects of glutathione (GSH) and the corresponding protective mechanisms.Methods A total of 40 male SD rats were randomly by computer randomization into 4 groups of ethanol control,+ 5 Gz value exposure,+ 10 Gz value exposure and GSH protection (n =10 each).GSH protection group received adaptive feeding for 7 days and then an intraperitoneal injection of GSH for 3 consecutive days.All 4 groups fasted for 24 hours within 10 days,water deprivation for 12 hours and a gastric lavage of anhydrous ethanol (0.4 ml/ 100 g) for 1 hour,ethanol control group had no acceleration,+5 Gz value exposure group at + 5 Gz and the latter two groups respectively at + 10 Gz for around 3 min.Each group underwent anesthesia of pentobarbital after centrifuge immediately.Abdominal aortic blood samples were collected and gastric tissues harvested for observation of mucosal injury.Mucosal damage index was calculated by the GUTH method.And the plasma content of HSP70 was measured by radioimmunoassay.Results (1) Gastric mucosa of each groups rats were injured.Damage was significantly reduced by GSH pretreatment,ethanol control group had less injury,the injury of + 5 Gz value exposure group was aggravated compared with the control group (gastric mucosal injury index:25.4 (14.0-30.0) vs 10.0 (9.2-13.9),P =0.001); + 10 Gz value exposure group mucosal injury was heaviest(47.2 (41.5-60.1)).There were diffuse hyperemia,edema and erosion with a large area of bleeding spots and fiat mucosal folds.It had statistically significant differences with the first two groups (all P＜0.01) ; GSH protection group was lightest at 9.5 (7.5-14.1).Compared with the + 10 Gz value exposure group,mucosal damage was milder (P ＜0.01).(2) The plasma levels of HSP70 of + 5 Gz value exposure had no significant differences with the control and ethanol groups ((6.5 ± 0.5) ng/ml,P =0.897) ; HSP70 plasma level((5.9 ±_0.5) ng/ml) of + 10 Gz value exposure was significantly lower than those of the first two groups (P =0.018,0.014) ; GSH protection group ((7.0 _± 0.5) ng/ml) was significantly higher than the level of + 10 Gz value exposure group (P ＜ 0.01).Conclusions + Gz exposure may cause the altered levels of plasma HSP70.High + Gz value exposure reduces its content and aggravates gastric mucosal injury.And glutathione reduces the injury of gastric mucosa through elevated plasma HSP70.